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Veterinary Medicine Year 2 > ENI - Gastrointestinal hormones > Flashcards

ENI - Gastrointestinal hormones Flashcards

1
Q

What is GIT function regulated by?

A
  • Enteric nervous system
  • Enteric endorine system, which controls secretions, motility and appetite
  • Some CNS control via the nervous and endocrine system
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2
Q

Compare the endo and exocrine function of the GIT

A
  • Mainly based on location of secretory granules within the cell
  • Exocrine: on apical side
  • Endocrine: on basolateral side
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3
Q

List the GI hormones

A
  • Insulin
  • Glucagon
  • Gastrin
  • Secretin
  • Cholecystokinin
  • Incretins (Gastric Inhibiting Peptide and Glucagon-Like Peptide-1)
  • Motilin
  • Ghrelin
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4
Q

Where is gastrin produced?

A

G cells in stomach (fundus and corpus)

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5
Q

What are the stimuli for gastrin release?

A
  • Presence of peptides and AAs in gastric lumen
  • Stomach distension
  • Vagal stimulation i.e. sight, smell, taste, chewing of food
  • Hypercalcaemia
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6
Q

What are the major effects fo gastrin?

A
  • Stimulates release of gastric acid from parietal cells

- Stimulates release of pepsinogen from chief cells

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7
Q

Describe the inhibition of gastrin

A
  • Once pH ~3 secretion inhibited

- Negative feedback to prevent dropping pH too far as would damage tissues

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8
Q

Describe gastrinomas

A
  • TUmour of gastrin secreting cells
  • Dogs and cats
  • Excessive gastrin and thus excessive HCl and pepsinogen
  • Can lead to ulcers, vomiting (may contain blood), poor appetite, dark blood in faeces
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9
Q

Describe secretin (production site, stimulus and major effect)

A
  • Produced in duodenum
  • Stimulus for release if H+ in small intestine
  • Stimulates release of bicarb rich pancreatic and biliary fluid i.e. reverse action of gastrin
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10
Q

Describe cholecystokinin (production site, stimulus and effects)

A
  • Produced in duodenum
  • Stimulated by fatty acids, monoglycoerides and AAs in small intestine (products of digestion)
  • Stimulates secretion of pancreatic enzymes and contraction and emptying of gall bladder
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11
Q

Describe Gastric Inhibitory Polypeptide (production site, stimulus, effects)

A
  • Producedi in proximal small intestine
  • Stimulus for release is fat, glycose and AAs in small intestine (products of digestion)
  • Stops digestion, signals “overload” of digestive products
  • Inhibits gastric secretion of motility
  • Potentiates release of insulin in reponse to elevated blood glucose
  • Stimulates lipoprotin lipase activity in adipocytes
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12
Q

Describe motilin (production site, stimulus, effects)

A
  • Produced by Mo cells of small intestine
  • Release stimuli unclear, secretion associated with fasting
  • Maintains motility in stomach and small intestine
  • Stimulates production of pepsin
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13
Q

List the factors involved in appetite regulation

A
  • Incretins
  • Hypothalamic inputs
  • 4 theories: lipostat, gut peptides, glucostat and thermostat
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14
Q

Describe the role of GLP-1 in appetite regulation

A
  • Promotes insulin secretion
  • Suppresses glucagon drive of gluconeogenesis
  • Slowed gastric emptying (fuller for longer)
  • Promotes satiety (hypothalamus by decreasing pleasure of food, motivation to eat and quantity and frequency of food consumption)
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15
Q

What are the hypothalamic inputs into appetite regulation?

A
  • Neurons in arcuate nucleus
  • Satiety centre
  • Appetite
    centre
  • Biological clock
  • Processes from other cerebral loci
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16
Q

What is the effect of hormones at the level of the hypothalamus in appetite regulation?

A
  • Leptin causes satiety (anorexigenic)

- Ghrelin stimulates appetite (orexigenic)

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17
Q

Outline the satiety centre within the hypothalamus

A
  • Responds to high glucose levels

- Inhibits eating

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18
Q

Outline the appetite centre within the hypothalamus

A
  • Responds to low glucose levels

- Stimulates eating

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19
Q

Outline the effect of other cerebral loci in appetite regulation

A
  • Processses from other loci project into hypothalamus and modify appete
  • e.g. limbic system (linked to emotions)
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20
Q

What are the 4 theories of appetite?

A
  • Lipostat (fat deposits and leptin)
  • Gut peptides (CCK, PYY, Ghrelin)
  • Glucostat (glucose, VFAs, AAs)
  • Thermostat
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21
Q

Describe the lipostat theory of appetite

A
  • Adipose tissue producing leptin proportional to fat
  • Acts on membrane bound receptors in hypothalamus to decrease food intake and increase energy output
  • In general related to fat mass, but also increased in night (suppress appetite) and during starvation (even if have lots of stores, want to maintain these and use other energy)
22
Q

What is the effect of starvation and leptin?

A
  • HPA axis stimulated

- Suppresses reproductive functions, thyroid axis and immune functions

23
Q

What is the result of genetic lack of leptin?

A
  • Obesity

- Hyperphagia, hypothermia and infertile

24
Q

Expalin the importance of varying leptin resistance in seasonal reproduction

A
  • Leptin varies with season

- Allows building of fat stores coming up to breeding in order to sustain pregnancy (also occurs with hibernation)

25
Q

Explain the role of cholecystokinin in satiety

A
  • Acts on G-protein coupeld receptors
  • Released rapidly in response to meal
  • Leads to gall bladder contraction, secretion of pancreatic enzymes and bicarbonates, slow gastric emptying, inhibits gastric acid secretion, reduces food intale
  • Also found in some cells in brain and expansion of stomach after meal causes release of CCK from these
26
Q

Explain the role of peptide YY (PYY) in satiety

A
  • Secreted by L cells in GIT
  • Released after meal in proportion to calories ingested and meal composition (higher after high fat meal, even if calories are the same)
  • Stimulates satiety and decreases food intake
27
Q

Explain the role of Ghrelin in satiety

A
  • produced by stomach motly but also intestine and hypothalamic nuclei
  • Increased before a meal but decreases after
  • Stimulates appetite and removal then stimulates satiey
28
Q

Explain the role of ghrelin in hedonic pleasure of food

A
  • Receptors found in hippocampus and regions in vovled in reward systems, as well as hypothalamus
  • May activate reward links that communicate pleasure and reinforcing aspects of natural rewards e.g.food
    (As well as addictive drugs such as ethanol)
29
Q

Outline the glucostat theory of satiety

A
  • High glucose stimulates satiety centre
  • Requires insulin
  • VFAs in ruminants
  • AAs do the same
30
Q

Outline the thermostat theory of satiety

A
  • Fall in body temp below set point stimulates appetite

- Increase above normal inhibits appetite

31
Q

What are the hormonal responses to negative energy balance?

A
  • Insulin decrease
  • Thyroxine decrease
  • Glucagon increase
  • Growth hormone increase
  • Cortisol increase
  • Catecholamine increase
32
Q

What are the metabolic responses to negative energy balance?

A
  • Initially use up carbohydrate stores e.g glycogen found in liver and muscle
  • Then use fat and protein (muscle mass will decrease)
33
Q

What are some reasons for negative energy balance in the dairy cow?

A
  • Energy demands of foetus in late gestation
  • Energy demands of milk production
  • Transient anorexia at time of parturition
  • Periparturient diseases
  • Low dry matter intake combined with increased energy demands
34
Q

Which of the volatile fatty acids are glucogenic and which are ketogenic?

A
  • Glucogenic: proprionate
  • Ketogenic: acetate, butyrate
  • Ketogenic:glucogenic ratio 4:1
35
Q

Outline the use of proprionate in gluconeogenesis

A
  • Converted to oxaloacete

- Converted to glucose

36
Q

What is the fate of the ketogenic VFAs?

A
  • Converted to acetyl CoA
  • Enters TCA cycle
  • ATP produced
  • Or stored as fats
  • Or converted to ketones
37
Q

What hormones stimulate HSL?

A
  • Low insulin and high glucagon
  • Catecholamines
  • Growth hormone
  • Cortisol
38
Q

What inhibits HSL?

A

High insulin and low glucagon

39
Q

What are the 2 key risk factors for lipid metabolism disorders with negative energy balance?

A
  • Obesity

- Insulin resistance

40
Q

Outline the effect of obesity on lipid metabolism

A
  • Larger TAG present for mobilisation
  • No negative feedback/fine control of this
  • Amount released if proportional to what is available
  • More fat present, more released
  • Accumulation of lipid in adipocytes alters density of insulin receptors on membranes and insulin signalling
41
Q

Outline the pathophysiology of lipids in negative energy balance

A
  • Excessive mobilisation of fatty acids from adipose tissue
  • Increase in blood non-esterified fatty acids
  • Increased fatty acid uptake by liver
  • Attempt to increase energy production via beta oxidation
  • Pathways overwhelmed as oxaloacetate is deficient
  • Excess fatty acids converted back to TAG
  • Accumulation interferes with liver function
42
Q

Outline the link between periparturient events and negative energy balance

A
  • NEB in late pregnancy
  • Increased energy demand of foetus but decreased intake
  • Shift in blood hormones at parturition: insulin, IGF-1, thyroid hormones decrease
  • GH, prolactin and cortisol increase
  • More lipid mobilisation, less intake of food
  • Increased insulin resistance in late gestation as cortisol more present
43
Q

What is the common presentation for hepatic lipidosis in dairy cows?

A
  • Periparturient cow

- Non-specific complaints: lower milk production, loss of appetite and mild depression

44
Q

What are the common findings of hepatic lipidosis on physical examination?

A
  • Decreased rumen motility
  • Ketosis
  • Concurrent disease e.g. dystocia, LDA, retained placenta
  • Metritis or mastitis
45
Q

What are common risk factors for hepatic lipidosis

A
  • Obesity (high BCS, older cow)
  • Insulin resistance (obesity induced, stress, pregnancy related, parturition peak in cortisol)
  • Concurrent disease e.g. metritis (stress, inflammatory mediators)
  • Improper housing (stress)
  • Poor nutrition
46
Q

Outline secondary ketosis in obesity

A
  • Fatty acids converted to acetyl CoAto make ATP
  • Propionate precursor for oxaloacetate, acetate and butyrate aare precursors for acetyl CoA
  • Low proprionate if eating less, acetyl CoA into TCA inhibited = bottleneck
  • Mobilised fat nowhere to go
  • Converted back to TAG and stored in hepatocytes, or back to ciruclation in horse
  • Excess acetyle CoA diverted to ketones
47
Q

What are the effects of secondary ketosis?

A
  • Fruity smell to breath (acetone)
  • Ketones weak acids, excess amounts induce ketoacidosis
  • Lower PH of blood affecting enzymatic actions
  • CNS depression
  • Lower appetute
48
Q

Describe the temporary export pathway for TAGs

A
  • TAGs exported from liver in VLDLs
  • Serve as TAG overflow system for liver, not very responsive in cows
  • TAG levels in blood reflect VLDL
  • VLDL levels do not increase
  • Plasma TAG levels fo not rise in cows, but in horses lots of TAG in blood and tissues end up filled leading to organ dysfunction
49
Q

Describe the pathology within a fatty liver

A
  • Cell swelling
  • Disrupted cell metabolism
  • Elevated liver enzyme levels (leak from damaged cells)
  • Loss of hepatic function
  • Capsule rupte
50
Q

Describe feline hepatic lipidosis

A
  • Obesity and NEB main risk factors
  • Fat and then suddenly off food for other reason e.g. illness such as pancreatitis
  • Friable fatty liver
51
Q

Describe hyperlipidaemia in horses and ponies

A
  • Following choke or anorexia due to pain (laminitis)
  • Stop eating leading to NEB
  • Repackage fat out of liver as VLDL
  • Organ dysfunction due to systemic hyperlipidaemia

Veterinary Medicine Year 2 (30 decks)

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