Rania Mohamed El-Sharkawy

rania.elsharkawy@alex-mri.edu.eg
Lecturer of clinical chemistry, MRI-Alexandria
University ,CPH...
Gut Control of Satiety
What is satiety ………
GENERALY……..
•After ingestion of a certain amount of
food , suppression of hunger occurs that
will lea...
How does satiety happens ………
The peripheral control is either long
term or short term signals

•Central control of food in...
Short term regulation of Satiety
•Mechano- and chemoreceptors
•Gastric peptides
•Nutrients and food intake
How does satiety happens ………
•Short term Peripheral control
•Mechanoreceptors and chemoreceptors
signaling as well as the ...
How does satiety happens ………
•Short term Peripheral control

•Short term regulatory mechanisms are
insufficient to regulat...
How does satiety happens ………
GENERAL CONCEPTS
The chemical constituents of food are detected by
specialized secretory cell...
Satiety signals Satiety signals
•Gastric distension
•Gut peptides, hormones, and
factors
•Ileal brake mechanism
Satiety signals
•Most come from the GI tract.

•Secreted in response to food
ingestion, create a sensation of
fullness or ...
Stomac
h
Mechano-and chemoreceptors
Entry of food to the stomach and to the proximal
small intestine….

•This will lead to stretch ...
Gastrointestinal peptides
Nutrients ingestion stimulates secretion of the blood
stream gastrointestinal peptides….
•Most o...
Gastrin-releasing polypeptides and
bombesin
Produced from gastric mucosa ….

• Regulates secretion of gastrin
• Peripheral...
Gastrin-releasing polypeptides and
bombesin
Produced from gastric mucosa ….

• Biological actions:
•  gastrin, CCK, PYY, ...
Intestinal
factors
Intestinal factors……?
 Cholecystokinin (CCK),.
5-hydroxytryptamine (5-HT),
 glucagon like peptide-1 (GLP-1),

 polypep...
Cholecystokinin (CCK) - A well-characterized
satiety factor
•Released from I cells in the duodenum in response to
nutrient...
Cholecystokinin (CCK) - A well-characterized
satiety factor

• Diffuses locally to activate CCK-A receptors present on
the...
Cholecystokinin (CCK) - A well-characterized
satiety factor

•CCK stimulate vagus nerve to pancreas (via CCKA receptor) → ...
CCK action
liver

 Bile
gall
bladder

fat &
protein
digestion

+

+

- HCl

bile &
enzymes

fats &
peptides

FOOD
STEPS OF CONSTRUCTION

Approximately 90% of
the human body's total serotonin is
located in the enterochromaffin cells in
t...
Serotonin (5 hydroxytryptamine)
•Inhibit secretion of gastrin, VIP, GIP, secretin,
motilin, GH, insulin, glucagon
•↑ fluid...
Glucagon like peptide GLP
•It is released in response to ingestion of meals
which potentiate glucose-induced insulin relea...
Glucagon like peptide GLP
inhibition of gastric emptying may in itself
cause a limitation of food intake, through
either n...
Action of GLP-1
Amylin and calcitonin gene
related peptide
Released from beta cell of the pancreas with
insulin, it acts on brain receptor...
Pancreatic polypeptide
•Released from the pancreas in response to food
ingestion
•Released in response to vagal stimulatio...
Polypeptide YY 3-36
•Released from the L-cells of small intestine
•Peak plasma levels appear postprandially after 1 h

•Ci...
Polypeptide YY 3-36
•Ingestion of nutrients causes L-cells in the
gastrointestinal tract to release PYY(1–36), which is
an...
Polypeptide YY 3-36
•However, a cleavage product of PYY(1–36),
PYY(3–36), is relatively selective for the NPY Y2
receptor....
Polypeptide YY 3-36
•Circulating PYY(3–36) is thought to
suppress appetite through inhibition of
ARH NPY neurons
Polypeptide YY 3-36
•↓ vagally mediated gastric acid secretion,
gastric emptying
• ↓ pancreatic enzyme and fluid secretion...
Increased feeding
(orexigenic effect)
Ghrelin
• Secreted by oxyntic cell in gastric
fundus
• Can be found in pancreas, int...
Ghrelin
Factors influencing it secretion

•Food intake
•Ghrelin level increases 1-2 hr prior to
meal, max just before eati...
Increased feeding
(orexigenic effect)
Ghrelin

•Acting at arcuate nucleus by
stimulation of NPY/AGRP neurons
(neuropeptide...
•Meal

Termination:
Long term
satiety….
Adipose tissue
over view…..
Meal Termination: Long term satiety….

Adipose tissue signals:
Leptin, secreted by fat cells
Malonyl-CoA, blo...
Leptin …..
Discovered in 1994 by Jeffrey Friedman
Cytokine, produced by fat cells, placenta and ?stomach
Diurnal variation...
Meal Termination: Long term
satiety….
Signals from Adipose Tissue
Leptin:
A hormone secreted by adipose tissue;
decreases ...
Conclusion….
Both………

The long term and the short term
regulators for food intake has to be work
in synergy for the long ...
Gut satiety control corrected
Gut satiety control corrected
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Gut satiety control corrected

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Gut satiety control corrected

  1. 1. Rania Mohamed El-Sharkawy rania.elsharkawy@alex-mri.edu.eg Lecturer of clinical chemistry, MRI-Alexandria University ,CPHQ,LSSGB Health governance –MRI-Alex university unit coordinator IHI Egypt & NAHQ member
  2. 2. Gut Control of Satiety
  3. 3. What is satiety ……… GENERALY…….. •After ingestion of a certain amount of food , suppression of hunger occurs that will lead to termination of food intake this process is referred as `satiation` .the time of satiation is followed by a period of variable duration that is characterized by the absence of hunger , and this is referred as `satiety`.
  4. 4. How does satiety happens ……… The peripheral control is either long term or short term signals •Central control of food intake and energy balance •Peripheral control of food intake and energy balance
  5. 5. Short term regulation of Satiety •Mechano- and chemoreceptors •Gastric peptides •Nutrients and food intake
  6. 6. How does satiety happens ……… •Short term Peripheral control •Mechanoreceptors and chemoreceptors signaling as well as the presence of food in the GIT tract contribute to satiety in the postprandial period. •Nutrients (glucose, aa..) and GIT peptides are also involved in the short term regulation of food intake.
  7. 7. How does satiety happens ……… •Short term Peripheral control •Short term regulatory mechanisms are insufficient to regulate energy balance and body adiposity •They should act with the long term regulatory mechanisms ( (leptin, insulin, ..) for determination of body adiposity and energy consumed over a period of time.
  8. 8. How does satiety happens ……… GENERAL CONCEPTS The chemical constituents of food are detected by specialized secretory cells in the gut epithelium releasing satiety mediators many of which act through the stimulation of the vagal afferents
  9. 9. Satiety signals Satiety signals •Gastric distension •Gut peptides, hormones, and factors •Ileal brake mechanism
  10. 10. Satiety signals •Most come from the GI tract. •Secreted in response to food ingestion, create a sensation of fullness or satiety. •Act within the time frame of a single meal
  11. 11. Stomac h
  12. 12. Mechano-and chemoreceptors Entry of food to the stomach and to the proximal small intestine…. •This will lead to stretch of the mechnoreceptors , also gastrointestinal chemoreceptors in response to nutrient products of digestion ( sugars, FA,..) •Signals from these gastrointestinal receptors are transmitted via vagal afferent nerves to the hindbrain where integration of this visceral input occurs and leads to satiety sensation .
  13. 13. Gastrointestinal peptides Nutrients ingestion stimulates secretion of the blood stream gastrointestinal peptides…. •Most of these peptides causes meal termination and hence called satiety signals.
  14. 14. Gastrin-releasing polypeptides and bombesin Produced from gastric mucosa …. • Regulates secretion of gastrin • Peripheral administration inhibits food intake and reduces appetite .
  15. 15. Gastrin-releasing polypeptides and bombesin Produced from gastric mucosa …. • Biological actions: •  gastrin, CCK, PYY, insulin release , inhibition of food intake, satiety
  16. 16. Intestinal factors
  17. 17. Intestinal factors……?  Cholecystokinin (CCK),. 5-hydroxytryptamine (5-HT),  glucagon like peptide-1 (GLP-1),  polypeptide YY (3-36)
  18. 18. Cholecystokinin (CCK) - A well-characterized satiety factor •Released from I cells in the duodenum in response to nutrients particularly fat and protein •Enters the blood, acts on gut motility, decrease the gastric emptying , gallbladder contraction, gastric and pancreatic enzyme secretion •CCK8, CCK22, CCK33 : principal circulating forms secreted in response to meal
  19. 19. Cholecystokinin (CCK) - A well-characterized satiety factor • Diffuses locally to activate CCK-A receptors present on the vagal sensory nerves • Secreted after food intake → signal transmitted by vagus → stop food intake
  20. 20. Cholecystokinin (CCK) - A well-characterized satiety factor •CCK stimulate vagus nerve to pancreas (via CCKA receptor) → release of Ach, GRP, VIP → fusion of granule with membrane and release of pancreatic enzyme
  21. 21. CCK action liver  Bile gall bladder fat & protein digestion + + - HCl bile & enzymes fats & peptides FOOD
  22. 22. STEPS OF CONSTRUCTION Approximately 90% of the human body's total serotonin is located in the enterochromaffin cells in the alimentary canal (gut) , where it is used to regulate intestinal movements.
  23. 23. Serotonin (5 hydroxytryptamine) •Inhibit secretion of gastrin, VIP, GIP, secretin, motilin, GH, insulin, glucagon •↑ fluid absorption and ↓ secretion from intestine •↓ endocrine and exocrine pancreatic secretion •↓ bile flow and gall bladder contraction •↓ gastric acid secretion and motility •↓ absorption of glucose, amino acid, triglyceride
  24. 24. Glucagon like peptide GLP •It is released in response to ingestion of meals which potentiate glucose-induced insulin release •GLP-1 is also believed to play an important role as one of the hormones of the “ileal brake mechanism,” an endocrine mechanism that is activated by the presence of nutrients in the ileal lumen and which serves to inhibit gastric motility and secretion
  25. 25. Glucagon like peptide GLP inhibition of gastric emptying may in itself cause a limitation of food intake, through either neural or endocrine signaling pathways, perhaps associated with distention of the stomach
  26. 26. Action of GLP-1
  27. 27. Amylin and calcitonin gene related peptide Released from beta cell of the pancreas with insulin, it acts on brain receptors to reduce food intake
  28. 28. Pancreatic polypeptide •Released from the pancreas in response to food ingestion •Released in response to vagal stimulation, gastric distention, fat/amino acid/glucose •It was shown to be reduced in conditions associated with increased food intake •Action : decrease pancreatic enzyme and HCO3 secretion
  29. 29. Polypeptide YY 3-36 •Released from the L-cells of small intestine •Peak plasma levels appear postprandially after 1 h •Circulating levels of PYY are sensitive to nutrient intake
  30. 30. Polypeptide YY 3-36 •Ingestion of nutrients causes L-cells in the gastrointestinal tract to release PYY(1–36), which is an endogenous ligand for several NPY receptors (Y1, Y2, and Y5)
  31. 31. Polypeptide YY 3-36 •However, a cleavage product of PYY(1–36), PYY(3–36), is relatively selective for the NPY Y2 receptor. The NPY Y2 receptor is expressed in the ARH (arcuate nucleus of the hypothamalmous)
  32. 32. Polypeptide YY 3-36 •Circulating PYY(3–36) is thought to suppress appetite through inhibition of ARH NPY neurons
  33. 33. Polypeptide YY 3-36 •↓ vagally mediated gastric acid secretion, gastric emptying • ↓ pancreatic enzyme and fluid secretion by inhibiting neural pathway to pancreas and ↓ pancreatic blood flow •↓ intestinal motility, food intake
  34. 34. Increased feeding (orexigenic effect) Ghrelin • Secreted by oxyntic cell in gastric fundus • Can be found in pancreas, intestine, hypothalamus, pituitary gland
  35. 35. Ghrelin Factors influencing it secretion •Food intake •Ghrelin level increases 1-2 hr prior to meal, max just before eating and decreases dramatically within 1 hr after meal •Degree of ghrelin level decrease is in proportion with calories and composition of food (CHO can decrease ghrelin > fat)
  36. 36. Increased feeding (orexigenic effect) Ghrelin •Acting at arcuate nucleus by stimulation of NPY/AGRP neurons (neuropeptide Y/ Agouti-related peptide) →↑ appetite (orexigenic effect)
  37. 37. •Meal Termination: Long term satiety….
  38. 38. Adipose tissue
  39. 39. over view….. Meal Termination: Long term satiety…. Adipose tissue signals: Leptin, secreted by fat cells Malonyl-CoA, blood levels rise during absorptive phase
  40. 40. Leptin ….. Discovered in 1994 by Jeffrey Friedman Cytokine, produced by fat cells, placenta and ?stomach Diurnal variation: peak in nighttime Receptors (gp130) located in most tissues, with a long form of the receptor in hypothalamus Bigger fat cells produced more leptin Leptin levels correlate with body fat content
  41. 41. Meal Termination: Long term satiety…. Signals from Adipose Tissue Leptin: A hormone secreted by adipose tissue; decreases food intake and increases metabolic rate, primarily by inhibiting Neuropeptide Y (NPY)-secreting neurons in the arcuate nucleus of the hypothalamus
  42. 42. Conclusion…. Both……… The long term and the short term regulators for food intake has to be work in synergy for the long term regulation of food intake as well as energy expenditure

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