25 Gastrointestinal Peptides Chan Flashcards

1
Q

What are the characteristics of Gut Peptide Hormones?

A

Diverse cellular sources. Wide scope of biological activities. Multiple structural forms. Multiple receptor subtypes. Multiple ligand-receptor specificity. Few therapeutic applications

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2
Q

What is Gastrin secreted by?

A

G cells in the stomach

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3
Q

What are the effects of Gastrin?

A

Increases acid secretion, increases mucus growth

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4
Q

What is the stimulus for Gastrin release?

A

Peptides and amino acids in lumen; Gastrin releasing peptide and ACh in nervous reflexes

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5
Q

What is Cholecystokinin (CCK) secreted by?

A

Endocrine cells of the small intestine (Duodenum/Jejunum); neurons of the brain and gut

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6
Q

What are the effects of Cholescystokinin (CCK)?

A

Stimulates pancreatic enzyme and HCO3 secretion. Stimulates bladder contractions; inhibits stomach emptying (promotes satiety)

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7
Q

What is the stimulus for Cholescystokinin (CCK) release?

A

Fatty Acids and some Amino Acids

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8
Q

What is Secretin secreted by?

A

Endocrine cells of the small intestine (Duodenum/Jejunum)

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9
Q

What are the effects of Secretin?

A

Stimulates pancreatic and hepatic HCO3 secretion; inhibits acid secretion; Pancreatic growth. Stimulates gallbladder contraction; inhibits stomach emptying

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10
Q

What is the stimulus for Secretin release?

A

Acid in small intestine

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11
Q

What is Gastric Inhibitory Peptide secreted by?

A

Endocrine K Cells of the small intestine

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12
Q

What are the effects of Gastric Inhibitory Peptide?

A

Stimulates pancreatic insulin release. Inhibits Acid secretion. Satiety and lipid metabolism

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13
Q

What is the stimulus for Gastric Inhibitory Peptide release?

A

Glucose, Fatty Acid, and Amino Acids in small intestine

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14
Q

What is Motilin secreted by?

A

Endocrine cells in the small intestine (Duodenum/Jejunum)

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15
Q

What are the effects of Motilin?

A

Stimulates migrating motor complex for motility

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16
Q

What is the stimulus for Motilin release?

A

Fasting: cyclic release every 1.5-2 hours by neural stimulus

17
Q

What is Glucagon Like Peptide 1 secreted by?

A

Endocrine cells in small intestine

18
Q

What are the effects of Glucagon Like Peptide 1?

A

Stimulates insulin release; inhibits glucagon release. Possibly inhibits acid secretion. Slows gastric emptying. Satiety

19
Q

What is the stimulus for Glucagon Like Peptide 1 release?

A

Mixed meals of fats and carbohydrates

20
Q

What secretes Somatostatin and where are they located?

A

D cells, located throughout the GI tract

21
Q

Which GI regulatory peptide has endocrine, paracrine, neurocrine, and autocrine activity?

A

Somatostatin

22
Q

Where are GI regulatory peptides with neurocrine activity secreted?

A

Synpatic cleft

23
Q

How does Gastrin release regulate itself?

A

When released from G cells, Gastrin can act on the CCK2R on the D cell which releases Somatostatin. Somatostatin can then bind to SSTR2 on the G cell which inhibits further Gastrin release

24
Q

Besides Gastrin release from the G cell, what else can stimulate Somatostatin release from the D cell?

A

ACh acting on the GRP nerve can activate the GRP receptor on D cells which causes Somatostatin release. This same nerve can also act on GRP receptors on G cells which can cause Gastrin release

25
Q

How does Gastrin increase acid release?

A

Gastrin acts on CCK2R’s on Parietal cells which cause H+ release

26
Q

How can Somatostatin decrease acid release?

A

Somatostatin released from D cells can act on the SSTR2’s on Parietal cells which inhibit H+ release

27
Q

How can Histamine cause acid release?

A

Histamine acts on the HRH2’s on parietal cells, causing H+ release (also act on the HRH2’s on D cells, causing Somatostatin release)

28
Q

What are the effects of Octreotide on plasma levels of growth hormone in acromegaly?

A

By 108 weeks of treatment, the amount of growth hormone is normalized

29
Q

How are GI Peptides and Body Weight Control related?

A

Obesity is associated with the metabolic syndrome, chronic diseases like DM, HTN, and heart disease. Highly resistant to treatment with most of the weight lost regained within 5 years after dieting. Binge eating is implicated for more than 25% of the over weight population and is related to dysfunction of GI peptide signaling

30
Q

What are the Incretins?

A

A group of GI hormones (GLP-1, GIP) that lower blood glucose by: increasing insulin release and inhibiting glucagon release after eating, slowing the rate of nutrient absorption and reducing food intake by reducing gastric emptying

31
Q

What is the GI peptide control of food intake (GLP-1)?

A

Released in the lower gut. Decreases food intake by slowing gastric emptying; reduced hunger and increased fullness ratings

32
Q

How is GLP-1 degraded?

A

Rapidly by dipeptidyl peptidase 4 (DPP-4). Half-life of 1-2 minutes

33
Q

What are some synthetic analogues of GLP-1?

A

Extenatide (Byetta): injectable, with a half life of 2.4 hours; multiple injections required. Liraglutide (Victoza): injectable, with a half-life of 11-15 hours; once a day injection

34
Q

What are some Dipeptidyl Peptidase-4 (DPP-4) Inhibitors?

A

Sitagliptin (Januvia): effective in improving blood glucose control when used alone or with other diabetes meds. Saxagliptin (Onglyza): used alone or in combination with other oral diabetes medicines; may worsen peripheral edema when used with TDZ

35
Q

What is the GI peptide control of food intake (Ghrelin)?

A

Produced mainly by the stomach. Increased food intake when administered to humans. Level rises before meals and falls following meals. The higher the energy value of a meal the larger the postprandial decline. Level increases from the morning to the evening, reaches higher peak before dinner than before breakfast. Level rises following weight loss in obese subjects. Insulin and somatostatin strongly inhibit Ghrelin expression and secretion

36
Q

What is the GI peptide control of food intake (Cholecystokinin (CCK))?

A

After a meal, CCK is released from endocrine 1 cells of the duodenum and the jejunum. Reduces the sensation of hunger in part by inhibiting gastric emptying. Administration to humans inhibits food intake. A decrease in plasma CCK correlates with a decreased fullness and increased hunger

37
Q

What is the GI peptide control of food intake (Peptide YY (3-36))?

A

Secreted from specialized endocrine L cells of the large bowel. Circulating levels suppressed during fasting. Released into circulation within 15 minutes after meals and peaks in about 1 hour. Infusion of PYY in normal weight humans reduced 24-hour food intake. PYY levels in obese humans are reduced but anorectic effect is preserved

38
Q

What is known as the “hunger hormone”?

A

Ghrelin. When this hormone level is high it indicates the need to eat. Causes an increase in food intake