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Facts about Type I Diabetes Mellitus. “ Diabetes was long thought to be a kidney disease (Greek & Arabic Methodology). “ Thomas Willis (1621 - 1679), discovered the sweetness of urine, hence, the name Diabetes Mellitus arised”. “Mathew Dobson (1776), identified glycosuria. - PowerPoint PPT Presentation
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Facts about Type I
Diabetes Mellitus
“ Diabetes was long thought to be a kidney disease
(Greek & Arabic Methodology).
“ Thomas Willis (1621 - 1679), discovered the
sweetness of urine, hence, the name Diabetes Mellitus
arised”
“Mathew Dobson (1776), identified glycosuria.
“Claude Bernard and Von Mering (1889), discovered in
the same year that pancreatectomy causes
diabetes”
“Fredrick Banting (1921), successfully, extracted
insulin, gaining the Nobel prize for this great
discovery”.
“Leonard Thompson (14 year old boy) & Elizabeth Hughes (aged
14 years), were the first patients to be treated with insulin in
1922.
Dear Mom, ..I look entirely different gaining
every hour strength & weight..
..it is truly miraculous....I wish you could see the expression
on there faces, they are so astounded in my unheard of
progress..Leonard,
April, 1922
Insulin Secretion•Site : B cells (Pancreatic Islets of
Langerhan’s).•Mechanism : from secretory
granules of Proinsulin (in the Golgi complex of B cells).
•Factors Related : glucose, gut hormones, A. As., F.As., ketone
bodies, nerve supply& glucagon.
Insulin Secretion
INSULIN SECRETION
GLUCOSE GKG-6-P
PK
PYRUVATES
ATP
Ca2+DEPOLARIZATION
++ +
__
_
K +
INSULIN
Glu t2
Blood Glucose
Biphasic Glucose Stimulation
1st phase: Rapid onset (with peak level after 1-2 minutes) & Short duration.
2nd phase:Delayed onset & Longer duration.
Insulin Secretion Curve
Biphasic insulin response to a constant glucose stimulation(IVGTT - hyperglycemic Clamp)
Insulin rate
Time (min)
Basal
4 60
Response to I.V. Glucose
Insulin Mechanism of action
Carbohydrate metabolismLipid metabolismProtein metabolism
Insulin Receptors
•Receptor-mediated endocytosis.•Gene transcription.•Glucose transporters.
Insulin Receptors
Insulin Hypoglycemic Action
Glucose storage .. Anabolic effect & Anticatabolic effect .
Insulin Lack
Insulin Deficiency
Insulin Defect Complications
Sorbitol Pathway
Diabetes Mellitus
“A metabolic disorder, with high risk of complications &
chronic hyperglycemia (with or without glycosuria).“
Prevalence of Insulin Disorders
“The prevalence worldwide varies from 2-5% in developing countries, to 5-10% in
developed countries.”
N.B. ( A cross-sectional study revealed incidence of 7million cases in the Egyptian
population at the year of 1992).
Diabetes: Clinical Features•Symptoms:
–Polyuria–Polydypsia=thirst–Polyphagia=appetite–Asthenia & Loss of weight
•Signs:
No specific signs may besigns of complications
•Signs:
No specific signs may be signs of complications
Stage/Test Fasting Plasma Glucose (FPG)
(Preferred)
Casual Plasma Glucose
Oral Glucose Tolerance Test
(OGTT)
Diabetes FPG > 126 mg/dL
(7.0 mmol/L)
Casual Plasma Glucose > 200
mg/dL (11.1 mmol/L) plus symptoms.
Two-hour Plasma (2hPG) >200 mg/dl
Impaired Glucose Homeostasis
Impaired Fasting Glucose
(IFG) = FPG > 110 and <126
mg/dl
Impaired glucose Tolerance (IGT) =
2hPG>140mg/dl and <200 mg/dL
Normal FPG< 110 mg/dL 2hPG<140 md/dl
Diagnosis of D. Mellitus
American Diabetes Association
Investigation of Diabetes
•Fasting Blood Glucose level
•Post prandial blood glucose level
•Glycosuria
•Glycosylated haemoglobin.
Glycosylated Haemoglobin
•Hb + G = HbA1 (non reversible)
•In hyperglycemia up to 20% or more.
•Occurs in the active life span of the RBCs.
•Gives information about the state of BGL
•during the previous 2 months.
Predisposing FactorsIDDM
•Heredity.•Histocomptability.•Virus infection.•Sesonality.•Cell-mediated immunity.
Seasonality
Stages of IDDM development
Age and insulin content