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Questions and Answers
What is primarily responsible for stimulating pancreatic secretion during the intestinal phase?
What is primarily responsible for stimulating pancreatic secretion during the intestinal phase?
Which two hormones play a significant role in the stimulation of pancreatic secretion?
Which two hormones play a significant role in the stimulation of pancreatic secretion?
What role does secretin play in pancreatic secretion?
What role does secretin play in pancreatic secretion?
What initiates the vagovagal reflexes that stimulate pancreatic secretion during the gastric phase?
What initiates the vagovagal reflexes that stimulate pancreatic secretion during the gastric phase?
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How does CCK affect the gall bladder during digestion?
How does CCK affect the gall bladder during digestion?
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Which component of bile is most crucial for fat digestion?
Which component of bile is most crucial for fat digestion?
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What is the primary source of CCK secretion?
What is the primary source of CCK secretion?
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Which of the following statements about gastrin's role in pancreatic secretion is accurate?
Which of the following statements about gastrin's role in pancreatic secretion is accurate?
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What effect does neuropeptide Y (NPY) have on metabolism?
What effect does neuropeptide Y (NPY) have on metabolism?
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Which peptide acts as an antagonist of the MC4 receptor?
Which peptide acts as an antagonist of the MC4 receptor?
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What is the relationship between the POMC pathway and the NPY system?
What is the relationship between the POMC pathway and the NPY system?
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What role do peptides that stimulate the melanocortin system play in relation to the NPY system?
What role do peptides that stimulate the melanocortin system play in relation to the NPY system?
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Which pathway is activated for increased food intake?
Which pathway is activated for increased food intake?
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What initiates the cephalic phase of gastric secretion?
What initiates the cephalic phase of gastric secretion?
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During which phase does the stimulation of peristalsis occur?
During which phase does the stimulation of peristalsis occur?
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What is the function of cholecystokinin (CCK) in the intestinal phase?
What is the function of cholecystokinin (CCK) in the intestinal phase?
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Which sequence of amino acids is crucial for the activity of both gastrin and CCK?
Which sequence of amino acids is crucial for the activity of both gastrin and CCK?
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Where is the densest collection of gastrin-containing cells located?
Where is the densest collection of gastrin-containing cells located?
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What stimulates the release of gastrin during the gastric phase?
What stimulates the release of gastrin during the gastric phase?
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Which type of receptor does CCK predominantly act upon in the gallbladder?
Which type of receptor does CCK predominantly act upon in the gallbladder?
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What is the primary stimulus for gastrin release during the intestinal phase?
What is the primary stimulus for gastrin release during the intestinal phase?
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What receptor does gastrin primarily act on to increase acid secretion in the stomach?
What receptor does gastrin primarily act on to increase acid secretion in the stomach?
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Which hormone increases blood flow and stimulates gastric acid secretion through overlapping actions with gastrin?
Which hormone increases blood flow and stimulates gastric acid secretion through overlapping actions with gastrin?
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What is the primary action of secretin?
What is the primary action of secretin?
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Which statement about motilin is correct?
Which statement about motilin is correct?
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What effect does gastric inhibitory peptide (GIP) primarily have on insulin secretion?
What effect does gastric inhibitory peptide (GIP) primarily have on insulin secretion?
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Which hormone is released from I cells in the upper small intestine?
Which hormone is released from I cells in the upper small intestine?
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Which of these hormones is known for its inhibitory effects on gastrointestinal motility and secretions?
Which of these hormones is known for its inhibitory effects on gastrointestinal motility and secretions?
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What is a common stimulus for the secretion of cholecystokinin (CCK)?
What is a common stimulus for the secretion of cholecystokinin (CCK)?
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Which hormone's release is primarily triggered by increased blood glucose and amino acids?
Which hormone's release is primarily triggered by increased blood glucose and amino acids?
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What role does serotonin (5-HT) play in gastrointestinal physiology?
What role does serotonin (5-HT) play in gastrointestinal physiology?
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Which of the following hormones enter the systemic circulation?
Which of the following hormones enter the systemic circulation?
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Secretin primarily influences the secretion of which substance?
Secretin primarily influences the secretion of which substance?
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Where are enteroendocrine cells predominantly located?
Where are enteroendocrine cells predominantly located?
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What type of hormonal communication occurs between neighboring cells?
What type of hormonal communication occurs between neighboring cells?
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Which gastrointestinal hormone is primarily responsible for stimulating gastric acid secretion?
Which gastrointestinal hormone is primarily responsible for stimulating gastric acid secretion?
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Which hormone is NOT primarily considered a gastrointestinal hormone?
Which hormone is NOT primarily considered a gastrointestinal hormone?
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Which hormones are involved in the regulation of food intake?
Which hormones are involved in the regulation of food intake?
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Where is the highest release of gastrin typically observed?
Where is the highest release of gastrin typically observed?
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Which phase of gastric secretion is triggered by the sight, smell, or thoughts of food?
Which phase of gastric secretion is triggered by the sight, smell, or thoughts of food?
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What is the primary type of receptor that CCK predominantly acts upon in the gallbladder?
What is the primary type of receptor that CCK predominantly acts upon in the gallbladder?
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The secretion of gastrin during the gastric phase is triggered by which of the following stimuli?
The secretion of gastrin during the gastric phase is triggered by which of the following stimuli?
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Which characteristic is not true about the structural relationship between gastrin and CCK?
Which characteristic is not true about the structural relationship between gastrin and CCK?
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During which phase is gastric secretion inhibited by CCK and secretin due to activation of receptors in the small intestines?
During which phase is gastric secretion inhibited by CCK and secretin due to activation of receptors in the small intestines?
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Which amino acids sequence is crucial for the biological activity of both gastrin and CCK?
Which amino acids sequence is crucial for the biological activity of both gastrin and CCK?
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Where in the digestive system is the densest collection of gastrin-containing cells located?
Where in the digestive system is the densest collection of gastrin-containing cells located?
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In which situation is gastrin most likely released from G cells?
In which situation is gastrin most likely released from G cells?
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What is primarily secreted by pancreatic acinar cells?
What is primarily secreted by pancreatic acinar cells?
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During which phase does the vagus nerve stimulate pancreatic secretion primarily through acetylcholine?
During which phase does the vagus nerve stimulate pancreatic secretion primarily through acetylcholine?
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Which component of pancreatic secretion helps to neutralize gastric acid in the small intestine?
Which component of pancreatic secretion helps to neutralize gastric acid in the small intestine?
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What stimulates the release of pancreatic enzymes during the intestinal phase?
What stimulates the release of pancreatic enzymes during the intestinal phase?
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Which substance is NOT typically a component of exocrine pancreatic secretions?
Which substance is NOT typically a component of exocrine pancreatic secretions?
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What overall effect does the parasympathetic nervous system have on pancreatic secretion?
What overall effect does the parasympathetic nervous system have on pancreatic secretion?
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What is the primary purpose of the basal secretion of pancreatic enzymes?
What is the primary purpose of the basal secretion of pancreatic enzymes?
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What initiates the cephalic phase in relation to pancreatic function?
What initiates the cephalic phase in relation to pancreatic function?
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During the intestinal phase, what primarily accounts for 70-80% of the stimulation of pancreatic secretion?
During the intestinal phase, what primarily accounts for 70-80% of the stimulation of pancreatic secretion?
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What is the role of secretin in pancreatic secretion?
What is the role of secretin in pancreatic secretion?
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Which hormone is predominantly responsible for enzyme secretion during the intestinal phase?
Which hormone is predominantly responsible for enzyme secretion during the intestinal phase?
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How does CCK facilitate bile release?
How does CCK facilitate bile release?
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Which statement about the gastric phase's effect on pancreatic secretion is correct?
Which statement about the gastric phase's effect on pancreatic secretion is correct?
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What type of interactions are indicated by the dashed lines in the described mechanisms?
What type of interactions are indicated by the dashed lines in the described mechanisms?
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Which component of bile is crucial for its function in fat digestion?
Which component of bile is crucial for its function in fat digestion?
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What primarily stimulates the release of secretin?
What primarily stimulates the release of secretin?
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What is the effect of blocking the vagal afferent fibers on satiety?
What is the effect of blocking the vagal afferent fibers on satiety?
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Which hormone directly acts on the hypothalamus to induce satiety after a meal?
Which hormone directly acts on the hypothalamus to induce satiety after a meal?
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How does CCK contribute to the inhibition of feeding?
How does CCK contribute to the inhibition of feeding?
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What role does Ghrelin play in food intake regulation?
What role does Ghrelin play in food intake regulation?
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What is the primary action of Leptin in terms of appetite regulation?
What is the primary action of Leptin in terms of appetite regulation?
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What is the role of Peptide YY in regulating appetite?
What is the role of Peptide YY in regulating appetite?
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Which peptide is known to be released by the enteroendocrine cells of the ileum and colon in response to fat digestion?
Which peptide is known to be released by the enteroendocrine cells of the ileum and colon in response to fat digestion?
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What effect does the stimulation of the vagus nerve have on eating behavior?
What effect does the stimulation of the vagus nerve have on eating behavior?
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How do the mechanisms of action differ between fasted and fed states in relation to ghrelin?
How do the mechanisms of action differ between fasted and fed states in relation to ghrelin?
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Which hormone is primarily responsible for stimulating insulin release after carbohydrate intake?
Which hormone is primarily responsible for stimulating insulin release after carbohydrate intake?
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Which hormone governs gastric motility during states of acid secretion?
Which hormone governs gastric motility during states of acid secretion?
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What physiological effect does GIP have on food intake regulation in comparison to leptin?
What physiological effect does GIP have on food intake regulation in comparison to leptin?
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Which of the following is true regarding the role of motilin within the gastrointestinal tract?
Which of the following is true regarding the role of motilin within the gastrointestinal tract?
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Which step is crucial in determining whether a substance is classified as a gastrointestinal hormone?
Which step is crucial in determining whether a substance is classified as a gastrointestinal hormone?
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What impact does glucose and amino acid presence have on gastrointestinal hormone release?
What impact does glucose and amino acid presence have on gastrointestinal hormone release?
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What is the key effect of leptin on food intake in relation to NPY and POMC?
What is the key effect of leptin on food intake in relation to NPY and POMC?
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Study Notes
### GIT Hormones
- Autocrine communication is within a single cell.
- Paracrine communication is between neighbouring cells.
- Endocrine communication is between distant cells via hormones in the bloodstream.
- The term hormone can refer to all three types of signaling.
### Types of GIT hormones
- There are many GI peptides/amines with various functions.
- Only five are considered to be true hormones (enter circulation): gastrin, cholecystokinin (CCK), secretin, glucose-dependent insulinotropic peptide (GIP), and motilin.
- Some peptides are endocrine, some paracrine, and some neural.
- These peptides are released from enteroendocrine cells distributed throughout the mucosa, not organized in glands.
- The duodenum and jejunum are the primary sites for hormone release.
Gastric Phases of Digestion
- Cephalic Phase: Begins with sight, smell, or thought of food. Triggers gastrin release and secretion of mucus, HCl, and pepsinogen.
- Gastric Phase: Stomach stretching activates stretch receptors, stimulating peristalsis (mixing) and gastric emptying
- Intestinal Phase: Begins with activation of receptors in the small intestine. Inhibition of gastric secretion by CCK and secretin slows gastric emptying.
### Gastrin and CCK
- Gastrin and CCK are structurally related peptides that act on CCK receptors.
- Both have a shared C-terminal sequence (Gly-Trp-Met-Asp-Phe), essential for activity.
- Gastrin (17 amino acids) and CCK (33 amino acids) can both act on each other's receptors.
- CCK-1 receptors are primarily found in the gallbladder (CCK).
- CCK-2 (or gastrin) receptors are primarily found in the stomach (gastrin).
### Gastrin Release
- G cells in the antrum of the stomach contain the highest concentration of gastrin.
- G cells are also found in the duodenum.
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Stimuli for Gastrin Release:
- Cephalic Phase: Gastrin-releasing peptide (GRP) is the neurotransmitter released via vagovagal stimulation.
- Gastric Phase: Stomach stretching stimulates GRP release.
- Gastric and Intestinal Phase: Breakdown of proteins to amino acids also stimulates gastrin release.
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Gastrin Actions:
- Increases acid secretion from oxyntic/parietal cells via CCK-2 receptors.
- Stimulates histamine release from ECL cells, leading to further acid secretion.
- Acts as a trophic agent, promoting growth of stomach mucosa.
- Stimulates splanchnic blood flow.
### Cholecystokinin (CCK) Release
- I cells located in the upper small intestine (duodenum and jejunum) release CCK.
- CCK release is stimulated by proteins and fats (peptides, single amino acids, fatty acids, monoglycerides).
- Sensory afferents (nerve fibers) are activated, and I cells may directly sense substrates during absorption.
### Cholecystokinin (CCK) Actions
- Most actions are on the gallbladder and pancreas.
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Effects on Gastric Acid Secretion:
- Stimulates acid secretion via CCK-2 receptors.
- Inhibits acid secretion via CCK-1 receptors, stimulating somatostatin release from D cells.
- Increases splanchnic blood flow.
### Secretin
- Secretin shares amino acid residues with GIP, VIP, and glucagon.
- S cells in the duodenum release secretin.
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Stimuli for Secretin Release:
- Low pH and, to a lesser extent, fatty acids.
- Secretin-releasing peptide activates sensory afferent fibers.
- S cells may directly sense pH and fatty acids.
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Secretin Actions:
- Stimulates pancreatic secretions (aqueous solution, bicarbonate).
- Stimulates insulin release.
- Decreases gastric acid secretion and gastric motility (via somatostatin and vagal pathways).
- Increases splanchnic blood flow.
### Other Hormones
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Somatostatin is released from delta (D) cells in the pancreas and stomach.
- Stimulated by CCK and ACh (released in response to increased blood glucose and amino acids).
- Acts as an inhibitor, decreasing motility, acid secretion, and blood flow.
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Motilin is released from enteroendocrine (“Mo”) cells in the mucosa of the upper GI tract.
- Released in 90-minute cycles, and inhibited by food intake.
- Responsible for the migrating motor complex, which assists in clearing foreign bodies.
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Gastric Inhibitory Peptide (GIP), now called glucose-dependent insulinotropic polypeptide (GIP), is released from K cells in the duodenum and jejunum.
- Stimulated by the presence of food in the upper small intestine.
- Inhibits gastric secretions and motility.
- Primarily stimulates insulin secretion.
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Serotonin (5-HT) is released from enterochromaffin cells.
- Involved in vomiting.
- Some anti-emetics (e.g., ondansetron) block 5-HT3 receptors on sensory afferent fibers.
Pancreatic Secretion
- Gastric Phase: Stomach distension activates vagovagal reflexes, stimulating pancreatic secretion. Gastrin plays a minimal role.
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Intestinal Phase: The presence of digestion products (70-80% of stimulation) and H+ in the small intestine stimulates pancreatic secretion.
- Secretin released by acid stimulates ductal cells, increasing aqueous volume and pH (due to HCO3-).
- CCK released by fat and protein digestion stimulates acinar cells to increase enzyme secretion.
- CCK acts indirectly via vagal afferent fibers.
### Bile Secretion
-
Bile is produced by hepatocytes (liver cells), stored in the gallbladder, and released into the duodenum.
- Bile is crucial for fat digestion and consists of: water, bilirubin, cholesterol, bile salts, and other fats.
- Secretin stimulates water and bicarbonate secretion from bile ducts.
- CCK acts on CCK-1 receptors in the gallbladder to contract it and relax the sphincter of Oddi, releasing bile acids into the small intestine.
### Central Control of Food Intake
- The hypothalamus plays a crucial role in regulating food intake.
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Neuropeptide Y (NPY) and proopiomelanocortin (POMC) systems:
- NPY system: stimulates food intake.
- POMC system: inhibits food intake.
- These systems have antagonistic effects.
- CCK inhibits food intake by activating POMC neurons.
- CCK also acts on the vagus nerve, contributing to satiety.
Neurohumoral Signals
- The cephalic phase of gastric secretion is initiated by sight, smell or thoughts of food, releasing gastrin into the blood and stimulating secretion of mucus, HCl and pepsinogen.
- During the gastric phase, stretching of the stomach activates stretch receptors, stimulating peristalsis (mixing) and gastric emptying.
- The intestinal phase begins with activation of receptors in the small intestines, inhibiting gastric secretion by CCK and secretin, and slowing gastric emptying.
Gastrin and Cholecystokinin (CCK)
- Gastrin and CCK are structurally related peptide hormones that act at the CCK receptors.
- They share the C-terminal sequence, essential for activity: Gly – Trp – Met – Asp – Phe.
- CCK-1 receptor is found in the gallbladder, predominantly activated by CCK.
- CCK-2 (or gastrin) receptor is found in the stomach, predominantly activated by gastrin.
Gastrin Release
- Gastrin-containing cells (G cells) are densest in the antrum of the stomach, with some in the duodenum.
- Gastrin release is triggered by different stimuli across each gastric phase:
- Cephalic and gastric phases: vagovagal stimulation, gastrin releasing hormone (GRP) as neurotransmitter.
- Gastric and intestinal phases: breakdown of protein to amino acids also stimulates gastrin release.
Pancreatic Secretions
- The pancreas has both endocrine and exocrine secretions.
- Endocrine secretions (glucagon and insulin) are not the focus here.
- Exocrine secretions consist of:
- An aqueous component (mainly Na+ and HCO3- secreted by ductal epithelial cells).
- A proteinaceous/enzymatic component (inactive precursors of digestive enzymes secreted by acinar cells).
Control of Pancreatic Secretion
- The pancreas produces a basal secretion of enzymes and fluid during the interdigestive period, coordinated by the parasympathetic nervous system, aided by CCK.
- Pancreatic juice secretion increases up to 20 times during a meal, driven by stimulatory and inhibitory mechanisms across cephalic, gastric, and intestinal phases.
Cephalic Phase of Pancreatic Secretion
- Stimuli: conditioned reflexes, smell, taste, chewing, and swallowing.
- Afferent impulses travel to the vagal nucleus.
- Vagal ACh stimulates both acinar and ductal secretions.
- Gastrin (released by the vagus) stimulates acinar cells, the role in humans is unclear.
Gastric Phase of Pancreatic Secretion
- Stimulation is mediated by the same mechanisms as the cephalic phase.
- Distension of the stomach wall initiates vagovagal reflexes to the pancreas.
- Gastrin plays little to no role in stimulating the pancreas.
Intestinal Phase of Pancreatic Secretion
- Presence of digestion products and H+ in the small intestine accounts for 70-80% of pancreatic secretion stimulation.
- Secretin and CCK account for almost all hormonal stimulation:
- Secretin release, stimulated by acid and long chain fatty acids, stimulates the ductal cells to increase the aqueous solution, increasing volume and pH.
- CCK, stimulated by fat and protein digestion, stimulates the acinar cells to increase enzyme secretion.
Bile
- Secreted by liver cells (hepatocytes), stored in the gall bladder, and released into the duodenum.
- Crucial for fat digestion, consisting of water, bilirubin, cholesterol, bile salts, and other fats.
- Secretin stimulates water and bicarbonate secretion from bile ducts.
- CCK constricts the gall bladder and relaxes the sphincter of Oddi, releasing bile acids.
Food Intake - Peripheral Regulation
- The vagus nerve carries afferent fibers relaying information to the nucleus tractus solitarius in the brain.
- Input can also cause efferent signals by vagal nerves, resulting in changes in gut function: "vagovagal reflex."
- Vagal stimulation induces satiety and inhibits feeding.
- Blocking of vagal afferents eliminates satiety.
- Insulin, released from pancreatic β-cells after a meal, acts directly on the hypothalamus to induce satiety.
- Leptin, released from adipocytes, stimulates the POMC pathway, inhibits the NPY pathway, inducing satiety.
Food Intake - Gastric (Inhibitors)
- Local gastric stimuli pass information back to the hypothalamus.
- Distension of the stomach stimulates vagal afferents and inhibits feeding.
- CCK, released due to food presence in the small intestine, stimulates satiety and inhibits feeding, by stimulating vagal afferents and insulin release.
- Peptide YY, released by enteroendocrine cells of the ileum and colon by fat digestion products, stimulates satiety, directly inhibiting NPY orexigenic nerves.
Food Intake - Stimulants
- Ghrelin is released from oxyntic glands in the stomach, also released from extra-gastric sites.
- Stimulates release of growth hormone and directly stimulates 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) influence the hypothalamus, affected by ghrelin, leptin etc.
Summary
- Gastrin: stimulated by acid, protein, distension, nervous input.
- CCK: stimulated by fats, carbohydrates, distension, nervous input.
- Secretin: stimulated by acid, carbohydrates, distension, nervous input.
- GIP: stimulated by carbohydrates, distension, nervous input.
- Motilin: stimulated by fats, carbohydrates, distension, nervous input.
Summary
- Gastrin: decreases gastric emptying, increases gastric motility, increases acid secretion.
- CCK: decreases gastric emptying, increases pancreatic secretion, increases gallbladder contraction.
- Secretin: increases pancreatic secretion, increases bicarbonate secretion, increases bile duct secretion.
- GIP: increases insulin release.
- Motilin: increases intestinal motility.
GI Hormone Criteria
- Step 1: Does a meal or other physiological event provide a stimulus for one part of the GI tract to affect another?
- Step 2: Does this affect persist after nervous communication between those parts is removed?
- Step 3: Can you isolate a substance from the site of the stimulus that when injected mimics the effect of the stimulus?
- Step 4: Can you identify the substance chemically and synthesise it?
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Description
Explore the intricate roles of GIT hormones in digestion with this quiz. Learn about the different types of communication within the body, the distinction between true hormones, and their functions. This quiz covers the gastric phases of digestion, focusing on key peptides and their actions.