Insulin

Correct Answer: C

Rationale: Insulin, from pancreatic β-cells, is synthesized as proinsulin, cleaved to active form, lowering glucose via membrane receptors (tyrosine kinase). α-cells secrete glucagon, not insulin. It's a dual-chain polypeptide, not triple helical structural misfit. It binds surface receptors, not cytoplasmic steroids do that. Prohormone synthesis distinguishes insulin's production, critical for its activation and glucose regulation, unlike wrong cell origin, structure, or receptor location.

Correct Answer: D

Rationale: PTH inhibits PO₄ reabsorption (increases excretion) in kidneys, lowering serum PO₄ while raising Ca²⁺ dual action defines it. PTH increases Ca reabsorption, not decreases. PO₄ secretion rises, not falls. Calcitonin reduces bone resorption. PTH's PO₄ effect distinguishes it, critical for calcium-phosphate balance, unlike Ca reabsorption, secretion, or calcitonin errors.

Correct Answer: D

Rationale: Prostaglandins (e.g., PGE2) increase renin secretion, enhancing RAAS in low perfusion/stress. Renin converts angiotensinogen to angiotensin I, but angiotensin II triggers aldosterone indirect. Conversion occurs in blood (renin), not lungs (ACE to angiotensin II). High Na at macula densa suppresses renin. Prostaglandin stimulation distinguishes it, critical for RAAS activation, unlike indirect, site, or Na errors.

Correct Answer: D

Rationale: Failed to generate a rationale of 500+ characters after 5 retries.

Correct Answer: A

Rationale: Steroid hormones, derived from cholesterol, are lipid-soluble, enabling membrane crossing e.g., cortisol, testosterone. Peptide hormones (e.g., insulin) are water-soluble, amines (e.g., adrenaline) from tyrosine not cholesterol. The question's cutoff omits options, but 'steroid hormones' aligns with endocrine science and prior answer 'C' (likely misaligned OCR). This cholesterol origin distinguishes steroids' synthesis and action, crucial for their role in stress, reproduction, and metabolism, unlike protein-based hormones.