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Molecular Endocrinology > Gut Hormones (7-8) > Flashcards

Gut Hormones (7-8) Flashcards

1
Q

What are some features of gut hormones?

A

→ all peptide hormones
→ many found elsewhere (e.g. brain)
→ act in both paracrine and endocrine fashion

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2
Q

What are some hormones of the upper gut/stomach?

A

Ghrelin → hunger, growth hormone releasing
Gastrin → acid secretion

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3
Q

What are some hormones of the middle gut/duodenum?

A

Secretin → pancreatic exocrine secretion
GIP → incretin activity
Motilin → gastrointestinal motility

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4
Q

What is the gross anatomy of the GI tract?

A

GI = gastrointestinal
→ a long continuous muscular digestive tube

involved in: ingestion, propulsion, mechanical digestion, chemical digestion, absorption, defecation

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5
Q

What are some functional considerations of the GI tract?

A

→ substances in the GI tract lumen are outside of the body
→ multiple sensors and receptors line the GI tract to monitor contents and respond to conditions
→ controls: intrinsic (local control) and extrinsic (CNS)

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6
Q

What are the four tunics of the GI tract?

A

Mucosa → epithelium, lamina propria, muscular mucosae
Submucosa → glands, receptors
Muscularis externa → longitudinal muscle, circular muscle
Serosa → epithelium, connective tissue

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7
Q

Does the innermost mucosa differ throughout the GI tract?

A

The histology/morphology is slightly different throughout
→ oesophagus, stomach, small intestine, large intestine differ - functional diversity
→ same tunics are there
→ e.g. small intestine - more absorpative

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8
Q

Where are the endocrine cells found?

A

Gastric pits in the stomach lining
→ gastric pits lead to gastric glands

Cells in gastric gland change as you go down
→ mucous cells, parietal cells, chief cells and enteroendocrine cells

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9
Q

What is the function of parietal cells?

A

Produce HCL
→ maintain acidic environment for proper digestion and nutrient absorption
→ controlled by enteroendocrine cells
→ acidity changes biology of Na H+ pumps

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10
Q

What is the function of chief cells?

A

Role in secreting enzyme pepsinogen
→ becomes active form pepsin in acidic environment

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11
Q

What is the function of enteroendocrine cells?

A

Paracrine
Neuronal → afferent vagal, splanchnic and enteric nerves
Endocrine → enters blood

Regulates digestive and metabolic functions, appetite and energy homeostasis

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12
Q

What are 7TM chemosenesors?

A

G-protein couples receptors found on entero-endocrine cells in the GI tract
→ have 7 transmembrane domains
→ involved in detecting luminal contents - nutrients, metabolites etc

e.g. short chain fatty acids → GPR41
proteolytic products → GPR93
bile acids → GPR131

activation causes release of GI-tract hormones

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13
Q

What are G-cell endocrine cells?

A

Type of endocrine cell found in stomach responsible for releasing gastrin

Food enters stomach
→ signals in pit to G cell
→ G cells sense increase Ca2+
→ release gastrin
→ gastrin regulates parietal cells
→ release of HCl

regulate gastric acid secretion and maintaining digestive function

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14
Q

How does gastrin work?

A

Controls acid secretion directly → via CCK receptors on parietal cells
Control acid secretion indirectly → through inducing histamine containing ECL cells

Regulated by pH and somatostatin
Also drives mucosal growth and effects gastric motility

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15
Q

What signals to parietal cells?

A

Parietal cells have many signals - lots of things controlling them
→ direct from gastrin
→ histamine from ECL
→ neural input
→ feedback via somatostatin from D cells

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16
Q

How is the movement of membrane and vesicles regulated in parietal cells?

A

Primarily driven by the action of proton pumps and transporters in the cell membrane

Proton pump → H+ out of cytoplasm, K+ into cytoplasm contributing to the acidic environment
Chloride ions → Cl out of cytoplasm into stomach lumen following gradient established by proton pumps

Fusion of vesicles leads to secretion of HCl

Regulated by hormones like gastrin, somatostatin and histamine

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17
Q

What are proton pump inhibitors?

A

Used for indigestion, peptic uncles and increased acid secretion

e.g. omeprazole
massive industry

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18
Q

How do parietal cells regulate vitamin B12 absorption?

A

Parietal cells secrete intrinsic factor
→ glycoprotein hormone required for vitamin B12 absorption in the ilium

Loss of parietal cells can lead to pernicious anaemia (changes avg volume of RBC)

19
Q

How is gastrin synthesised?

A

Gastrin gene transcribed and translated in G cell nucleus - forms preprogastrin (precursor of gastrin)

Preprogastrin undergoes post-translational modifications as it moves through ER → signal peptide removed forming progastrin

Further processing produces mature gastrin peptides - gastrin34gly, gastrin34, gastrin17

Stored in secretory vesicles in G cells

Metabolised by kidney, intestine and liver

20
Q

How is somatostatin regulated in the stomach?

A

Low gastric pH stimulates delta cells (found in antrum where they are open to the lumen) that secrete somatostatin and inhibit gastrin release

Also influenced by
→ mechanical stimulation
→ dietary components of a meal
→ other hormones and neurotransmitters

21
Q

What are the functions of somatostatin?

A

In the gut somatostatin has broad inhibitory action
→ reduces gastric acid production
→ reduces pepsinogen secretion (form chief cells)
→ inhibits pancreatic enzyme, fluid and bicarbonate secretion
→ reduces bile flow
→ inhibits gut motility
→ reduces intestinal transport of nutrients and fluid
→ inhibits tissue growth and proliferation

22
Q

What is Zollinger-Ellison syndrome?

A

Gastrin secreting tumours in the pancreas/duodenum
→ excessive secretion of gastrin - stimulates stomach acid production
→ results in severe peptic ulcers

23
Q

How is glucose controlled after a meal?

A

Stimulation of insulin secretion from pancreatic beta cells

Inhibition of hepatic gluconeogenesis by suppression of glucagon secretion

Delaying delivery of carbohydrates to the small intestine by inhibiting gastric emptying

24
Q

What is the entero-insular axis?

A

The communication pathway between the entero-endocrine cells in the GI tract and the pancreas
→ allows for coordinated regulation insulin and glucagon secretion in response to changing nutrient availability

→ 50% of insulin release driven by GI hormones called incretins e.g. GLP-1, GIP

25
Q

What are incretins?

A

Hormones produced by the GI tract in response to ingestion of food
→ play a crucial role in regulating glucose metabolism by stimulating insulin

GLP-1 (glucagon like peptide) → stimulates insulin secretion from pancreatic beta cells, inhibits glucagon secretion, delaying gastric emptying

GIP (gastric inhibitory peptide) → stimulates insulin secretion from pancreatic beta cells in response to elevated blood glucose, promotes fat storage in adipose tissue

26
Q

What is the structure of insulin?

A

2 chains → A and B, linked with disulphide bonds

Intermediate C-peptide → cleaved to make insulin correctly, clean C peptide can assume insulin made right

27
Q

What is the incretin effect?

A

Oral ingestion of nutrients results in a greater stimulation of insulin secretion compared to intravenous - with the same amount of nutrients
→ attributed to the action of incretin hormones like GLP-1 and GIP which stimulate insulin secretion from pancreatic beta cells when glucose levels are high
→ significant role in glucose homeostasis

28
Q

How are glucagon and GLP-1 made from the same pro hormone?

A

Glucagon and GLP-1 are made from the same gene and pre protein but have opposite actions
→ tissue specific processing of glucagon pro hormone allows for this

alpha cells → glucagon, pancreas
→ released from pancreas, binds G protein-coupled receptors in skeletal muscle and liver, exerting its glucoregulatory effect
L cells → GLP-1, small intestine
→ stimulates insulin secretion and augments the insulin-releasing effects of glucose on the pancreatic beta cells

29
Q

What are the outputs of GLP-1?

A

Pancreas → stimulates insulin secretion (tropic)
→ promotes beta-cell mass increase (trophic - driving mitosis)
→ inhibits alpha-cell glucagon secretion

Nervous system → slows down gastric motility/stomach emptying

30
Q

How does the glucagon gene undergo tissue specific processing?

A

Preproglucagon undergoes tissue specific processing depending on where its expressed, due to different prohormone convertases present, for example;

Pancreatic alpha cells → preproglucagon mRNA is processed into proglucagon which is cleaved by Psck2 to produce glucagon

Intestinal L cells → preproglucagon processed into different peptides, Psck1/3 cleaved proglucagon into smaller peptides including GLP-1, GLP-2

Overall ensures the actions of glucagon and its derivatives are tailored to the specific metabolic needs of the different tissues

31
Q

What is the role of DPP-4 enzyme?

A

Incretin degrader → particularly inactivates GLP-1 and GIP, rapidly cleaves aa on their N-terminus
→ reducing their ability to induce insulin secretion

Potential therapeutic target with DPP-4 inhibitors → inhibit DPP-4 to promotes incretin effect in diabetes

32
Q

What are the actions of GLP-2?

A

Secreted by gut endocrine L cells
→ promotes intestinal growth
→ mucus proliferation
→ maintaining integrity of the intestinal barrier
→ contributes to intestinal motility

33
Q

What are the roles of GIP?

A

GIP (gastric inhibitory peptide) is secreted by enteroendocrine K cells proximal intestine/duodenum
→ stimulates insulin secretion from pancreatic beta cells (incretin hormone)
→ inhibits motility and secretion of H+ stomach secretion

34
Q

What is the potential therapeutic target for type 2 diabetes involving GIP?

A

DPP IV resistant stable GIP agonists
→ enzyme resistant analogues (with additional amine group to prolong half life) of GIP possessing enhanced agonist activity
→ increase insulin secretion, beta cell mass and glucose-responsiveness

35
Q

What is ghrelin?

A

28aa peptide hormone released by the stomach
→ stimulates hunger
→ binds to neurones in hypothalamus to stimulate feelings of hunger
→ as stomach emptying (fasting) ghrelin levels rise - driving appetite

Also plays a role in regulating growth hormone release from anterior pituitary

36
Q

What structure of ghrelin determines its interaction with membrane and receptors?

A

Octanoic acid on Ser3
→ anchors to membrane - how it attaches to receptors

37
Q

How does ghrelin reach its receptor in the brain?

A

Not good at crossing the blood brain barrier
→ to moves to brain via vagal nerve
→ ghrelin activates NPY and agouti-related protein-producing neurones in the arcuate nucleus of the hypothalamus - involved in regulation of feeding (balanced by leptin)

38
Q

How can surgery reduce appetite?

A

Bariatic surgery like proximal gastric bypass surgery (gastric band) or sleeve gastrectomy can reduce circulating ghrelin
→ leading to a reduction in appetite

39
Q

What is cholecystokinin?

A

Peptide hormone produced by )-cells of the small intestine
→ secreted into blood following ingestion of a meal
→ forms of CCK ranging in size from 58 to 8 have similar biological activities
→ all forms produced from a a single gene by post-translational processing of a pre-pro-hormone

40
Q

What are the effects of cholecystokinin?

A

CCK binds specific CCK1 receptors

Gallbladder → stimulates gallbladder contraction
Pancreas → pancreatic secretion
Smooth muscle of the stomach → regulates gastric emptying
Peripheral nerves → bowel motility
CCK induces satiety (works against ghrelin)
Inhibits gastric secretion → binding to CCK receptors on somatostatin

→ coordinate ingestion, digestion and absorption of dietary nutrients

41
Q

What is motilin?

A

22aa peptide hormone produced by M-cells of the duodenum
→ secretion not induced by eating
→ synchronised with inter digestive migrating motor complex under fasting conditions

42
Q

What is the effect of motilin?

A

Binds specific receptors on smooth muscle cells of the oesophagus, stomach and intestines to enhance propulsive activity
→ erythromycin and related antibodies act as non-peptide motlilin agonists

43
Q
A

Molecular Endocrinology (7 decks)

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