18B12: Exam Report
Outline the control of blood glucose
53% of candidates passed this question.
A definition of normal glucose levels was expected, mentioning how it is regulated despite variable intake. Most answers incorporated the roles of insulin/glucagon and the glucostat function of the liver. Sufficient detail regarding the mechanism of insulin release was often lacking. Extra marks were awarded for description of the role of the satiety centre in the hypothalamus, glucokinase and processes in fasting and starvation that maintain blood glucose levels.
Marks were not awarded for describing effects of insulin and glucagon unrelated to glucose control.
U1iii / 18B12: Describe the body’s mechanism for regulating blood glucose
- Blood glucose levels are maintained in a tight range (4 – 7mmol/L)
- Controlled by feedback mechanism which balances insulin (anabolic) & glucagon (catabolic)
- Sensor = Islets of Langerhans
- Integrator = Endocrine pancreas (and SNS)
- Effector = Endocrine pancreas, adrenaline, anterior pituitary cells (ACTH, GH), liver “glycostat” – maintains BGL in strict range
Hormone Control
Insulin
- Stored in B cells of pancreas
- Release:
- BGL >5mmol/L
- Arginine, leucine, lysine & phenylalanine amino acids
- Glucagon
- Gastrin, secretin, cholecystokinin
- ACh
Act to:
- CHO
- Increase glucose uptake by insertion of GLUT 4 receptors to muscle & AT cells (not in RBC, brain – freely permeable to glucose)
- ↑Glycogen synthesis via ↑glycogen synthase activity
- ↑Glucokinase activity in hepatocytes which traps glucose inside hepatocytes
- ↓Gluconeogenesis & glycogenolysis
- Protein
- ↑tissue uptake & ↓oxidation of amino acids
- ↑protein synthesis
- ↓protein breakdown
- Fats
- ↑glucose entry to AT → ↑fat synthesis
- Activation of lipoprotein lipase & FA synthase to facilitate breakdown TAG → FA for uptake by AT cells
- Inhibits Hormone Sensitive Lipase → ↓hydrolysis of TAGs stored in AT
- CHO
Glucagon
- Synthesised by α-cells of pancreas
- Secreted with hypoglycaemia, inhibited by hyperglycaemia
- CHO
- Acts in liver to stimulate breakdown of stored glycogen → G6P → glucose
- Acts in skeletal muscle & AT to break down peripheral glycogen → pyruvate & lactate → pyruvate goes to Krebs & lactate to liver for gluconeogenesis via CORI CYCLE
- Inhibits cellular utilisation of glucose during hypoglycaemia → most cells to use FAs/ketones as 1° energy source
- Lipid
- Stimulates Hormone Sensitive Lipase → break down AT → FFAs & glycerol → Acetyl CoA → Krebs
- Lipid
Growth Hormone & ACTH
- Released by anterior pituitary
- ACTH causes cortisol release from Adrenal Cortex
- Cortisol & GH inhibit glucose uptake by ↓[GLUT4] receptors on cell membrane
Thyroxine
- Released from thyroid
- ↑GIT absorption of glucose
Oestrogen/Progesterone
- Mild insulin resistance
Neural Control
- Adrenaline → released by Adrenal cortex & sympathetic nerve terminals
- ↑glucagon breakdown
- ↑gluconeogenesis
- ↑HORMONE SENSITIVE LIPASE to breakdown AT
- Hunger, nausea, agitation, tachycardia