Hormones and Metabolic Integration: Insulin, Glucagon, Thyroid and Steroid Hormones
What this domain tests
Hormone questions test the actions of insulin, glucagon, thyroid hormones, and steroid hormones, and how they integrate fuel use in fed and fasting states.
Core rules
- Insulin is made by pancreatic beta cells. It promotes glucose uptake in muscle and adipose via GLUT4, glycogen synthesis, lipogenesis, and protein synthesis; it lowers blood glucose.
- Glucagon is made by alpha cells. It raises cAMP, stimulates glycogenolysis and gluconeogenesis in the liver, and promotes lipolysis. It opposes insulin.
- Thyroid hormones T3 and T4 increase basal metabolic rate and calorigenesis; secretion is controlled by TSH from the pituitary and TRH from the hypothalamus. Calcitonin comes from thyroid C cells and lowers calcium.
- Steroid hormones are lipophilic, travel bound to carriers, enter cells, and bind intracellular receptors that act as transcription factors. Cortisol promotes gluconeogenesis and is anti-inflammatory.
- In fasting, insulin falls and glucagon rises; liver glycogen is depleted, gluconeogenesis and ketogenesis increase, and adipose releases fatty acids.
Worked example
After an overnight fast, blood glucose is maintained mainly by hepatic glucose output. Glucagon stimulates glycogenolysis first, then gluconeogenesis from lactate, glycerol, and amino acids. Adipose lipolysis supplies fatty acids for oxidation and glycerol for gluconeogenesis. The brain continues to use glucose and, after prolonged fasting, ketone bodies. Insulin is low, so GLUT4-mediated uptake in muscle and fat is reduced.
Traps
Insulin does not control all glucose uptake; brain GLUT3 is insulin-independent. The thyroid does not secrete calcitonin from follicular cells. Steroid hormones do not act through cell-surface receptors. Glucagon does not directly break down muscle glycogen; muscle lacks glucose-6-phosphatase.