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1
خدا نام به
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CONTROL OF FOOD INTAKE AND APPETITE
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What’s the underlying cause?
Fast forward 15 years to 2030 Humans are sicker than ever
Life expectancy has decreased and productivity is down
Obesity
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Traditionally, a distinction has been made between
homeostatic & nonhomeostatic control of appetite and food
intake
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Deviation from homeostatic control
physiologic nonphysiologic
obesity
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CENTRAL CONTROLS OF FOOD INTAKE AND APPETITE
Coordination by the
Hypothalamus
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The hypothalamus is widely recognized as the
in the control of food intake and appetite
“gate keeper”
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the lateral hypothalamus as the
“hunger center” and
the medial hypothalamus as the
“satiety center”
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A network of communicationamong the gut,
pancreas, adipose tissue, brainstem, and hypothalamus is well
established
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Additionally, further communication
exists between the
hypothalamus and higher cortical centers
pertaining tofood memory of food, with resulting
overall coordinated
control of food intake
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Role of the Brainstem
is the main organ responsible for facilitating the communication between peripheral signals
of food intake and hypothalamic nuclei
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The arcuate nucleus (ARC) is thought to be the
main hypothalamic
area controlling food intake
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Within the ARC, two groups of neurons are pivotalin regulating food intake
One group of neurons contains
neuropeptide Y (NPY), and most of these also contain
Agouti-related peptide (AgRP)
The second group is formed by neurons containing pro-opiomelanocortin
(POMC)
Activation of these neurons
enhances food ntake
(orexigenic)
Activation of these neurons
reduces food intake
(anorexigenic)
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NPY
is the most powerful central stimulant of
appetite
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Neuropeptides Implicated in the Control ofFood Intake
• Agouti-Related Peptide• Cocaine- and Amphetamine-Regulated Transcript
• Hypothalamic Releasing Hormones• Orexins• Melanin-Concentrating Hormone• Brain-Derived Neurotrophic Factor• Ciliary Neurotrophic Factor• Central Neurotransmitters
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PERIPHERAL CONTROLS OF FOOD INTAKEAND APPETITE
Nutrient, hormonal signals from the gastrointestinal system, endocrine
organs, and adipose tissueall have essential roles in influencing
food intake and appetite
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These peripheral signals target areas of the hypothalamus to regulate
appetite They include signals conveying afeeling of fullness (satiety signals)
and hunger (orexigenic signals)
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meal size
These signals can control
&
meal number
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Neural Signals
Orosensory and Optic Stimuli
Orosensory and optic stimuli provide the brain with
sensory information regarding the
nature of foodThese stimuli include
appearance, taste, smell, and textural stimuli
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The information isused by the brain to decision
to eat or not eat to continue or to stop eating
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Gastric Distention
Volume-related postprandial gastric distention results in satiety during a meal
bariatric surgical
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Nutrient Signals
Most nutrient signals exert their effects on the gastrointestinal
system and the brain and induce the secretion of gastrointestinal
hormones and appetite regulation
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Gut Hormones
• the largest endocrine organ
• secretes more than 30 different regulatory
peptide hormones
• digestion and absorption
• affect short-term feelings of hunger and satiety
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These hormones are
the subject of extensive research, given their
potential as
physiologic antiobesity therapies
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Cholecystokinin (CCK)
• It is released postprandially• slowed gastric emptying
• CCK reduces food intake
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Ghrelin• Increases appetite• “hunger hormone”• considered as one of the most powerful
physiologic orexigenic agents • increases food intake and body weight
in rodents• Plasma ghrelin levels are also noted to
increase on weight loss (regain weight )
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Peptide YY (PYY)
• released postprandially• PYY administration decreases food
intake• Obese patients demonstrate a blunted
postprandial rise in PYY• PYY-based antiobesity agents are
currently under development
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Glucagon-like Peptide-1(GLP-1)
• reduces food intake• released postprandially • reduces gastric emptying• analogs of GLP-1 are used in the
treatment of type 2 diabetes• currently undergoing clinical trials for
the treatment of obesity
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Pancreatic Hormones
• major function is to control glucose homeostasis (Insulin & Glucagon)
• pancreatic polypeptide and amylin, also affect appetite ( are satiety signal and reduces food intake)
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Hormones from Adipose Tissue (leptin)
• a circulating protein produced by adipocytes (fat cells)
• is a signal from the adipose tissue to the brain that reflects the state of energy stores
• increased by overfeeding• absence of leptin lead to severe obesity
• Leptin acts on ARC LepR to stimulate POMC neurons and inhibit NPY/AgRP neurons to decrease food intake
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Other HormonesThyroid hormones, gonadal steroids
and glucocorticoids regulate metabolic rate, reproductive state and stress
responses, respectively These processes rely on adequate
energy supplies. Therefore, it is not surprising that hormones regulating these processes are also
involved in theendocrine regulation of appetite
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Signals from the Immune System
Anorexia or decreased food intake during infectious,
inflammatory, and neoplastic disease states is very evident.
Anorexia appears to result from the action of cytokines in the brain
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Hedonic Mechanisms
visual, smell, and taste
signals can override satiety signals to maintain
food intake
The word “hedonic” relates to pleasant (or unpleasant)
sensations
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CONCLUSION
The regulation of food intake and appetite occurs through
the integration of various
central and peripheral signals
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These signals interact at the level of the
brainstem and hypothalamus to produce an overall response of
hunger or fullness
Additionally,
these neuronal networks are hugely modified by other influences such as sensory
inputs, food memory, rewarding aspects
of food, and numerous environmental and emotional factors
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This modification is a particular feature of modernhuman eating behavior and
may underpin the dysregulationof energy balance that is
responsible for the current
obesity epidemic
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By means of ever-expanding current research , it is hoped that our understanding of the complex and intricate signaling pathways governing appetite control will improve and pave the way for
better antiobesity drug treatments
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