The Ambulatory Reversal Program

The Ambulatory Reversal Program

www.themegallery.com

Overview

In today’s society, where inactive lifestyles and obesity are becoming increasingly common, the incidence of diabetes is growing rapidly. Recent economic data shows soaring numbers of money spent and lost to fight diabetes both in the United States and Worldwide.

Diabetes Wellness Clinics of America


Pedro J Martinez, M.D., C.M.C.M.

Board Certified Internal Medicine Board Certified in Managed Care Medicine Board eligible Geriatrics Health Ministries Director, Arizona Conference Office Director, Apologetics, Arizona Conference Commissioned Minister, Arizona Conference Medical Evangelist, Arizona Conference

Guatemala Mexico

Chairman – Health Advisory Committee, NAD Hope Medical Institute, Medical Director Hope Diabetes Center Medical Director PM Ministries [Internet Ministries], Director License Minister Doctor in Practical Ministries –Candidate Master of Art in Biblical Counseling - Candidate


Diabetes Diabetes MellitusMellitus


Diabetes is a serious disease with far-reaching Diabetes is a serious disease with far-reaching consequences.consequences.

In 2007, the disease and its complications cost the In 2007, the disease and its complications cost the United States about United States about $174 billion$174 billion. Direct costs had . Direct costs had doubled since 2000 and costs are expected to continue to doubled since 2000 and costs are expected to continue to increase.increase.

Type 1 and type 2 diabetes currently affect over Type 1 and type 2 diabetes currently affect over 24 24 million Americansmillion Americans, or 8% of the population., or 8% of the population.

Additionally, an estimated 5.2 million people remain undiagnosed, and more than 60 million Americans have pre-diabetes, a precursor condition characterized by plasma glucose levels that are above normal but below the values diagnostic of diabetes



Diabetes – an Unfolding Diabetes – an Unfolding EpidemicEpidemic

world wide will reach 300 world wide will reach 300 million by 2025million by 2025World Health Organisation, World Health Organisation, September 1998September 1998

WHO estimates that the WHO estimates that the number of diabetics number of diabetics

Increase in the number of Increase in the number of people with diabetes from 150 people with diabetes from 150

million million tto 220 million – 10 years o 220 million – 10 years from now – yearly growth of from now – yearly growth of

3.9%.3.9%.Source: Amos A.., McCarty DJ, Source: Amos A.., McCarty DJ,

Zimmet P: Diabet. Med. 1997; 14Zimmet P: Diabet. Med. 1997; 14

150150

220220

20002000 20102010

The cost of treating people with diabetes is The cost of treating people with diabetes is expected to expected to amount to about USD 1 trillion amount to about USD 1 trillion annually – in the US in 2025annually – in the US in 2025Dr G Bernstein, former president of ADADr G Bernstein, former president of ADA



The evolution of mankind

2.5 mn years 50 years



Prevalence of obesity increased by 61% since 1991

More than 50% of US adults are overweight

Body mass index (BMI) and weight gain are major risk factors for diabetes:

BMI 25-30 is overweight

BMI >30 is obese

The Prevalence of Diabetes and Obesity

Mokdad AH, et al. Diabetes Care. 2000;23:1278-1283.Mokdad AH, et al. JAMA. 1999;282:1519-1522.Mokdad AH, et al. JAMA. 2001;286:1195-1200.

72

73

74

75

76

77

78

Pre

vale

nce

(%

)

DiabetesMean Body Weight

kg

Year

4.0

4.5

5.0

5.5

6.0

6.5

7.0

7.5

1990 1992 1994 1996 1998 2000


NormalNormal Type 2 DiabetesType 2 Diabetes

Courtesy of Wilfred Y. Fujimoto, MD.Courtesy of Wilfred Y. Fujimoto, MD.

Visceral Fat Distribution:Visceral Fat Distribution:Normal vs Type 2 DiabetesNormal vs Type 2 Diabetes


Total Prevalence of Diabetes in Americans Aged =20 Years by Age Group (2005)


Current Treatment Goalsfor Glycemic Control

HDC

<6.0%

<100 mg/dL

<140 mg/dL


Metabolic Complications

KetoacidosisHyperosmolar nonketotic syndromeHypoglycemia

Macrovascular Complications

Cardiovascular diseaseCerebrovascular diseasePeripheral vascular disease

Microvascular Complications

Diabetic neuropathyDiabetic retinopathyDiabetic nephropathy

Diabetic Metabolic, Macrovascular, andMicrovascular Complications

Abbott KC, et al. BMC Endocr Disord. 2003;3:1. Reusch JEB. J Clin Invest. 2003;112:986-988. Sheetz MJ, King GL. JAMA. 2002;288:2579-2588.Williams R, et al. Diabetologia. 2002;45:S13-S17.



The Defect

Insulin ResistanceInsulin Resistance

Liver Liver DysfunctionDysfunction

PancreasPancreasDysfunctionDysfunction

Small BowelSmall BowelHormonal ImbalanceHormonal Imbalance



Unmet Therapeutic Needsin Type 2 Diabetes


b-Cell Function Declines Regardless of Intervention in Type 2 Diabetes

Ambulatory Reversal Program

The Ambulatory

Reversal Program

Hope Medical InstituteHope Medical Institute

ARPARP

OverviewOverview The Ambulatory Reversal ProgramThe Ambulatory Reversal Program [[ARPARP] is the ] is the

most cost effective non-residential [out-patient], most cost effective non-residential [out-patient], functional lifestyle and health maintenance functional lifestyle and health maintenance program of its kind.program of its kind.

Based on the Genesis Agenda with the ARP Based on the Genesis Agenda with the ARP protocolsprotocols

It is a broad base, scientifically sounded, evidence It is a broad base, scientifically sounded, evidence based, affordable comprehensive and easy to based, affordable comprehensive and easy to follow lifestyle program follow lifestyle program

Facilitate the transition from a live-in [Residential] Facilitate the transition from a live-in [Residential] to the “real life”to the “real life”

Culturally sensitiveCulturally sensitive Enhances the replication, preservation, and Enhances the replication, preservation, and

regeneration [neogenesis] of the beta cellregeneration [neogenesis] of the beta cell


OverviewOverview

Naturally control the appetite, facilitating a Naturally control the appetite, facilitating a significant amount of weight losssignificant amount of weight loss

Reduce or eliminate the insulin resistanceReduce or eliminate the insulin resistance Is fast, fun, motivating with a high degree of Is fast, fun, motivating with a high degree of

compliancecompliance Our programs emphasize a non-new age Our programs emphasize a non-new age

progressive functional lifestyle, exercise and progressive functional lifestyle, exercise and stress reduction program. stress reduction program.

Although it is not a requirement to be a vegetarian.Although it is not a requirement to be a vegetarian. Our goal is to guide our patient in that direction by Our goal is to guide our patient in that direction by

a gradual, cultural based well balanced process.a gradual, cultural based well balanced process.


OverviewOverview

OffersOffersFreedom of ChoiceFreedom of Choice

Relaxing atmosphereRelaxing atmosphere

Quick SatisfactionQuick Satisfaction

Warranty FullnessWarranty Fullness


Stabilize

Preserve

Damage Control [Restore]

Reversibility

Phases of ARP


1.1. StabilizeStabilize: the first immediate goal is to : the first immediate goal is to stabilize the patient [safety is always our main stabilize the patient [safety is always our main concern] in order to prevent those conditions concern] in order to prevent those conditions that can and will put the patient life in that can and will put the patient life in jeopardy. Results can be seen within days, jeopardy. Results can be seen within days, not weeks, months or yearsnot weeks, months or years

2.2. PreservePreserve. Our intensive program is . Our intensive program is designed to preservedesigned to preserve beta cells that remain in beta cells that remain in your pancreas by slowing and/or eliminating your pancreas by slowing and/or eliminating the destruction of itthe destruction of it

3.3. RestoreRestore: Beta cell regeneration is not : Beta cell regeneration is not Science Fiction. Since 1998 evidence has Science Fiction. Since 1998 evidence has been accumulated pointing in that direction. been accumulated pointing in that direction. – The patient will be empowered with all the tools The patient will be empowered with all the tools

necessary to actively participate in the healing necessary to actively participate in the healing process that will prevent and/or reverse diabetesprocess that will prevent and/or reverse diabetes

4.4. RebuildRebuild: Quality of life is essential to us. : Quality of life is essential to us. – Physically:Physically: A well balance exercise program will A well balance exercise program will

be tailor to every patient needs. be tailor to every patient needs. – Mentally:Mentally: Patient will be able to enjoy the true Patient will be able to enjoy the true

understanding of the positive thinking [based on understanding of the positive thinking [based on evidence not on theory] evidence not on theory]

The Deadly Quartet

Abdominal ObesityAbdominal Obesity Men: > 102 cm [>40 in] Men: > 102 cm [>40 in] Female: >88 cm [35 in]Female: >88 cm [35 in]

DyslipidemiaDyslipidemia Triglycerides > 150Triglycerides > 150 HDL <40 in men, < 50 in femaleHDL <40 in men, < 50 in female

Fasting glucose >110Fasting glucose >110High blood pressure >130/85High blood pressure >130/85

Our Goal

A normal glycated hemoglobin

(HbA1c), the same as a person

without diabetes

MissionTo improve the quality of lives and

to reduce or eliminate diabetes complications through a new

community outreach, evidence and scientifically based program. ARP is

based on an innovative and new treatment paradigm, education and

research, leading to the prevention and/or reversal of Diabetes Mellitus

Our Philosophy “One of the mantras of diabetes care is that the

patient should be in charge”

Patient-Centered Care

Synchronized Secuence of Event


The Issues

Diagnosis1. Type I2. Type II

Production• Apoptosis• Neo-genesis• Stress• Gluco-

toxicity• Lipo-toxicity

Diabetes

Utilization•Insulin resistance•Visceral Obesity

Hormonal Balance

•Glucagon•GLP-1•Adrenal system

11 Reduce Apoptosis

New Treatment ParadigmNew Treatment Paradigm

22 Increase Beta Cell Replication

33 Increase GLP-1

44 Reduce Glucagon

55 Decrease Free Fatty Acids

66 Decrease Insulin Resistance

77 Reduce Hyperinsulinemia

Woerle H, et al., Diabetes 2003;52”[Suppl 1]:A351

Synchronized Sequence

Reversibility

Regenerator

Damage control

Stabilization

Psychological /Spirit

Complementary Med

DiaFiber Plus

ARP Protocol

Clinical Flow

7 days

Collect Inform

ation

Stabilization

Focus on Physiology

Stabilization

Initiate Level 1S

tabilization

Monitor P

rogress

Dam

age Control

First visit 2nd Visit 3rd Visit 4» Visit

14 days14 days 21 days21 days

Services and Programs


Fundamental Defect

Increased PP

Overprod Glu

High Elev SPM

Insulin Resistance

•Acquired•Obesity•Unhealthy lifestyle•Medication•Glucose toxicities•Lipo-toxicities

Impaired Insulin Release

•Genetics•Glucose toxicities•Lipo-toxicities

Glucagon AbnormalitiesGlucagon Abnormalities

Pre & Post HyperglycemiaPre & Post Hyperglycemia

Woerle H, et al., Diabetes 2003;52”[Suppl 1]:A351

Pancreatic Dysfunction

PancreasPancreas

DISDIS

DSGDSG

CBCMCBCM

ACAACA

IERIIERIImpaired

Early Release of Insulin

Decreased Insulin Secretion

Decreased Beta Cell Mass

Decreased Sensitivity to

Glucose

Decreased secretion of

Amylin

Beta Cell function

1

Apoptosis [program death of cell]

Prevention•Fiber•Post-prandial walk

2

Beta Cell Replication

Prevention•Fiber•GLP-1

3

Neogenesis

Prevention•Fiber•GLP-1•Altern. Med.

Butler AE, et al. Diabetes. 2003,52:102-110

Postprandial Abnormalities in People with Type 2 Diabetes

Reduced early insulin release, increased glucagon secretion

Increased glucose release From meal -- reduced hepatic sequestration Endogenously produced

• Liver -- increased glycogenolysis and gluconeogenesis • Kidney -- increased gluconeogenesis

Abnormal routes of glucose disposal Decreased oxidation Increased nonoxidative glycolysis Increased hepatic glycogen cycling Decreased muscle glucose uptake Increased glucose uptake in other tissues (eg, kidney)

Real Issues

Methods

How are we doing this?

Portion

Calories

Appetite

Education

Compliance

Satisfaction

A Century of Diabetes CareA Century of Diabetes Care

DCCT

UKPDS

Pump thera

py

Human insulin

Insulin analogsType 1

20001900 19501920

Insulin therapy

Sulfonylureas

Alpha-glucosidase InhibitorsBiguanide

GlitazonesMeglitinides

Insulin therapy

1920

Type 2

20001900 1950

Diet

The CostDiabetes Wellness Clinics of America

The Cost

Diabetes MellitusDiabetes Mellitus•Production [Homa B]Production [Homa B]

•Absolute deficiency of insulinAbsolute deficiency of insulin•Relative deficiency of insulinRelative deficiency of insulin

•Utilization [Homa R]Utilization [Homa R]•Insulin resistance Insulin resistance

““Ticking Clock” Ticking Clock” HypothesisHypothesis

WHO. WHO. DiabetologiaDiabetologia 1985;28:615-640; Haffner SM et al. 1985;28:615-640; Haffner SM et al. JAMA JAMA 1990;263:2893-2898.1990;263:2893-2898.

ForFor

Microvascular Microvascular complicationscomplications

Macrovascular Macrovascular complicationscomplications

The “clock starts ticking”The “clock starts ticking”

At onset of hyperglycemiaAt onset of hyperglycemia

Before the diagnosis of Before the diagnosis of hyperglycemiahyperglycemia

ARP -PhysicianARP -Physician

1st Structured –office 1st Structured –office basedbased

Provider orientedProvider oriented provider to intervene on provider to intervene on

timetime Evidence basedEvidence based Scientifically groundedScientifically grounded Clinically testedClinically tested HelpHelp

Helps to target the root Helps to target the root of the problems, no just of the problems, no just the numbersthe numbers

Empower physicianEmpower physician Financially attractiveFinancially attractive FastFast

– Glycemic controlGlycemic control– Weight controlWeight control

ARP -PatientARP -Patient

Facilitate gradual Facilitate gradual lifestyle changeslifestyle changes

Eliminate craving and Eliminate craving and food addiction food addiction

Helps patient to feel free Helps patient to feel free of counting caloriesof counting calories

Empower patientEmpower patient Helps to eliminate in a Helps to eliminate in a

safe and timely fashion, safe and timely fashion, unnecessary drugsunnecessary drugs

Culturally sensitiveCulturally sensitive High complianceHigh compliance Fast Fast Simple and affordableSimple and affordable Improve self-esteemImprove self-esteem Always full and Always full and

satisfiedsatisfied Appetite control Appetite control

without drugs = without drugs = weight lossweight loss

The Toxic Effect of Sugar


Metabolic Pathways Leading to Metabolic Pathways Leading to Diabetic Microvascular Complications Diabetic Microvascular Complications

The Fiber Facto

Increase in fiber intake reduces the Increase in fiber intake reduces the risk of having diabetes by 39% (P = risk of having diabetes by 39% (P = 0.026) whereas the same increase in 0.026) whereas the same increase in protein intake increases the risk by protein intake increases the risk by 38% 38%

Low dietary fiber and high protein Low dietary fiber and high protein intakes associated withintakes associated with newly newly diagnosed diabetes in a remote diagnosed diabetes in a remote aboriginal community.aboriginal community.

The Importance of Fiber

The New England The New England Journal of Medicine Journal of Medicine 5/11/005/11/00

A high intake of dietary fiber A high intake of dietary fiber (50gms), particularly of the (50gms), particularly of the soluble type, above the level soluble type, above the level recommended by the ADA recommended by the ADA (35gm), in patients with type 2 (35gm), in patients with type 2 diabetes.diabetes.– improves glycemic controlimproves glycemic control– decreases hyperinsulinemiadecreases hyperinsulinemia– lowers plasma lipid lowers plasma lipid

concentrationsconcentrations

IncomeIncome

US DiabeticsUS Diabetics

Thank You!!!! Martin Pintos305-766-9643

[email protected]

Martin Pintos305-766-9643

[email protected]

Ambulatory care is any medical care delivered on an outpatient basis. Many medical conditions do not require hospital admission and can be managed without admission to a hospital.

Ambulatory care is any medical care delivered on an outpatient basis. Many medical conditions do not require hospital admission and can be managed without admission to a hospital.

Ambulatory

Insulin resistance (IR) is the condition in which normal amounts of insulin are inadequate to produce a normal insulin response from fat, muscle and liver cells.

Insulin resistance in fat cells reduces the effects of insulin and results in elevated hydrolysis of stored triglycerides in the absence of measures which either increase insulin sensitivity or which provide additional insulin. Increased mobilization of stored lipids in these cells elevates free fatty acids in the blood plasma.

Insulin resistance in muscle cells reduces glucose uptake (and so local storage of glucose as glycogen), whereas insulin resistance in liver cells results in impaired glycogen synthesis and a failure to suppress glucose production. High plasma levels of insulin and glucose due to insulin resistance are believed to be the origin of metabolic syndrome and type 2 diabetes, including its complications.




Insulin resistance (IR)Insulin resistance is a condition in which the body produces insulin but does not use

it properly.







Insulin resistance (IR)Part I

Insulin resistance is a condition in which the body produces insulin but does not use it properly. Insulin, a hormone made by the pancreas, helps the body use glucose for energy. Glucose is a form of sugar that is the body’s main source of energy.

The body’s digestive system breaks food down into glucose, which then travels in the bloodstream to cells throughout the body. Glucose in the blood is called blood glucose, also known as blood sugar. As the blood glucose level rises after a meal, the pancreas releases insulin to help cells take in and use the glucose.

When people are insulin resistant, their muscle, fat, and liver cells do not respond properly to insulin. As a result, their bodies need more insulin to help glucose enter cells. The pancreas tries to keep up with this increased demand for insulin by producing more. Eventually, the pancreas fails to keep up with the body’s need for insulin. Excess glucose builds up in the bloodstream, setting the stage for diabetes. Many people with insulin resistance have high levels of both glucose and insulin circulating in their blood at the same time.

Insulin resistance increases the chance of developing type 2 diabetes and heart disease. Learning about insulin resistance is the first step toward making lifestyle changes that can help prevent diabetes and other health problems.

Insulin resistance is a condition in which the body produces insulin but does not use it properly. Insulin, a hormone made by the pancreas, helps the body use glucose for energy. Glucose is a form of sugar that is the body’s main source of energy.

The body’s digestive system breaks food down into glucose, which then travels in the bloodstream to cells throughout the body. Glucose in the blood is called blood glucose, also known as blood sugar. As the blood glucose level rises after a meal, the pancreas releases insulin to help cells take in and use the glucose.

When people are insulin resistant, their muscle, fat, and liver cells do not respond properly to insulin. As a result, their bodies need more insulin to help glucose enter cells. The pancreas tries to keep up with this increased demand for insulin by producing more. Eventually, the pancreas fails to keep up with the body’s need for insulin. Excess glucose builds up in the bloodstream, setting the stage for diabetes. Many people with insulin resistance have high levels of both glucose and insulin circulating in their blood at the same time.

Insulin resistance increases the chance of developing type 2 diabetes and heart disease. Learning about insulin resistance is the first step toward making lifestyle changes that can help prevent diabetes and other health problems.

Insulin resistance (IR)Part II

Impaired fasting blood sugar, impaired glucose tolerance, or type 2 diabetes. This occurs because the pancreas is unable to turn out enough insulin to overcome the insulin resistance. Blood sugar levels rise and diabetes is diagnosed.

High blood pressure. The mechanism is unclear, but studies suggest that the worse the blood pressure, the worse the insulin resistance.

Abnormal cholesterol levels. The typical cholesterol levels of a person with insulin resistance are low HDL, or good cholesterol, and high levels of another blood fat called triglycerides.

Heart disease. The insulin resistance syndrome can result in atherosclerosis (hardening of the arteries) and an increased risk of blood clots.

Obesity. A major factor in the development of insulin resistance syndrome is obesity -- especially abdominal obesity or belly fat. Obesity promotes insulin resistance and negatively impacts insulin responsiveness in a person. Weight loss can improve the body's ability to recognize and use insulin appropriately.

Kidney damage. Protein in the urine is a sign that kidney damage has occurred, although not everyone uses this component to define insulin resistant syndrome.

Insulin resistance (IR)What Are The Signs of Insulin Resistance

Syndrome?

Part III

Apoptosis .[1] is the process of programmed cell death (PCD) that may occur in multicellular organisms. Programmed cell death involves a series of biochemical events leading to a characteristic cell morphology and death, in more specific terms, a series of biochemical events that lead to a variety of morphological changes, including blebbing, changes to the cell membrane such as loss of membrane asymmetry and attachment, cell shrinkage, nuclear fragmentation, chromatin condensation, and chromosomal DNA fragmentation (1-4).

Apoptosis .[1] is the process of programmed cell death (PCD) that may occur in multicellular organisms. Programmed cell death involves a series of biochemical events leading to a characteristic cell morphology and death, in more specific terms, a series of biochemical events that lead to a variety of morphological changes, including blebbing, changes to the cell membrane such as loss of membrane asymmetry and attachment, cell shrinkage, nuclear fragmentation, chromatin condensation, and chromosomal DNA fragmentation (1-4).

Apoptosis

Glucagon-like peptide-1 (GLP-1) is derived from the transcription product of the proglucagon gene. Proglucagon is a precursor of glucagon, and several other components. It is generated in the alpha cells of the pancreas, and it consists of the following: Oxyntomodulin is a naturally occurring 37 amino acid peptide hormone found in the colon, produced by the oxyntic (fundic) cells of the oxyntic (fundic) mucosa. It has been found to suppress appetite.

The major source of GLP-1 in the body is the intestinal L cell that secretes GLP-1 as a gut hormone. GLP-1 secretion by L cells is dependent on the presence of nutrients in the lumen of the small intestine. The secretagogues (agents that cause or stimulate secretion) of this hormone include major nutrients like carbohydrate, protein and lipid. Once in the circulation, GLP-1 has a half life of less than 2 minutes, due to rapid degradation by the enzyme dipeptidyl peptidase-4.

Glucagon-like peptide-1 (GLP-1) is derived from the transcription product of the proglucagon gene. Proglucagon is a precursor of glucagon, and several other components. It is generated in the alpha cells of the pancreas, and it consists of the following: Oxyntomodulin is a naturally occurring 37 amino acid peptide hormone found in the colon, produced by the oxyntic (fundic) cells of the oxyntic (fundic) mucosa. It has been found to suppress appetite.

The major source of GLP-1 in the body is the intestinal L cell that secretes GLP-1 as a gut hormone. GLP-1 secretion by L cells is dependent on the presence of nutrients in the lumen of the small intestine. The secretagogues (agents that cause or stimulate secretion) of this hormone include major nutrients like carbohydrate, protein and lipid. Once in the circulation, GLP-1 has a half life of less than 2 minutes, due to rapid degradation by the enzyme dipeptidyl peptidase-4.

Glucagon-like peptide-1 (GLP-1)

Glucagon is an important hormone involved in carbohydrate metabolism. Produced by the pancreas, it is released when the glucose level in the blood is low (hypoglycemia), causing the liver to convert stored glycogen into glucose and release it into the bloodstream. The action of glucagon is thus opposite to that of insulin, which instructs the body's cells to take in glucose from the blood. However, glucagon also paradoxically stimulates the release of insulin, so that newly available glucose in the bloodstream can be up taken and used by insulin-dependent tissues.

Glucagon is an important hormone involved in carbohydrate metabolism. Produced by the pancreas, it is released when the glucose level in the blood is low (hypoglycemia), causing the liver to convert stored glycogen into glucose and release it into the bloodstream. The action of glucagon is thus opposite to that of insulin, which instructs the body's cells to take in glucose from the blood. However, glucagon also paradoxically stimulates the release of insulin, so that newly available glucose in the bloodstream can be up taken and used by insulin-dependent tissues.

Glucagon

Fatty acids can be bound or attached to other molecules, such as in triglycerides or phospholipids. When they are not attached to other molecules, they are known as "free" fatty acids.

The uncombined fatty acids or free fatty acids may come from the breakdown of a triglyceride into its components (fatty acids and glycerol). However as fats are insoluble in water they must be bound to appropriate regions in the plasma protein albumin for transport around the body. The levels of "free fatty acid" in the blood are limited by the number of albumin binding sites available.

Free fatty acids are an important source of fuel for many tissues since they can yield relatively large quantities of ATP(Adenosine-5'-triphosphate ATP transports chemical energy within cells for metabolism).

Many cell types can use either glucose or fatty acids for this purpose. In particular, heart and skeletal muscle prefer fatty acids. The brain cannot use fatty acids as a source of fuel; it relies on glucose, or on ketone bodies. Ketone bodies are produced in the liver by fatty acid metabolism during starvation, or during periods of low carbohydrate intake.

Fatty acids can be bound or attached to other molecules, such as in triglycerides or phospholipids. When they are not attached to other molecules, they are known as "free" fatty acids.

The uncombined fatty acids or free fatty acids may come from the breakdown of a triglyceride into its components (fatty acids and glycerol). However as fats are insoluble in water they must be bound to appropriate regions in the plasma protein albumin for transport around the body. The levels of "free fatty acid" in the blood are limited by the number of albumin binding sites available.

Free fatty acids are an important source of fuel for many tissues since they can yield relatively large quantities of ATP(Adenosine-5'-triphosphate ATP transports chemical energy within cells for metabolism).

Many cell types can use either glucose or fatty acids for this purpose. In particular, heart and skeletal muscle prefer fatty acids. The brain cannot use fatty acids as a source of fuel; it relies on glucose, or on ketone bodies. Ketone bodies are produced in the liver by fatty acid metabolism during starvation, or during periods of low carbohydrate intake.

Fatty acids

Hyperinsulinemia, present in people with diabetes mellitus type 2 or insulin resistance where excess levels of circulating insulin are in the blood. It is not diabetes, but it is often associated with metabolic syndrome and type 2 Diabetes.

Hyperinsulinemia, present in people with diabetes mellitus type 2 or insulin resistance where excess levels of circulating insulin are in the blood. It is not diabetes, but it is often associated with metabolic syndrome and type 2 Diabetes.

Hyperinsulinemia

The term Sagittal Abdominal Diameter (SAD) is a measure of Visceral Obesity[1]. In layman's terms, this is the size of one's belly. More specifically, SAD represents the distance from your back to your upper abdomen, midway between the top of the pelvis and the bottom of the ribs, measured while standing[2]. The term Sagittal Abdominal Diameter (SAD) is a measure of Visceral Obesity

The term Sagittal Abdominal Diameter (SAD) is a measure of Visceral Obesity[1]. In layman's terms, this is the size of one's belly. More specifically, SAD represents the distance from your back to your upper abdomen, midway between the top of the pelvis and the bottom of the ribs, measured while standing[2]. The term Sagittal Abdominal Diameter (SAD) is a measure of Visceral Obesity

Sagittal Abdominal Diameter (SAD)

In mammals, the adrenal glands (also known as suprarenal glands) are the star-shaped endocrine glands that sit on top of the kidneys; their name indicates that position (ad-, "near" or "at" + renes, "kidneys"; and as concerns supra-, meaning "above"). They are chiefly responsible for regulating the stress response through the synthesis of corticosteroids and catecholamines, including cortisol and adrenaline, respectively.

In mammals, the adrenal glands (also known as suprarenal glands) are the star-shaped endocrine glands that sit on top of the kidneys; their name indicates that position (ad-, "near" or "at" + renes, "kidneys"; and as concerns supra-, meaning "above"). They are chiefly responsible for regulating the stress response through the synthesis of corticosteroids and catecholamines, including cortisol and adrenaline, respectively.

Adrenal glands

Insulin is a hormone with extensive effects on both metabolism and several other body systems (eg, vascular compliance). Insulin causes most of the body's cells to take up glucose from the blood (including liver, muscle, and fat tissue cells), storing it as glycogen in the liver and muscle, and stops use of fat as an energy source. When insulin is absent (or low), glucose is not taken up by most body cells and the body begins to use fat as an energy source (ie, transfer of lipids from adipose tissue to the liver for mobilization as an energy source). As its level is a central metabolic control mechanism, its status is also used as a control signal to other body systems (such as amino acid uptake by body cells). It has several other anabolic effects throughout the body. When control of insulin levels fails, diabetes mellitus results.

Insulin is used medically to treat some forms of diabetes mellitus. Patients with Type 1 diabetes mellitus depend on external insulin (most commonly injected subcutaneously) for their survival because the hormone is no longer produced internally. Patients with Type 2 diabetes mellitus are insulin resistant, have relatively low insulin production, or both; some patients with Type 2 diabetes may eventually require insulin when other medications fail to control blood glucose levels adequately. Insulin is a peptide hormone composed of 51 amino acid residues.

Insulin is a hormone with extensive effects on both metabolism and several other body systems (eg, vascular compliance). Insulin causes most of the body's cells to take up glucose from the blood (including liver, muscle, and fat tissue cells), storing it as glycogen in the liver and muscle, and stops use of fat as an energy source. When insulin is absent (or low), glucose is not taken up by most body cells and the body begins to use fat as an energy source (ie, transfer of lipids from adipose tissue to the liver for mobilization as an energy source). As its level is a central metabolic control mechanism, its status is also used as a control signal to other body systems (such as amino acid uptake by body cells). It has several other anabolic effects throughout the body. When control of insulin levels fails, diabetes mellitus results.

Insulin is used medically to treat some forms of diabetes mellitus. Patients with Type 1 diabetes mellitus depend on external insulin (most commonly injected subcutaneously) for their survival because the hormone is no longer produced internally. Patients with Type 2 diabetes mellitus are insulin resistant, have relatively low insulin production, or both; some patients with Type 2 diabetes may eventually require insulin when other medications fail to control blood glucose levels adequately. Insulin is a peptide hormone composed of 51 amino acid residues.

Insulin

Sulfonylurea (UK: Sulphonylurea) derivatives are a class of antidiabetic drugs that are used in the management of diabetes mellitus type 2 ("adult-onset"). They act by increasing insulin release from the beta cells in the pancreas.

Sulfonylurea (UK: Sulphonylurea) derivatives are a class of antidiabetic drugs that are used in the management of diabetes mellitus type 2 ("adult-onset"). They act by increasing insulin release from the beta cells in the pancreas.

Sulfonylurea(Drug)

Metformin (INN; trade names Glucophage, Riomet, Fortamet, Glumetza, Obimet, Dianben, Diabex, Diaformin, and others) is an oral anti-diabetic drug from the biguanide class. It is the first-line drug for the treatment of type 2 diabetes, particularly in overweight and obese people and those with normal kidney function,[1][2][3] and evidence suggests it may be the best choice for people with heart failure.[4] Metformin is the most popular anti-diabetic drug in the United States and one of the most prescribed drugs in the country overall, with nearly 35 million prescriptions filled in 2006 for generic metformin alone.[5] It is also used in the treatment of polycystic ovary syndrome.

Metformin (INN; trade names Glucophage, Riomet, Fortamet, Glumetza, Obimet, Dianben, Diabex, Diaformin, and others) is an oral anti-diabetic drug from the biguanide class. It is the first-line drug for the treatment of type 2 diabetes, particularly in overweight and obese people and those with normal kidney function,[1][2][3] and evidence suggests it may be the best choice for people with heart failure.[4] Metformin is the most popular anti-diabetic drug in the United States and one of the most prescribed drugs in the country overall, with nearly 35 million prescriptions filled in 2006 for generic metformin alone.[5] It is also used in the treatment of polycystic ovary syndrome.

Metformin(Drug)

Glibenclamide (INN), also known as glyburide (USAN), is an anti-diabetic drug in a class of medications known as sulfonylureas, It is sold in doses of 1.25 mg, 2.5 mg and 5 mg, under the trade names Diabeta, Glynase and Micronase in the United States and Daonil, Semi-Daonil and Euglucon in the United Kingdom. It is also sold in combination with metformin under the trade name Glucovance.

Glibenclamide (INN), also known as glyburide (USAN), is an anti-diabetic drug in a class of medications known as sulfonylureas, It is sold in doses of 1.25 mg, 2.5 mg and 5 mg, under the trade names Diabeta, Glynase and Micronase in the United States and Daonil, Semi-Daonil and Euglucon in the United Kingdom. It is also sold in combination with metformin under the trade name Glucovance.

Glibenclamide(Drug)

Chlorpropamide is an example of a drug class called sulphonylureas (derivatives are a class of antidiabetic drugs that are used in the management of diabetes mellitus type 2 . They act by increasing insulin release from the beta cells in the pancreas).

Chlorpropamide is an example of a drug class called sulphonylureas (derivatives are a class of antidiabetic drugs that are used in the management of diabetes mellitus type 2 . They act by increasing insulin release from the beta cells in the pancreas).

Chlorpropamide(Drug)

Edema formerly known as dropsy or hydropsy, is an abnormal accumulation of fluid beneath the skin, or in one or more cavities of the body. Generally, the amount of interstitial fluid is determined by the balance of fluid homeostasis, and increased secretion of fluid into the interstitium or impaired removal of this fluid may cause edema.

Five factors can contribute to the formation of edema. It may be facilitated by increased hydrostatic pressure or reduced oncotic pressure within blood vessels, increased blood vessel wall permeability as in inflammation, obstruction of fluid clearance via the lymphatic or changes in the water retaining properties of the tissues themselves. Raised hydrostatic pressure often reflects retention of water and sodium by the kidney.[1

Edema formerly known as dropsy or hydropsy, is an abnormal accumulation of fluid beneath the skin, or in one or more cavities of the body. Generally, the amount of interstitial fluid is determined by the balance of fluid homeostasis, and increased secretion of fluid into the interstitium or impaired removal of this fluid may cause edema.

Five factors can contribute to the formation of edema. It may be facilitated by increased hydrostatic pressure or reduced oncotic pressure within blood vessels, increased blood vessel wall permeability as in inflammation, obstruction of fluid clearance via the lymphatic or changes in the water retaining properties of the tissues themselves. Raised hydrostatic pressure often reflects retention of water and sodium by the kidney.[1

Edema

Metabolism is the set of chemical reactions that occur in living organisms in order to maintain life. These processes allow organisms to grow and reproduce, maintain their structures, and respond to their environments. Metabolism is usually divided into two categories. Catabolism breaks down organic matter, for example to harvest energy in cellular respiration. Anabolism, on the other hand, uses energy to construct components of cells such as proteins and nucleic acids.

The chemical reactions of metabolism are organized into metabolic pathways, in which one chemical is transformed into another by a sequence of enzymes. Enzymes are crucial to metabolism because they allow organisms to drive desirable but thermodynamically unfavorable reactions by coupling them to favorable ones, and because they act as catalysts to allow these reactions to proceed quickly and efficiently. Enzymes also allow the regulation of metabolic pathways in response to changes in the cell's environment or signals from other cells.

Metabolism is the set of chemical reactions that occur in living organisms in order to maintain life. These processes allow organisms to grow and reproduce, maintain their structures, and respond to their environments. Metabolism is usually divided into two categories. Catabolism breaks down organic matter, for example to harvest energy in cellular respiration. Anabolism, on the other hand, uses energy to construct components of cells such as proteins and nucleic acids.

The chemical reactions of metabolism are organized into metabolic pathways, in which one chemical is transformed into another by a sequence of enzymes. Enzymes are crucial to metabolism because they allow organisms to drive desirable but thermodynamically unfavorable reactions by coupling them to favorable ones, and because they act as catalysts to allow these reactions to proceed quickly and efficiently. Enzymes also allow the regulation of metabolic pathways in response to changes in the cell's environment or signals from other cells.

Metabolism

Macrovascular disease is a disease of any large (macro) blood vessels in the body.

This sometimes occurs when a person has had diabetes for a long time. Fat and blood clots build up in the large blood vessels and stick to the vessel walls.

Three common macrovascular diseases are coronary disease (in the heart), cerebrovascular disease (in the brain), and peripheral vascular disease (in the limbs)

Macrovascular disease is a disease of any large (macro) blood vessels in the body.

This sometimes occurs when a person has had diabetes for a long time. Fat and blood clots build up in the large blood vessels and stick to the vessel walls.

Three common macrovascular diseases are coronary disease (in the heart), cerebrovascular disease (in the brain), and peripheral vascular disease (in the limbs)

Macrovascular

Microangiopathy (or microvascular disease) is an angiopathy affecting small blood vessels in the body.[1] It can be contrasted to macroangiopathy.

Microangiopathy (or microvascular disease) is an angiopathy affecting small blood vessels in the body.[1] It can be contrasted to macroangiopathy.

Microangiopathy

Pathophysiology - This sometimes occurs when a person has had diabetes mellitus for a long time. High blood glucose levels cause the endothelial cells lining the blood vessels to take in more glucose than normal (these cells do not depend on insulin). They then form more glycoproteins on their surface than normal, and also cause the basement membrane to grow thicker and weaker. The walls of the vessels become abnormally thick but weak, and therefore they bleed, leak protein, and slow the flow of blood through the body. Then some cells, for example in the retina (diabetic retinopathy) or kidney (diabetic nephropathy), may not get enough blood and may be damaged. Nerves, if not sufficiently supplied with blood, are also damaged which may lead to loss of function (diabetic neuropathy).

Pathophysiology - This sometimes occurs when a person has had diabetes mellitus for a long time. High blood glucose levels cause the endothelial cells lining the blood vessels to take in more glucose than normal (these cells do not depend on insulin). They then form more glycoproteins on their surface than normal, and also cause the basement membrane to grow thicker and weaker. The walls of the vessels become abnormally thick but weak, and therefore they bleed, leak protein, and slow the flow of blood through the body. Then some cells, for example in the retina (diabetic retinopathy) or kidney (diabetic nephropathy), may not get enough blood and may be damaged. Nerves, if not sufficiently supplied with blood, are also damaged which may lead to loss of function (diabetic neuropathy).

Pathophysiology

Hypoglycemia can produce a variety of symptoms and effects but the principal problems arise from an inadequate supply of glucose as fuel to the brain, resulting in impairment of function (neuroglycopenia). Derangements of function can range from vaguely "feeling bad" to coma, anymous seizures, and (rarely) permanent brain damage or death.

The most common forms of moderate and severe hypoglycemia occur as a complication of treatment of diabetes mellitus treated with insulin or less frequently with certain oral medications. Hypoglycemia is usually treated by the ingestion or administration of dextrose, or foods quickly digestible to glucose.

Endocrinologists (specialists in hormones, including those which regulate glucose metabolism) typically consider the following criteria (referred to as Whipple's triad) as proving that individual's symptoms can be attributed to hypoglycemia:1. Symptoms known to be caused by hypoglycemia 2. Low glucose at the time the symptoms occur 3. Reversal or improvement of symptoms or problems when the glucose is

restored to normal

Hypoglycemia can produce a variety of symptoms and effects but the principal problems arise from an inadequate supply of glucose as fuel to the brain, resulting in impairment of function (neuroglycopenia). Derangements of function can range from vaguely "feeling bad" to coma, anymous seizures, and (rarely) permanent brain damage or death.

The most common forms of moderate and severe hypoglycemia occur as a complication of treatment of diabetes mellitus treated with insulin or less frequently with certain oral medications. Hypoglycemia is usually treated by the ingestion or administration of dextrose, or foods quickly digestible to glucose.

Endocrinologists (specialists in hormones, including those which regulate glucose metabolism) typically consider the following criteria (referred to as Whipple's triad) as proving that individual's symptoms can be attributed to hypoglycemia:1. Symptoms known to be caused by hypoglycemia 2. Low glucose at the time the symptoms occur 3. Reversal or improvement of symptoms or problems when the glucose is

restored to normal

Hypoglycemia

Nonketotic hyperosmolar coma (nonketotic hyperglycaemia) is a type of diabetic coma associated with a high mortality seen in diabetes mellitus type 2. The preferred term used by the American Diabetes Association is hyperosmolar nonketotic state (HNS). Other commonly used names are hyperosmolar hyperglycemic nonketotic coma (HHNKC)[1] or hyperosmotic non-ketotic (HONK).It is also called Hyperglycaemic Hyperosmolar State(HHS),as some patients may have some ketonuria and it does not necessarily cause coma.

Nonketotic hyperosmolar coma (nonketotic hyperglycaemia) is a type of diabetic coma associated with a high mortality seen in diabetes mellitus type 2. The preferred term used by the American Diabetes Association is hyperosmolar nonketotic state (HNS). Other commonly used names are hyperosmolar hyperglycemic nonketotic coma (HHNKC)[1] or hyperosmotic non-ketotic (HONK).It is also called Hyperglycaemic Hyperosmolar State(HHS),as some patients may have some ketonuria and it does not necessarily cause coma.

Nonketotic hyperosmolar coma

Ketoacidosis is a type of metabolic acidosis which is caused by high concentrations of ketone bodies, formed by the deamination of amino acids, and the breakdown of fatty acids. The two common ketones produced in humans are acetoacetic acid and β-hydroxybutyrate.

This is most common in untreated type 1 diabetes mellitus, when the liver breaks down fat and proteins in response to a perceived need for respiratory substrate. It can also occur with people undergoing hunger strikes, lasting over 3 days, or people in a starvation state as the body is forced to break down fat for sustenance due to their lack of outside nutrition.

Ketoacidosis can be smelled on a person's breath. This is due to acetone, a direct byproduct of the spontaneous decomposition of acetoacetic acid. It is often described as smelling like fruit or nail polish remover.[1]

Ketoacidosis should not be confused with ketosis, which is one of the body's normal processes for the metabolism of body fat. In ketoacidosis, the body fails to adequately regulate ketone production causing such a severe accumulation of keto acids that the pH of the blood is substantially decreased.

Ketoacidosis is a type of metabolic acidosis which is caused by high concentrations of ketone bodies, formed by the deamination of amino acids, and the breakdown of fatty acids. The two common ketones produced in humans are acetoacetic acid and β-hydroxybutyrate.

This is most common in untreated type 1 diabetes mellitus, when the liver breaks down fat and proteins in response to a perceived need for respiratory substrate. It can also occur with people undergoing hunger strikes, lasting over 3 days, or people in a starvation state as the body is forced to break down fat for sustenance due to their lack of outside nutrition.

Ketoacidosis can be smelled on a person's breath. This is due to acetone, a direct byproduct of the spontaneous decomposition of acetoacetic acid. It is often described as smelling like fruit or nail polish remover.[1]

Ketoacidosis should not be confused with ketosis, which is one of the body's normal processes for the metabolism of body fat. In ketoacidosis, the body fails to adequately regulate ketone production causing such a severe accumulation of keto acids that the pH of the blood is substantially decreased.

Ketoacidosis

Hb1c - Glycosylated (or glycated) hemoglobin (hemoglobin A1c, Hb1c , or HbA1c, A1C) is a form of

hemoglobin used primarily to identify the average plasma glucose concentration over prolonged periods of time. It is formed in a non-enzymatic pathway by hemoglobin's normal exposure to high plasma levels of glucose. Glycosylation of hemoglobin has been implicated in nephropathy and retinopathy in diabetes mellitus. Monitoring the HbA1c in type-1 diabetic patients may

improve treatment.[ Measuring A1c

Hb1c - Glycosylated (or glycated) hemoglobin (hemoglobin A1c, Hb1c , or HbA1c, A1C) is a form of

hemoglobin used primarily to identify the average plasma glucose concentration over prolonged periods of time. It is formed in a non-enzymatic pathway by hemoglobin's normal exposure to high plasma levels of glucose. Glycosylation of hemoglobin has been implicated in nephropathy and retinopathy in diabetes mellitus. Monitoring the HbA1c in type-1 diabetic patients may

improve treatment.[ Measuring A1c

HbA1c - Glycosylated

Impaired Glucose Tolerance (IGT) is a pre-diabetic state of dysglycemia, that is associated with insulin resistance and increased risk of cardiovascular pathology. IGT may precede type 2 diabetes mellitus by many years. IGT is also a risk factor for mortality.[

Impaired Glucose Tolerance (IGT) is a pre-diabetic state of dysglycemia, that is associated with insulin resistance and increased risk of cardiovascular pathology. IGT may precede type 2 diabetes mellitus by many years. IGT is also a risk factor for mortality.[

Impaired Glucose Tolerance (IGT)

Hypertension, also referred to as high blood pressure, HTN or HPN, is a medical condition in which the blood pressure is chronically elevated. In current usage, the word "hypertension"[1] without a qualifier normally refers to systemic, arterial hypertension.[2

Hypertension, also referred to as high blood pressure, HTN or HPN, is a medical condition in which the blood pressure is chronically elevated. In current usage, the word "hypertension"[1] without a qualifier normally refers to systemic, arterial hypertension.[2

Hypertension

Polycystic ovary syndrome (PCOS) is an endocrine disorder that affects approximately 5% of all women.[1] It occurs amongst all races and nationalities, is the most common hormonal disorder among women of reproductive age, and is a leading cause of infertility.[2][3]

The principal features are weight problems, lack of regular ovulation and/or menstruation, and excessive amounts or effects of androgenic (masculinizing) hormones. The symptoms and severity of the syndrome vary greatly among women. While the causes are unknown, insulin resistance, diabetes, and obesity are all strongly correlated with PCOS.

Polycystic ovary syndrome (PCOS) is an endocrine disorder that affects approximately 5% of all women.[1] It occurs amongst all races and nationalities, is the most common hormonal disorder among women of reproductive age, and is a leading cause of infertility.[2][3]

The principal features are weight problems, lack of regular ovulation and/or menstruation, and excessive amounts or effects of androgenic (masculinizing) hormones. The symptoms and severity of the syndrome vary greatly among women. While the causes are unknown, insulin resistance, diabetes, and obesity are all strongly correlated with PCOS.

Polycystic ovary syndrome (PCOS)

Beta cells (beta-cells, β-cells) are a type of cell in the pancreas in areas called the islets of Langerhans. They make up 65-80% of the cells in the islets. Beta cells make and release insulin, a hormone that controls the level of Glucose in the blood. There is a baseline level of Glucose maintained by the liver, but it can respond quickly to spikes in blood glucose by releasing stored insulin while simultaneously producing more. The response time is fairly quick, taking approximately 10 minutes.

Apart from insulin, beta cells release C-peptide, a byproduct of insulin production, into the bloodstream in equimolar quantities. C-peptide helps to prevent neuropathy, and other symptoms of diabetes related to vascular deterioration[1]. Measuring the levels of C-peptide can give a practitioner an idea of the viable beta cell mass. [2]

β-cells also produce amylin,[3] also known as IAPP, islet amyloid polypeptide. Amylin functions as part of the endocrine pancreas and contributes to glycemic control. Amylin's metabolic function is now somewhat well characterized as an inhibitor of the appearance of nutrient [especially glucose] in the plasma. It thus functions as a synergistic partner to insulin. Whereas insulin regulates long term food intake, increased amylin decreases food intake in the short term.

Beta cells (beta-cells, β-cells) are a type of cell in the pancreas in areas called the islets of Langerhans. They make up 65-80% of the cells in the islets. Beta cells make and release insulin, a hormone that controls the level of Glucose in the blood. There is a baseline level of Glucose maintained by the liver, but it can respond quickly to spikes in blood glucose by releasing stored insulin while simultaneously producing more. The response time is fairly quick, taking approximately 10 minutes.

Apart from insulin, beta cells release C-peptide, a byproduct of insulin production, into the bloodstream in equimolar quantities. C-peptide helps to prevent neuropathy, and other symptoms of diabetes related to vascular deterioration[1]. Measuring the levels of C-peptide can give a practitioner an idea of the viable beta cell mass. [2]

β-cells also produce amylin,[3] also known as IAPP, islet amyloid polypeptide. Amylin functions as part of the endocrine pancreas and contributes to glycemic control. Amylin's metabolic function is now somewhat well characterized as an inhibitor of the appearance of nutrient [especially glucose] in the plasma. It thus functions as a synergistic partner to insulin. Whereas insulin regulates long term food intake, increased amylin decreases food intake in the short term.

Beta cells

Amylin, or Islet Amyloid Polypeptide (IAPP), is a 37-residue peptide hormone secreted by pancreatic β-cells at the same time as insulin (in a roughly 1:100 amylin:insulin ratio). [1]

Islet, or insulinoma, amyloid polypeptide (IAPP, or amylin) is commonly found in pancreatic islets of patients suffering diabetes mellitus type 2, or harboring an insulinoma. While the association of amylin with the development of type 2 diabetes has been known for some time,[2] a direct causative role for amylin has been harder to establish. Recent results suggest that amylin, like the related beta-amyloid (Abeta) associated with Alzheimer's disease, can induce apoptotic cell-death in insulin-producing beta cells, an effect that may be relevant to the development of type 2 diabetes.[3]

Amylin, or Islet Amyloid Polypeptide (IAPP), is a 37-residue peptide hormone secreted by pancreatic β-cells at the same time as insulin (in a roughly 1:100 amylin:insulin ratio). [1]

Islet, or insulinoma, amyloid polypeptide (IAPP, or amylin) is commonly found in pancreatic islets of patients suffering diabetes mellitus type 2, or harboring an insulinoma. While the association of amylin with the development of type 2 diabetes has been known for some time,[2] a direct causative role for amylin has been harder to establish. Recent results suggest that amylin, like the related beta-amyloid (Abeta) associated with Alzheimer's disease, can induce apoptotic cell-death in insulin-producing beta cells, an effect that may be relevant to the development of type 2 diabetes.[3]

Islet Amyloid Polypeptide (IAPP)

C-peptide is a peptide which is made when proinsulin is split into insulin and C-peptide. They split before proinsulin is released from endocytic vesicles within the pancreas -- one C-peptide for each insulin molecule.

C-peptide is the abbreviation for "connecting peptide", although its name was probably also inspired by the fact that insulin is also composed of an "A" chain and a "B" chain. C-peptide was discovered in 1967. It should not be confused with c-reactive protein or Protein C. The first documented use of the C-peptide test was in 1972.

C-peptide is a peptide which is made when proinsulin is split into insulin and C-peptide. They split before proinsulin is released from endocytic vesicles within the pancreas -- one C-peptide for each insulin molecule.

C-peptide is the abbreviation for "connecting peptide", although its name was probably also inspired by the fact that insulin is also composed of an "A" chain and a "B" chain. C-peptide was discovered in 1967. It should not be confused with c-reactive protein or Protein C. The first documented use of the C-peptide test was in 1972.

C-peptide

Cardiovascular disease or cardiovascular diseases refers to the class of diseases that involve the heart or blood vessels (arteries and veins). [1]

While the term technically refers to any disease that affects the cardiovascular system (as used in MeSH), it is usually used to refer to those related to atherosclerosis (arterial disease). These conditions have similar causes, mechanisms, and treatments. In practice, cardiovascular disease is treated by cardiologists, thoracic surgeons, vascular surgeons, neurologists, and interventional radiologists, depending on the organ system that is being treated. There is considerable overlap in the specialties, and it is common for certain procedures to be performed by different types of specialists in the same hospital.

Cardiovascular disease or cardiovascular diseases refers to the class of diseases that involve the heart or blood vessels (arteries and veins). [1]

While the term technically refers to any disease that affects the cardiovascular system (as used in MeSH), it is usually used to refer to those related to atherosclerosis (arterial disease). These conditions have similar causes, mechanisms, and treatments. In practice, cardiovascular disease is treated by cardiologists, thoracic surgeons, vascular surgeons, neurologists, and interventional radiologists, depending on the organ system that is being treated. There is considerable overlap in the specialties, and it is common for certain procedures to be performed by different types of specialists in the same hospital.

Cardiovascular disease

Cerebrovascular disease is a group of brain dysfunctions related to disease of blood vessels supplying the brain. Hypertension is the most important cause that damages the blood vessel lining endothelium exposing the underlying collagen where platelets aggregate to initiate a repairing process which is not always complete and perfect. Sustained hypertension permanently changes the architecture of the blood vessels making them narrow, stiff, deformed and uneven which are more vulnerable to fluctuations of blood pressure. A fall in blood pressure during sleep can lead to marked reduction in blood flow in the narrowed blood vessels causing ischemic stroke in the morning whereas a sudden rise in blood pressure can cause tearing of the blood vessels causing intracranial hemorrhage during excitation at daytime. Primarily people who are elderly, diabetic, smoker, or have ischemic heart disease, have cerebrovascular disease.

All diseases related to artery dysfunction can be classified under a disease as known as Macrovascular disease. This is a simplistic study by which arteries are blocked by fatty deposits or by a blood clot. The results of cerebrovascular disease can include a stroke, or even sometimes a hemorrhagic stroke. Ischemia or other blood vessel dysfunctions can affect one during a cerebrovascular accident.

Cerebrovascular disease is a group of brain dysfunctions related to disease of blood vessels supplying the brain. Hypertension is the most important cause that damages the blood vessel lining endothelium exposing the underlying collagen where platelets aggregate to initiate a repairing process which is not always complete and perfect. Sustained hypertension permanently changes the architecture of the blood vessels making them narrow, stiff, deformed and uneven which are more vulnerable to fluctuations of blood pressure. A fall in blood pressure during sleep can lead to marked reduction in blood flow in the narrowed blood vessels causing ischemic stroke in the morning whereas a sudden rise in blood pressure can cause tearing of the blood vessels causing intracranial hemorrhage during excitation at daytime. Primarily people who are elderly, diabetic, smoker, or have ischemic heart disease, have cerebrovascular disease.

All diseases related to artery dysfunction can be classified under a disease as known as Macrovascular disease. This is a simplistic study by which arteries are blocked by fatty deposits or by a blood clot. The results of cerebrovascular disease can include a stroke, or even sometimes a hemorrhagic stroke. Ischemia or other blood vessel dysfunctions can affect one during a cerebrovascular accident.

Cerebrovascular disease

Peripheral vascular disease (PVD), also known as peripheral artery disease (PAD) or peripheral artery occlusive disease (PAOD), includes all diseases caused by the obstruction of large arteries in the arms and legs. PVD can result from atherosclerosis, inflammatory processes leading to stenosis, an embolism or thrombus formation. It causes either acute or chronic ischemia (lack of blood supply), typically of the legs.

Peripheral vascular disease (PVD), also known as peripheral artery disease (PAD) or peripheral artery occlusive disease (PAOD), includes all diseases caused by the obstruction of large arteries in the arms and legs. PVD can result from atherosclerosis, inflammatory processes leading to stenosis, an embolism or thrombus formation. It causes either acute or chronic ischemia (lack of blood supply), typically of the legs.

Peripheral vascular disease (PVD)

Diabetic neuropathies are neuropathic disorders that are associated with diabetes mellitus. These conditions are thought to result from diabetic microvascular injury involving small blood vessels that supply nerves (vasa nervorum). Relatively common conditions which may be associated with diabetic neuropathy include third nerve palsy; mononeuropathy; mononeuropathy multiplex; diabetic amyotrophy; a painful polyneuropathy; autonomic neuropathy; and thoracoabdominal neuropathy.

Diabetic neuropathies are neuropathic disorders that are associated with diabetes mellitus. These conditions are thought to result from diabetic microvascular injury involving small blood vessels that supply nerves (vasa nervorum). Relatively common conditions which may be associated with diabetic neuropathy include third nerve palsy; mononeuropathy; mononeuropathy multiplex; diabetic amyotrophy; a painful polyneuropathy; autonomic neuropathy; and thoracoabdominal neuropathy.

Diabetic neuropathies

Diabetic retinopathy is retinopathy (damage to the retina) caused by complications of diabetes mellitus, which can eventually lead to blindness. It is an ocular manifestation of systemic disease which affects up to 80% of all patients who have had diabetes for 10 years or more[1]. Despite these intimidating statistics, research indicates that at least 90% of these new cases could be reduced if there was proper and vigilant treatment and monitoring of the eyes[citation needed].

Diabetic retinopathy is retinopathy (damage to the retina) caused by complications of diabetes mellitus, which can eventually lead to blindness. It is an ocular manifestation of systemic disease which affects up to 80% of all patients who have had diabetes for 10 years or more[1]. Despite these intimidating statistics, research indicates that at least 90% of these new cases could be reduced if there was proper and vigilant treatment and monitoring of the eyes[citation needed].

Diabetic retinopathy

Diabetic nephropathy (nephropatia diabetica), also known as Kimmelstiel-Wilson syndrome and intercapillary glomerulonephritis, is a progressive kidney disease caused by angiopathy of capillaries in the kidney glomeruli. It is characterized by nephrotic syndrome and nodular glomerulosclerosis. It is due to longstanding diabetes mellitus, and is a prime cause for dialysis in many Western countries.

Diabetic nephropathy (nephropatia diabetica), also known as Kimmelstiel-Wilson syndrome and intercapillary glomerulonephritis, is a progressive kidney disease caused by angiopathy of capillaries in the kidney glomeruli. It is characterized by nephrotic syndrome and nodular glomerulosclerosis. It is due to longstanding diabetes mellitus, and is a prime cause for dialysis in many Western countries.

Diabetic nephropathy

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The Ambulatory Reversal Program