Central and Peripheral Controls of Food Intake and Appetite

 
CENTRAL CONTROLS OF FOOD
INTAKE AND APPETITE
Part-II
 
Dr Pramod Kumar
Asstt. Professor
Department of Veterinary Physiology
Bihar Veterinary College, Patna
 
 
 
Peripheral control of food intake and appetite
  
Neural, nutrient and hormonal signals from
the gastrointestinal system, endocrine organs,
adipose tissue and circulation all have essential
roles in influencing food intake and appetite.
 
Neural Signals
 
 
 Orosensory and Optic stimuli include
appearance, taste, smell and textural stimuli
 
 Visual information - signals in the afferent optic
fibers of cranial nerve I
 
Gustatory, olfactory and orosensory information
→ fibers of cranial nerves VII, IX, I and V → brain
important for taste, reward, flavor and →
mnemonic → dorsal vagal complex, limbic system
and OFC
 
 
Gastric Distention
 
 
 Volume-related postprandial gastric distention
results in satiety during a meal.
 
 Mechanoreceptors in the stomach wall sense
stretch volume and tension during a meal →
afferent fibers of the vagal & spinal visceral
nerves
 
 used in the management of severe obesity
 
 
Glucose
 alters the firing rate of neurons in the
ARC, LHA and NTS
 
 cellular influx of glucose alters the ratio of AMP
to ATP within the neuronal cell
 
 
ATP-dependent membrane channels that may
influence neuronal depolarization
 
 alter the activity of important nutrient sensing
enzymes (e.g., AMP-activated protein kinase)
 
 Some neurons (e.g., ARC POMC neurons) are
excited by glucose
 
 others (e.g., ARC NPY neurons) are inhibited by
glucose
 
 
Circulating lipids
 such as long-chain fatty acids
(LCFAs) can alter feeding behavior by directly
activating central neural pathways  by intra
cerebro-ventricular administration of an LCFA
(oleic acid) also decreased food intake
 
Gut Hormones
 
 
 
 
Ghrelin
 
 Peptide YY (PYY)
 
 Cholecystokinin (CCK)
 
 Pancreatic polypeptide (PP)
 
 Amylin
 
 Glucose-dependent insulinotropic polypeptide
(GIP)
 
 Glucagon-like peptide-1, 2 (GLP-1, 2)
 
 Oxyntomodulin
 
Cholecystokinin
 
 
 CCK is synthesized in the I cells of the small
intestine
 
 promote fat and protein digestion
 
 results in gallbladder contraction, relaxation of
the sphincter of Oddi, somastostatin release,
stimulation of pancreatic enzyme release and
slowed gastric emptying
 
 afferent fibers transmit signals → NTS (central
melanocortin system) → reduce food intake
 
 
 
Ghrelin
 is the only known gut hormone that
increases appetite “hunger hormone.”
 
 produced by the A-cells of gastric fundus
 
 increase gastric motility and stimulation of
growth hormone release
 
 increased fat storage and decrease in fat use
 
 Plasma ghrelin levels rise before meals and
decline after eating
 
 
Peptide YY (PYY)
 is a member of PP fold family
includes NPY and pancreatic polypeptide
 
 PYY is released postprandially
 
 release of PYY is augmented by dietary fat
 
 PYY administration decreases food intake in
rodents and humans
 
 PYY may reduce food intake by decreasing ARC
NPY levels via the ARC Y
2
 receptor or via its
effects on the vagus nerve
 
 it also delays gastric emptying.
 
 
Glucagon-like Peptide-1
 
 
Enteroendocrine L cells → preproglucagon →
GLP-1, GLP-2 and oxyntomodulin
 
 GLP1 released postprandially - It is an incretin
which results in increased glucose-dependent
insulin release
 
 reduces gastric emptying and gastric acid
secretion
 
 inhibits glucagon release.
 
 reduces food intake 
 oxyntomodulin Despite
similarly of GLP 1, it increases energy expenditure
and may suppress ghrelin release
 
Pancreatic Hormones
 
 
Insulin
: Effect on appetite and satiety
 
 Indirect : low blood glucose → increase in
food intake
 
 Direct : acts on ARC insulin receptors →
decrease food intake
 
 Glucagon: decreases meal size, and reduces
overall food intake and body weight
 
 
Pancreatic polypeptide
 : PP is secreted
postprandially
 
 delays gastric emptying and reduce appetite
 
 exerts its effects via acting on the Y
4
 receptors
in the ARC, in the AP or via the vagus
 
 Amylin: inhibits gastric secretion, delays gastric
emptying
 
 It is a satiety signal and reduces food intake
and body weight
 
Adipose Tissue Hormones
 
 
Leptin
 produce in adipose tissue
 
 exerts its effects by acting on the leptin
receptor (LepR)
 
 acts on ARC LepR to stimulate POMC
neurons and inhibit NPY/AgRP neurons to
decrease food intake
 
 failure of leptin to diminish appetite in
obesity is termed leptin resistance
 
 
 
Thyroid Hormone
 regulates basal metabolic
state
 
 Hyperthyroidism is associated with increased
food intake and decreased body weight
 
 Gonadal Steroids (orchiectomy) decreases food
intake, ovariectomy increases food intake
 
 Glucocorticoids generally stimulate food intake
and weight gain
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This article delves into the intricate mechanisms that regulate food intake and appetite, focusing on central and peripheral factors. Neural signals, gastric distention, glucose influence, circulating lipids' role, and gut hormones all play crucial roles in shaping our eating behavior. These signals from various systems work together to influence our food choices and satiety levels, highlighting the complexity of appetite regulation.

  • Food intake
  • Appetite control
  • Neural signals
  • Gastric distention
  • Glucose regulation

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  1. CENTRAL CONTROLS OF FOOD INTAKE AND APPETITE Part-II Dr Pramod Kumar Asstt. Professor Department of Veterinary Physiology Bihar Veterinary College, Patna

  2. Peripheral control of food intake and appetite Neural, nutrient and hormonal signals from the gastrointestinal system, endocrine organs, adipose tissue and circulation all have essential roles in influencing food intake and appetite.

  3. Neural Signals appearance, taste, smell and textural stimuli Visual information - signals in the afferent optic fibers of cranial nerve I Gustatory, olfactory and orosensory information fibers of cranial nerves VII, IX, I and V brain important for taste, reward, flavor and mnemonic dorsal vagal complex, limbic system and OFC Orosensory and Optic stimuli include

  4. Gastric Distention Volume-related postprandial gastric distention results in satiety during a meal. Mechanoreceptors in the stomach wall sense stretch volume and tension during a meal afferent fibers of the vagal & spinal visceral nerves used in the management of severe obesity

  5. Glucose alters the firing rate of neurons in the ARC, LHA and NTS cellular influx of glucose alters the ratio of AMP to ATP within the neuronal cell ATP-dependent membrane channels that may influence neuronal depolarization alter the activity of important nutrient sensing enzymes (e.g., AMP-activated protein kinase) Some neurons (e.g., ARC POMC neurons) are excited by glucose others (e.g., ARC NPY neurons) are inhibited by glucose

  6. Circulating lipids such as long-chain fatty acids (LCFAs) can alter feeding behavior by directly activating central neural pathways cerebro-ventricular administration of an LCFA (oleic acid) also decreased food intake by intra

  7. Gut Hormones Ghrelin Peptide YY (PYY) Cholecystokinin (CCK) Pancreatic polypeptide (PP) Amylin Glucose-dependent insulinotropic polypeptide (GIP) Glucagon-like peptide-1, 2 (GLP-1, 2) Oxyntomodulin

  8. Cholecystokinin CCK is synthesized in the I cells of the small intestine promote fat and protein digestion results in gallbladder contraction, relaxation of the sphincter of Oddi, somastostatin release, stimulation of pancreatic enzyme release and slowed gastric emptying afferent fibers transmit signals NTS (central melanocortin system) reduce food intake

  9. Ghrelin is the only known gut hormone that increases appetite hunger hormone. produced by the A-cells of gastric fundus increase gastric motility and stimulation of growth hormone release increased fat storage and decrease in fat use Plasma ghrelin levels rise before meals and decline after eating

  10. Peptide YY (PYY) is a member of PP fold family includes NPY and pancreatic polypeptide PYY is released postprandially release of PYY is augmented by dietary fat PYY administration decreases food intake in rodents and humans PYY may reduce food intake by decreasing ARC NPY levels via the ARC Y2receptor or via its effects on the vagus nerve it also delays gastric emptying.

  11. Glucagon-like Peptide-1 Enteroendocrine L cells preproglucagon GLP-1, GLP-2 and oxyntomodulin GLP1 released postprandially - It is an incretin which results in increased glucose-dependent insulin release reduces gastric emptying and gastric acid secretion inhibits glucagon release. reduces food intake oxyntomodulin Despite similarly of GLP 1, it increases energy expenditure and may suppress ghrelin release

  12. Pancreatic Hormones Insulin: Effect on appetite and satiety Indirect : low blood glucose increase in food intake Direct : acts on ARC insulin receptors decrease food intake Glucagon: decreases meal size, and reduces overall food intake and body weight

  13. Pancreatic postprandially delays gastric emptying and reduce appetite exerts its effects via acting on the Y4receptors in the ARC, in the AP or via the vagus Amylin: inhibits gastric secretion, delays gastric emptying It is a satiety signal and reduces food intake and body weight polypeptide : PP is secreted

  14. Adipose Tissue Hormones Leptin produce in adipose tissue exerts its effects by acting on the leptin receptor (LepR) acts on ARC LepR to stimulate POMC neurons and inhibit NPY/AgRP neurons to decrease food intake failure of leptin to diminish appetite in obesity is termed leptin resistance

  15. Thyroid Hormone regulates basal metabolic state Hyperthyroidism is associated with increased food intake and decreased body weight Gonadal Steroids (orchiectomy) decreases food intake, ovariectomy increases food intake Glucocorticoids generally stimulate food intake and weight gain

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