Short term satiety is regulated by mechano- and chemoreceptors in the stomach and small intestine that signal fullness after eating. Hormones like CCK, GLP-1, PYY are also involved in short term regulation by being released from the gut in response to food intake. Long term satiety is regulated by hormones like leptin released by adipose tissue and signals fullness over longer periods based on fat stores. Both short term gut signals and long term adipose signals need to work together to properly regulate long term energy balance and food intake.

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. Gut Control of Satiety

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. 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. Short term regulation of Satiety
•Mechano- and chemoreceptors
•Gastric peptides
•Nutrients and food intake

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. 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. 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. Satiety signals Satiety signals
•Gastric distension
•Gut peptides, hormones, and
factors
•Ileal brake mechanism

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. Stomac
h

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. 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. Gastrin-releasing polypeptides and
bombesin
Produced from gastric mucosa ….
• Regulates secretion of gastrin
• Peripheral administration inhibits food intake
and reduces appetite .

15. Gastrin-releasing polypeptides and
bombesin
Produced from gastric mucosa ….
• Biological actions:
•  gastrin, CCK, PYY, insulin release
, inhibition of food intake, satiety

16. Intestinal
factors

17. Intestinal factors……?
 Cholecystokinin (CCK),.
5-hydroxytryptamine (5-HT),
 glucagon like peptide-1 (GLP-1),
 polypeptide YY (3-36)

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. 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. 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. CCK action
liver
 Bile
gall
bladder
fat &
protein
digestion
+
+
- HCl
bile &
enzymes
fats &
peptides
FOOD

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. 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. 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. 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. Action of GLP-1

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. 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. 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. 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. 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. Polypeptide YY 3-36
•Circulating PYY(3–36) is thought to
suppress appetite through inhibition of
ARH NPY neurons

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

35. Increased feeding
(orexigenic effect)
Ghrelin
• Secreted by oxyntic cell in gastric
fundus
• Can be found in pancreas, intestine,
hypothalamus, pituitary gland

36. 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)

37. Increased feeding
(orexigenic effect)
Ghrelin
•Acting at arcuate nucleus by
stimulation of NPY/AGRP neurons
(neuropeptide Y/ Agouti-related
peptide) →↑ appetite (orexigenic
effect)

38. •Meal
Termination:
Long term
satiety….

39. Adipose tissue

40. over view…..
Meal Termination: Long term satiety….
Adipose tissue signals:
Leptin, secreted by fat cells
Malonyl-CoA, blood levels rise during
absorptive phase

41. 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

42. 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

43. 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