The sleep-wake cycle of the body is regulated by the hormone

Correct Answer: D

Rationale: Melatonin, from the pineal gland, regulates the sleep-wake cycle, increasing in darkness to promote sleep. Prolactin (pituitary) aids lactation, cortisol (adrenals) manages stress, progesterone (ovaries) supports pregnancy not sleep directly. Melatonin's circadian role distinguishes it, key to biological rhythms, with disruptions affecting sleep, unlike stress or reproductive hormones.

Correct Answer: C

Rationale: Temperature regulation involves endogenous pyrogens (e.g., IL-1) from monocytes, macrophages, and Kupffer cells, raising hypothalamic setpoints in fever. It's hypothalamic, not cortical posterior hypothalamus heats, anterior cools (stimulation causes vasodilation, not hypothermia). Body temperature fluctuates daily, not constant. Pyrogens' mediation distinguishes fever's mechanism, key to immune-thermoregulatory link, unlike integration, regional, or stability claims.

Correct Answer: D

Rationale: Insulin release from β-cells involves glucose metabolism, depolarizing the membrane, opening Ca²⁺ channels for exocytosis core mechanism. β-cells are ~60-80%, not 90%. D cells secrete somatostatin, not pancreatic polypeptide (PP cells). Pork insulin, not beef, is closer to human (1 amino acid difference vs. 3). Ca²⁺-driven release distinguishes insulin secretion, critical for glucose response, unlike cell proportion, hormone, or species errors.

Correct Answer: D

Rationale: ACE inhibitors reduce angiotensin II, decreasing thirst in hypovolemia angiotensin II acts on subfornical organ, not just supraoptic nucleus (ADH site). Drinking and ADH differ thirst is behavioral, ADH hormonal. Dry membranes signal hypothalamus (e.g., via osmoreceptors), but angiotensin II's role is primary in volume loss. ACE inhibition distinguishes thirst modulation, key to RAAS-thirst link, unlike site, regulation, or membrane claims.

Correct Answer: A

Rationale: Insulin uses tyrosine kinase receptors (membrane-bound), driving glucose uptake via signaling cascades. Glucagon, PTH, and ACTH use G-protein-coupled receptors (GPCRs), activating cAMP similar mechanism. Insulin's distinct receptor type distinguishes it, key to its anabolic action, unlike cAMP-mediated hormones.