josh endocrine Flashcards
(20 cards)
describe how CHO are metabolised
Glucose transporters bring glucose into cell
Oxidised for energy
- Generates CO2 (as waste) & H2O
Substrate for other metabolic reactions
Converted to glycogen
Recovered from glycogen stores
describe how proteins are metabolised
AAs transported in blood into cells
AAs used for protein synthesis
Catabolised for E (proteolysis)
AAs recovered from I/C proteins
describe how fats are metabolised
Triglycerides (TGs) broken down by lipoprotein lipase
FAs taken up by cells (glycerol liver)
FAs oxidised for E or:
Combined with glycerol forms new TGs, stored in fat droplets in cytosol
Stored TGs B/↓ into glycerol and FAs, catabolised for E or:
Released back into blood
What is GE and what is its formula
Gross Energy of feed (GE): Is the heat generated when a unit mass of feed is completely combusted in oxygen to yield water and carbon dioxide under std. conditions of temperature and pressure.
(total energy in body gain) / (total energy in feed)
what is DE and what is its formula
Digestible energy (DE): Not all substances in the feed enter the metabolic processes of the animal. Energy lost in the form of faeces has to be considered and subtracted from the Gross energy.
DE = gross energy of feed – gross energy of faeces
What is ME and what is its formula
Metabolizable energy (ME): – energy lost in the from of fermentation (ruminants) and through urine (urea- breakdown product of protein) is subtracted from the DE
ME = Digestible energy – urinary energy – energy of combustible gases
what is compensatory growth
Otherwise known as ‘catch up growth’ or ‘rebound growth’ or ‘rehabilitative growth’ is a result of the animal having insufficient food at a time period which disrupts the sigmoid growth curve. When food supply becomes plentiful again the animal rapidly accelerates growth, this is largely described in ruminants due to the inconsistency of pasture in seasons.
what are the two catergories of factors and what they include
Animal factors: maturity and fat depots
Nutrional factors: duration and severity of growth restriction and food access during rehabilitation
appetite has short term and long term control, why is that?
short term is based on the Gi tracts current influence, consider how increased stomach sectretions when empty increase hungar levels.
long term provides influence based on current fats depots.
list the hormones invloved in short term and long term appeties control
Long term: leptin
Short term: Ghrelin, cholecystokinin, peptide YY (PYY)
describe Ghrelin secretion, receptors and effect
Secretion: Produces primarily from cells in the stomach but also the small intestine.
Receptors:It is received by the anterior pituitary.
Effect: Increases food intake by stimulating GH from anterior pituitary and enhancing GnRH release. This increases feelings of hunger and increases gastric motility and acid secretion in preparation for digestion
describe Cholecystokinin secretion, receptors and effect
Secretion: Produced by the duodenum and jejunum in response to a meal it acts on the CCK
Receptor: In the CNS.
Effect: The signal to stop the feed intake by signaling in the CNS. This mediates digestion in the small intestine by inhibiting gastric emptying.
describe Peptide YY (PYY) secretion, receptors and effect
Secretion: Predominantly by the colon
Receptor: Acts centrally and locally
Effect: Acts centrally by inhibiting feed intake and acts locally by delaying gastric emptying and inhibiting bile secretions.
describe GIP (Glucose dependent insulinotropic polypeptide) secretion, receptors and effect
Secretion: Releases from the small intestine K cells
Receptor: GIP receptors (adiopose tissue and GI tract)
Effect: Decreases feed intake by increasing insulin secretion and increasing adipose tissue lipogenesis, also decreasing gastric acid secretion.
describe (glucagon-like peptide-1) secretion, receptors and effect
Secretion: Released by L cells in the intestine
Receptor:
Effect: Decreases feed intake by inhibiting gastric emptying and increasing insulin secretion.
describe Leptin secretion, receptors and effect
Secretion: Polypeptide released by the adipose tissue
Receptor: CNS
Effect: Reduces feed intake which allows for increased energy expenditure, increasing activity and resulting in weight loss.
Describe GH and its release. also its inhibitin
GH ( also called somatotropin) is released fro the somatotropic cells in the anterior pituitary, this release is induced by hypothalamic GnRH. Gh is inhibited by GHIH (growth hormone inhibiting hormone) also called somatostatin.
desribe the effect of GH metabolicly
Protein metabolism: in general GH stimulates protein anabolism in many tissues.
Fat metabolism: increases that utilisation of fat
Carbohydrate metabolism: Serves to maintain normal blood glucose
what is Insulin like growth factors role in bone growth
Largely regulated by GH and IGF - 1:
increased protein deposition by chondrocytic and osteogenic cells
increased mitotic rate in these cells
chondrocyte hypertrophy
conversion of chondrocytes to osteoblasts
stimulation of osteoblasts & osteoclasts
thyroid hormone also needed for hypertrophy and ossification.
