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Questions and Answers
Which phase of gastric secretion is primarily initiated by the sight, smell, or thoughts of food?
Which phase of gastric secretion is primarily initiated by the sight, smell, or thoughts of food?
What is the primary effect of the intestinal phase on gastric secretion?
What is the primary effect of the intestinal phase on gastric secretion?
What stimulates gastrin release during the gastric phase?
What stimulates gastrin release during the gastric phase?
Which receptors are primarily affected by cholecystokinin (CCK) and gastrin?
Which receptors are primarily affected by cholecystokinin (CCK) and gastrin?
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How many amino acids are present in the gastrin hormone?
How many amino acids are present in the gastrin hormone?
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Where is the densest concentration of gastrin-containing cells (G cells) located?
Where is the densest concentration of gastrin-containing cells (G cells) located?
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What effect does the breakdown of protein into amino acids have during gastric and intestinal phases?
What effect does the breakdown of protein into amino acids have during gastric and intestinal phases?
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Which hormone acts predominantly at the CCK-1 receptor in the gallbladder?
Which hormone acts predominantly at the CCK-1 receptor in the gallbladder?
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Which gastrointestinal hormones are primarily responsible for inhibiting gastric acid secretion?
Which gastrointestinal hormones are primarily responsible for inhibiting gastric acid secretion?
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Where are most gastrointestinal hormones released in the digestive tract?
Where are most gastrointestinal hormones released in the digestive tract?
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What type of communication involves hormones interacting with distant cells?
What type of communication involves hormones interacting with distant cells?
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Which of the following hormones is considered a major gastrointestinal hormone?
Which of the following hormones is considered a major gastrointestinal hormone?
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What is the primary role of the hormone secretin in the gastrointestinal system?
What is the primary role of the hormone secretin in the gastrointestinal system?
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Which of the following hormones primarily stimulates the release of pancreatic secretions?
Which of the following hormones primarily stimulates the release of pancreatic secretions?
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How do gastrointestinal hormones influence food intake?
How do gastrointestinal hormones influence food intake?
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What factor primarily influences the secretion of hormones like motilin and GIP?
What factor primarily influences the secretion of hormones like motilin and GIP?
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What primarily stimulates pancreatic secretion during the intestinal phase?
What primarily stimulates pancreatic secretion during the intestinal phase?
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Which hormone is mainly responsible for increasing enzyme secretion from the pancreas?
Which hormone is mainly responsible for increasing enzyme secretion from the pancreas?
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What role does secretin play in pancreatic function?
What role does secretin play in pancreatic function?
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Which factor plays a minimal role in stimulating pancreatic secretion during the gastric phase?
Which factor plays a minimal role in stimulating pancreatic secretion during the gastric phase?
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How is bile mainly released into the duodenum?
How is bile mainly released into the duodenum?
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Which component is NOT a main constituent of bile?
Which component is NOT a main constituent of bile?
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What initiates the vagovagal reflexes to the pancreas during the gastric phase?
What initiates the vagovagal reflexes to the pancreas during the gastric phase?
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Which of the following statements about the function of CCK is correct?
Which of the following statements about the function of CCK is correct?
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What is the primary function of Brunner’s glands in the duodenum?
What is the primary function of Brunner’s glands in the duodenum?
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What effect does vagal stimulation have on Brunner’s gland secretion?
What effect does vagal stimulation have on Brunner’s gland secretion?
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Which hormone is NOT classified as a major gastrointestinal hormone?
Which hormone is NOT classified as a major gastrointestinal hormone?
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Which type of signal does the anorexigenic pathway in the hypothalamus primarily respond to?
Which type of signal does the anorexigenic pathway in the hypothalamus primarily respond to?
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What neurotransmitter is primarily involved in stimulating the orexigenic pathway for food intake?
What neurotransmitter is primarily involved in stimulating the orexigenic pathway for food intake?
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Which hormone primarily inhibits food intake through the melanocortin pathway?
Which hormone primarily inhibits food intake through the melanocortin pathway?
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What is the role of the hypothalamus in the control of food intake?
What is the role of the hypothalamus in the control of food intake?
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Which of the following statements about increased secretion from Brunner's glands is TRUE?
Which of the following statements about increased secretion from Brunner's glands is TRUE?
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What effect does vagal stimulation have on food intake?
What effect does vagal stimulation have on food intake?
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Which hormone acts directly on the hypothalamus to promote satiety after a meal?
Which hormone acts directly on the hypothalamus to promote satiety after a meal?
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What is the role of ghrelin in food intake regulation?
What is the role of ghrelin in food intake regulation?
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Which peptides are known to stimulate satiety?
Which peptides are known to stimulate satiety?
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How does Leptin primarily function in the body?
How does Leptin primarily function in the body?
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Which condition results from the blocking of vagal afferents?
Which condition results from the blocking of vagal afferents?
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What role does CCK have in food intake regulation?
What role does CCK have in food intake regulation?
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Which of the following peptides is primarily involved in appetite loss?
Which of the following peptides is primarily involved in appetite loss?
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What type of communication occurs when a hormone interacts with the same cell that released it?
What type of communication occurs when a hormone interacts with the same cell that released it?
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Which hormone is predominantly associated with stimulating bile release into the duodenum?
Which hormone is predominantly associated with stimulating bile release into the duodenum?
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The secretion of which hormone is primarily influenced by the entry of fats into the duodenum?
The secretion of which hormone is primarily influenced by the entry of fats into the duodenum?
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Which hormone is known to have an inhibitory effect on gastric acid secretion?
Which hormone is known to have an inhibitory effect on gastric acid secretion?
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Which additional gastrointestinal hormone plays a role in the modulation of gastrointestinal motility?
Which additional gastrointestinal hormone plays a role in the modulation of gastrointestinal motility?
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Where in the gastrointestinal tract are enteroendocrine cells responsible for hormone release primarily located?
Where in the gastrointestinal tract are enteroendocrine cells responsible for hormone release primarily located?
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What is the primary physiological role of secretin in the gastrointestinal system?
What is the primary physiological role of secretin in the gastrointestinal system?
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Which of the following factors does NOT commonly influence the secretion of gastrointestinal hormones?
Which of the following factors does NOT commonly influence the secretion of gastrointestinal hormones?
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What substance do Brunner's glands secrete to protect the duodenum from acidity?
What substance do Brunner's glands secrete to protect the duodenum from acidity?
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Which pathway in the hypothalamus inhibits food intake and increases metabolism?
Which pathway in the hypothalamus inhibits food intake and increases metabolism?
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What role does neuropeptide Y (NPY) play in food intake regulation?
What role does neuropeptide Y (NPY) play in food intake regulation?
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Which effect does sympathetic stimulation have on Brunner's gland secretion?
Which effect does sympathetic stimulation have on Brunner's gland secretion?
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What is the main neurotransmitter involved in the orexigenic pathway for stimulating food intake?
What is the main neurotransmitter involved in the orexigenic pathway for stimulating food intake?
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What triggers the increase in secretion from Brunner's glands in the duodenum?
What triggers the increase in secretion from Brunner's glands in the duodenum?
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Which hormone is primarily released in response to higher caloric intake and acts to increase food intake?
Which hormone is primarily released in response to higher caloric intake and acts to increase food intake?
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Which hormone released from the hypothalamus is responsible for inhibiting food intake through the melanocortin pathway?
Which hormone released from the hypothalamus is responsible for inhibiting food intake through the melanocortin pathway?
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Which hormone is released from pancreatic β-cells and directly induces satiety?
Which hormone is released from pancreatic β-cells and directly induces satiety?
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What effect does blocking vagal afferents have on food intake?
What effect does blocking vagal afferents have on food intake?
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Which peptide is released by enteroendocrine cells of the ileum and colon, and stimulates satiety?
Which peptide is released by enteroendocrine cells of the ileum and colon, and stimulates satiety?
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What is the primary role of leptin in relation to food intake?
What is the primary role of leptin in relation to food intake?
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What is the outcome of CCK released in response to food intake?
What is the outcome of CCK released in response to food intake?
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Which hormone is primarily known for stimulating growth hormone release and increasing food intake?
Which hormone is primarily known for stimulating growth hormone release and increasing food intake?
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The vagovagal reflex is associated with what key function in relation to the gut?
The vagovagal reflex is associated with what key function in relation to the gut?
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Which of the following statements regarding ghrelin is true?
Which of the following statements regarding ghrelin is true?
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Which hormone primarily stimulates gastric emptying?
Which hormone primarily stimulates gastric emptying?
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Which mechanism is utilized to classify a substance as a gastrointestinal hormone?
Which mechanism is utilized to classify a substance as a gastrointestinal hormone?
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What is the role of GIP in carbohydrate digestion?
What is the role of GIP in carbohydrate digestion?
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What effect does ghrelin have in the fasted state?
What effect does ghrelin have in the fasted state?
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How does leptin primarily influence food intake regulation?
How does leptin primarily influence food intake regulation?
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What is the primary action of motilin in the gastrointestinal system?
What is the primary action of motilin in the gastrointestinal system?
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Which hormone is most likely to decrease in response to food intake?
Which hormone is most likely to decrease in response to food intake?
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Which gastrointestinal hormone is classified as a major inhibitor of gastric acid secretion?
Which gastrointestinal hormone is classified as a major inhibitor of gastric acid secretion?
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What is one of the primary roles of gastrin in the stomach?
What is one of the primary roles of gastrin in the stomach?
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How does cholecystokinin (CCK) primarily affect gastric acid secretion?
How does cholecystokinin (CCK) primarily affect gastric acid secretion?
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Which of the following correctly describes the release mechanism for secretin?
Which of the following correctly describes the release mechanism for secretin?
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Which hormone primarily inhibits gastric motility after eating?
Which hormone primarily inhibits gastric motility after eating?
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What is one known function of motilin in the gastrointestinal tract?
What is one known function of motilin in the gastrointestinal tract?
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How does somatostatin primarily influence digestive function?
How does somatostatin primarily influence digestive function?
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What role does serotonin (5-HT) play in the gastrointestinal system?
What role does serotonin (5-HT) play in the gastrointestinal system?
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Which amino acids does secretin share with other hormones?
Which amino acids does secretin share with other hormones?
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How does gastrin indirectly enhance gastric acid secretion?
How does gastrin indirectly enhance gastric acid secretion?
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What would be a direct consequence of somatostatin release in the digestive system?
What would be a direct consequence of somatostatin release in the digestive system?
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Study Notes
Hormone Communication
- Hormones can communicate with the same cell (autocrine), neighboring cells (paracrine), or distant cells (endocrine).
- Some GI tract peptides and amines have hormonal functions.
- Currently, five GI peptides are considered to be hormones: gastrin, cholecystokinin (CCK), secretin, glucose-dependent insulinotropic peptide (GIP), and motilin.
- These peptides are released from enteroendocrine cells scattered throughout the mucosa, not in organized glands.
- The duodenum and jejunum are the primary sites for hormone release.
- Some hormones are also released in the antrum of the stomach and ileum.
Gastric Phases
- Cephalic Phase: Initiated by sight, smell, or thought of food, it triggers gastrin release and stimulates secretion of mucus, HCl, and pepsinogen.
- Gastric Phase: Stretching of the stomach activates stretch receptors, stimulating peristalsis and gastric emptying.
- Intestinal Phase: Activated by intestinal receptors, it inhibits gastric secretion through CCK and secretin, slowing gastric emptying.
- Basal gastric acid secretion increases in anticipation of or during food consumption, driven by cephalic, gastric, and intestinal phase mechanisms.
Gastrin and CCK
- Gastrin and CCK are structurally related peptide hormones that act on CCK receptors.
- Both hormones share a C-terminal sequence essential for activity.
- Gastrin has 17 amino acids, and CCK has 33 amino acids.
- Due to homology, they can bind each other's receptors: CCK-1 receptors in the gallbladder (predominantly CCK), and CCK-2 (gastrin) receptors in the stomach (predominantly gastrin).
Gastrin Release
- The antrum of the stomach houses the highest concentration of gastrin-containing cells (G cells).
- Gastrin release is triggered by various stimuli during each gastric phase:
- Cephalic and Gastric Phases: Gastrin-releasing hormone (GRP) is the neurotransmitter released by vagovagal stimulation.
- Gastric and Intestinal Phases: Breakdown of protein to amino acids stimulates gastrin release.
Secretin
- Secretin is a hormone released from the duodenum in response to acidic chyme entering from the stomach.
- It stimulates the pancreas to produce bicarbonate-rich fluid, neutralizing the acidic chyme.
- Secretin also stimulates the gallbladder to release bile.
Cholecystokinin (CCK)
- CCK is released from the small intestine in response to the presence of fats and proteins.
- It triggers pancreatic acinar cells to release digestive enzymes, aiding in the breakdown of fats and proteins.
- CCK also causes contraction of the gallbladder, releasing bile into the duodenum for fat digestion.
Brunner's Glands
- Brunner's glands are located in the early duodenum and secrete mucus and bicarbonate.
- They protect the duodenum from acidic stomach contents.
- Their secretion is increased by food presence (distention or irritation), vagal stimulation, and secretin and CCK release.
- Sympathetic stimulation decreases Brunner's gland secretion.
Control of Food Intake
- Central regulation of food intake occurs in the hypothalamus.
- The hypothalamus receives afferent signals from various neuro-humoral pathways, including those involved in digestion, emotion, behavior, and reward.
- There are two efferent pathways from the hypothalamus:
- Anorexigenic Pathway: Inhibits food intake and increases metabolism.
- Orexigenic Pathway: Stimulates food intake and inhibits metabolism.
Inhibitory Pathway for Food Intake
- The anorexigenic pathway involves pro-opiomelanocortin (POMC) containing neurons in the hypothalamus.
- These neurons release α-melanocyte-stimulating hormone (α-MSH), binding to melanocortin receptors (MC4) on second-order neurons to suppress food intake and stimulate metabolism.
Stimulatory Pathway for Food Intake
- The orexigenic pathway involves neuropeptide Y (NPY).
- Hunger signals stimulate NPY release, which binds to Y1 receptors to increase feeding behavior and calorie storage.
Peripheral Regulation of Food Intake
- The vagus nerve carries afferent fibers relaying information to the nucleus tractus solitarius in the brain.
- This input can cause an efferent signal through vagal nerves, altering gut function, known as the vagovagal reflex.
- Vagal stimulation induces satiety and inhibits feeding.
- Blockage of vagal afferents eliminates satiety.
- Insulin released following a meal acts directly on the hypothalamus, inducing satiety.
- Leptin, released from adipocytes, stimulates the POMC pathway, inhibits the NPY pathway, and overall induces satiety.
Gastric Inhibition of Food Intake
- Distension of the stomach stimulates vagal afferents and inhibits feeding.
- CCK, released in response to food in the small intestine, stimulates satiety and inhibits feeding, both by stimulating vagal afferents and insulin release.
- Peptide YY, released by enteroendocrine cells of the ileum and colon in response to fat digestion, stimulates satiety by directly inhibiting NPY orexigenic nerves.
Gastric Stimulation of Food Intake
- Ghrelin is released from oxyntic glands in the stomach (and potentially other sites).
- It stimulates growth hormone release and directly stimulates orexigenic NPY neurons, increasing food intake.
- Ghrelin release is not affected by protein intake or distention.
- Dopaminergic neurons from the ventral tegmental area (VTA) of the midbrain (reward pathways) are influenced by sight, smell, and taste of food. They can influence the hypothalamus and are affected by ghrelin and leptin.
Additional Peptides
- Glucagon-like peptide 1 (GLP-1) inhibits food intake, stimulates insulin release, and inhibits gastric function.
- Oxyntomodulin (OXM) inhibits food intake.
- Pancreatic polypeptide (PP) inhibits food intake.
GIT Hormones
-
Hormonal Communication Types
- Autocrine: Communication with the same cell
- Paracrine: Communication with neighboring cells
- Endocrine: Communication with distant cells
-
GI Peptides/Amines
- Five are considered hormones: gastrin, CCK, secretin, GIP, and motilin
- Enter the systemic circulation
- Some act as endocrine, paracrine, or neural signals
- Released from enteroendocrine cells scattered throughout the mucosa
-
Duodenum and Jejunum are Sites of Hormone Release
- Some are also released in the stomach antrum and ileum
-
Gastrin
- Acts on CCK-2 (gastrin) receptors in the stomach
- Increases acid secretion from oxyntic/parietal cells
- Stimulates histamine release from ECL cells, further boosting acid secretion
- Acts as a trophic agent, stimulating stomach mucosal growth
- May also involve histamine in growth stimulation
- Overlaps with CCK actions, stimulating the CCK-1 receptor
- Increases splanchnic blood flow
-
Cholecystokinin (CCK)
- Released from I cells in the upper small intestine (duodenum and jejunum)
- Stimulated by proteins and fats
- Peptides and single amino acids for protein
- Fatty acids or monoglycerides for fats
- Involves activation of sensory afferents
- I cells may directly sense substrates as they are absorbed
- Primarily acts on the gallbladder and pancreas
- Complex effects on gastric acid secretion
- Stimulation via CCK-2 receptors increases acid secretion
- Inhibition via CCK-1 receptors that release somatostatin from D cells
- Increases splanchnic blood flow
-
Secretin
- Shares amino acid residues with GIP, VIP, and glucagon
- Released by S cells, mainly in the duodenum
- Stimulated by pH and fatty acids
- Secretin-releasing peptide triggers release following activation of sensory afferents
- S cells may also directly sense pH and fatty acids
- Primarily promotes pancreatic and gallbladder secretions
- Also stimulates insulin from the pancreas
- Decreases acid secretion (via somatostatin) and gastric motility (vagally)
- Increases blood flow
-
Somatostatin
- Released from delta or D cells in the pancreas and stomach
- Released in response to CCK and ACh stimulated by increased blood glucose and amino acids after meals
- Generally inhibitory, decreasing motility, acid secretions, and blood flow
-
Motilin
- Released from the mucosa of the upper GI tract (specifically, 'Mo' cells)
- Released in 90-minute cycles, inhibited by meal ingestion
- Causes the migrating motor complex (rumbling) that helps clear foreign bodies
- Its only known function
-
Gastric Inhibitory Peptide (GIP)
- Stimulated by food in the upper small intestine
- Released from K cells in the duodenum and jejunum
- Inhibits gastric secretions and motility
- Major action is stimulating insulin secretion
- Now called glucose-dependent insulinotropic polypeptide
-
Serotonin (5-HT)
- Released from enterochromaffin cells
- Involved in vomiting
- Some anti-emetics block the 5-HT3 receptor on sensory afferent fibers (ondansetron)
-
Brunner’s Glands
- Mucous-secreting glands in the early duodenum
- Secrete mucus and HCO3- to protect the duodenum from stomach acid
- Increased secretion by food in the duodenum (distention/irritation) and vagal stimulation, also secretin and CCK
- Decreased secretion by sympathetic stimulation
-
Control of Food Intake
- Central regulation occurs in the hypothalamus
- Receives signals from various neuro-humoral pathways, including digestion, emotion, behavior, and reward
- Two efferent pathways from the hypothalamus:
- Anorexigenic pathway: Inhibits food intake and increases metabolism
- Orexigenic pathway: Stimulates food intake and inhibits metabolism
-
Inhibitory (Anorexigenic) Pathway
- Melanocortin pathway
- POMC-containing neurons in the hypothalamus release α-MSH
- α-MSH binds to MC4 receptors on second-order neurons to inhibit food intake and stimulate metabolism
-
Stimulatory (Orexigenic) Pathway
- Neuropeptide Y (NPY)
- Hunger signals stimulate NPY release
- NPY binds to Y1 receptors to increase feeding behavior and calorie storage
-
Food Intake - Peripheral Regulation
- Vagal nerve transmits information to the brain's nucleus tractus solitarius
- Vagal stimulation induces satiety and inhibits feeding
- Blocking vagal afferents eliminates satiety
- Insulin from pancreatic β-cells acts directly on the hypothalamus to induce satiety
- Leptin from adipocytes stimulates the POMC pathway and inhibits the NPY pathway, overall inducing satiety
-
Food Intake - Gastric (Inhibitors)
- Local gastric stimuli pass information to the hypothalamus
- Stomach distension stimulates vagal afferents and inhibits feeding
- CCK release from the small intestine stimulates satiety and inhibits feeding
- Via stimulation of vagal afferents and insulin release
- Peptide YY released from the ileum and colon by fat digestion products stimulates satiety
- Directly inhibits the orexigenic NPY nerves
-
Food Intake - Stimulants
- Ghrelin released from oxyntic glands in the stomach (and possibly extra-gastric sites)
- Stimulates growth hormone release
- Directly stimulates the orexigenic NPY neurons (increased food intake)
- Ghrelin release is not affected by protein intake or distention
- Dopaminergic neurons from the ventral tegmental area (VTA) of the midbrain (reward pathways)
- Influenced by sight, smell, and taste of food
- Influence the hypothalamus but are also affected by ghrelin and leptin
- Ghrelin released from oxyntic glands in the stomach (and possibly extra-gastric sites)
-
Additional Peptides (Not Examinable)
- Glucagon-like peptide 1 (GLP-1): Inhibits food intake, stimulates insulin release, and inhibits gastric function
- Semaglutide/Ozempic is a GLP-1 agonist
- Tirzepatide/Mounjaro is a GIP and GLP-1 agonist
- Oxyntomodulin (OXM): Inhibits food intake
- Pancreatic polypeptide (PP): Inhibits food intake
- Glucagon-like peptide 1 (GLP-1): Inhibits food intake, stimulates insulin release, and inhibits gastric function
-
Summary Table
-
Trigger vs. Hormones: Gastrin, CCK, Secretin, GIP, Motilin
- Acid
- Carbohydrate
- Fats
- Protein
- Distension
- Nervous
-
Actions vs. Hormones: Gastrin, CCK, Secretin, GIP, Motilin
- Acid Secretion
- Gastric Emptying
- Pancreatic Secretion
- Gastric Motility
- Intestinal Motility
- Insulin Release
-
Trigger vs. Hormones: Gastrin, CCK, Secretin, GIP, Motilin
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Description
This quiz focuses on the mechanisms of hormone communication, including autocrine, paracrine, and endocrine signaling. It also covers the different phases of gastric activity: the cephalic, gastric, and intestinal phases, and their physiological implications related to digestion.