Gastrointestinal hormones Flashcards
(51 cards)
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
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
3
Q
List the GI hormones
A
- Insulin
- Glucagon
- Gastrin
- Secretin
- Cholecystokinin
- Incretins (Gastric Inhibiting Peptide and Glucagon-Like Peptide-1)
- Motilin
- Ghrelin
4
Q
Where is gastrin produced?
A
G cells in stomach (fundus and corpus)
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
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
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
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
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
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
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
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
13
Q
List the factors involved in appetite regulation
A
- Incretins
- Hypothalamic inputs
- 4 theories: lipostat, gut peptides, glucostat and thermostat
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)
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
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)
17
Q
Outline the satiety centre within the hypothalamus
A
- Responds to high glucose levels
- Inhibits eating
18
Q
Outline the appetite centre within the hypothalamus
A
- Responds to low glucose levels
- Stimulates eating
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)
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
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
Explain the role of cholecystokinin in satiety
- 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
Explain the role of peptide YY (PYY) in satiety
- 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
Explain the role of Ghrelin in satiety
- 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
Explain the role of ghrelin in hedonic pleasure of food
- 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
Outline the glucostat theory of satiety
- High glucose stimulates satiety centre
- Requires insulin
- VFAs in ruminants
- AAs do the same
30
Outline the thermostat theory of satiety
- Fall in body temp below set point stimulates appetite
| - Increase above normal inhibits appetite
31
What are the hormonal responses to negative energy balance?
- Insulin decrease
- Thyroxine decrease
- Glucagon increase
- Growth hormone increase
- Cortisol increase
- Catecholamine increase
32
What are the metabolic responses to negative energy balance?
- Initially use up carbohydrate stores e.g glycogen found in liver and muscle
- Then use fat and protein (muscle mass will decrease)
33
What are some reasons for negative energy balance in the dairy cow?
- 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
Which of the volatile fatty acids are glucogenic and which are ketogenic?
- Glucogenic: proprionate
- Ketogenic: acetate, butyrate
- Ketogenic:glucogenic ratio 4:1
35
Outline the use of proprionate in gluconeogenesis
- Converted to oxaloacete
| - Converted to glucose
36
What is the fate of the ketogenic VFAs?
- Converted to acetyl CoA
- Enters TCA cycle
- ATP produced
- Or stored as fats
- Or converted to ketones
37
What hormones stimulate HSL?
- Low insulin and high glucagon
- Catecholamines
- Growth hormone
- Cortisol
38
What inhibits HSL?
High insulin and low glucagon
39
What are the 2 key risk factors for lipid metabolism disorders with negative energy balance?
- Obesity
| - Insulin resistance
40
Outline the effect of obesity on lipid metabolism
- 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
Outline the pathophysiology of lipids in negative energy balance
- 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
Outline the link between periparturient events and negative energy balance
- 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
What is the common presentation for hepatic lipidosis in dairy cows?
- Periparturient cow
| - Non-specific complaints: lower milk production, loss of appetite and mild depression
44
What are the common findings of hepatic lipidosis on physical examination?
- Decreased rumen motility
- Ketosis
- Concurrent disease e.g. dystocia, LDA, retained placenta
- Metritis or mastitis
45
What are common risk factors for hepatic lipidosis
- 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
Outline secondary ketosis in obesity
- 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
What are the effects of secondary ketosis?
- Fruity smell to breath (acetone)
- Ketones weak acids, excess amounts induce ketoacidosis
- Lower PH of blood affecting enzymatic actions
- CNS depression
- Lower appetute
48
Describe the temporary export pathway for TAGs
- 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
Describe the pathology within a fatty liver
- Cell swelling
- Disrupted cell metabolism
- Elevated liver enzyme levels (leak from damaged cells)
- Loss of hepatic function
- Capsule rupte
50
Describe feline hepatic lipidosis
- 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
Describe hyperlipidaemia in horses and ponies
- 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
