Hormonal Regulation of Metabolism
High-Yield Summary
- Three hormone classes: peptide (water-soluble, surface receptors, fast), steroid (lipid-soluble, intracellular receptors, slow/gene-level), amino acid-derived (catecholamines act like peptide hormones; thyroid hormones act like steroid hormones).
- Insulin (pancreatic beta cells): lowers blood glucose via GLUT4 translocation; promotes glycogen/fat/protein synthesis; inhibits lipolysis and gluconeogenesis. Brain, RBCs, kidney tubules, intestinal mucosa, and pancreatic beta cells are insulin-INDEPENDENT for glucose uptake.
- Glucagon (pancreatic alpha cells): raises blood glucose via hepatic glycogenolysis, gluconeogenesis, ketogenesis — opposes insulin. The insulin:glucagon ratio is the master switch (high = storage mode, low = mobilization mode).
- Glucocorticoids (cortisol, adrenal cortex): raise glucose via slow, transcription-driven gluconeogenic enzyme expression; long-term stress response; stimulated by ACTH (HPA axis).
- Catecholamines (epinephrine/norepinephrine, adrenal medulla): rapid cAMP-mediated fight-or-flight response — glycogenolysis, lipolysis, increased heart rate/cardiac output.
- Thyroid hormones (T3/T4): set baseline metabolic rate (permissive, not acute); regulated by the hypothalamic-pituitary-thyroid axis (TRH → TSH → T3/T4, negative feedback).
Key Terms
- Insulin-independent tissues
- Brain, red blood cells, kidney tubules, intestinal mucosa, pancreatic beta cells — take up glucose regardless of insulin.
- Insulin-to-glucagon ratio
- Master regulator: high ratio = storage mode, low ratio = mobilization mode.
- HPA axis
- Hypothalamic-pituitary-adrenal axis; CRH → ACTH → cortisol.
- Hypothalamic-pituitary-thyroid axis
- TRH → TSH → T3/T4, with negative feedback on hypothalamus and pituitary.
Hormone Classes by Solubility
| Class | Solubility / Receptor / Speed |
|---|---|
| Peptide (insulin, glucagon) | Water-soluble / Cell surface / Rapid |
| Catecholamines | Water-soluble / Cell surface / Rapid |
| Steroid (cortisol) | Lipid-soluble / Intracellular / Slow, long-lasting |
| Thyroid (T3/T4) | Lipid-soluble / Intracellular / Slow, long-lasting |
Insulin vs. Glucagon
| Feature | Insulin vs. Glucagon |
|---|---|
| Source | Pancreatic beta cells / Pancreatic alpha cells |
| Trigger | High blood glucose (fed) / Low blood glucose (fasting) |
| Glycogen | Promotes synthesis, inhibits breakdown / Promotes breakdown (glycogenolysis) |
| Glucose production | Suppresses gluconeogenesis / Stimulates gluconeogenesis |
| Lipid effect | Inhibits lipolysis, promotes fat synthesis / Promotes lipolysis, ketogenesis |
Common MCAT Trap
- Thyroid hormones are amino acid-derived but lipid-soluble and act like steroids — don't classify all amino acid-derived hormones as fast-acting like catecholamines.
- Insulin-independent tissues still take up glucose in diabetes — a key clinical point often tested indirectly.
- Glucocorticoids raise blood glucose through slow transcriptional changes, NOT rapid glycogen breakdown like glucagon/epinephrine — different mechanism, same directional effect.
Quick Recall
Which five tissue types are insulin-independent for glucose uptake?
What determines whether the body is in storage or mobilization mode?
What is the role of thyroid hormones in metabolism?