Which of the following are considered effects of the release of the hormone glucagon?

Correct Answer: A

Rationale: Glucagon, from pancreatic alpha cells, raises blood glucose via glycogenolysis (breaking glycogen into glucose in the liver), gluconeogenesis (forming glucose from non-carbs), and liver glucose release countering insulin. Glucose transport into cells is insulin's role, not glucagon's it mobilizes, not stores. All three (glycogenolysis, gluconeogenesis, release) apply, but single-option format favors glycogenolysis as primary. Its glucose-mobilizing action distinguishes it, key to fasting glucose maintenance, unlike cellular uptake.

Correct Answer: C

Rationale: Adrenal glands sit atop the kidneys, one per side, producing hormones like cortisol and epinephrine. The thyroid is neck-based, liver below kidneys, and hypothalamus in the brain not adjacent. This renal positioning distinguishes adrenal anatomy, vital for stress and metabolic regulation, integrating with kidney function in endocrine control.

Correct Answer: D

Rationale: Alpha cells in the pancreas produce glucagon to raise blood glucose. Autoimmune targeting would impair glucagon, not somatostatin (delta cells), pancreatic polypeptide (PP cells), or insulin (beta cells). Glucagon's direct link to alpha cells distinguishes it, critical for glucose counterregulation, contrasting with other pancreatic hormones.

Correct Answer: B

Rationale: Paracrine signaling involves chemicals (e.g., prostaglandins) affecting nearby cells, like histamine in inflammation acting locally without entering blood. Autocrine signaling targets the secreting cell itself (e.g., cancer cells self-stimulating). Endocrine signaling uses blood to reach distant cells (e.g., insulin from pancreas). 'Neuron' isn't a signaling type neurons use neurotransmitters, often paracrine-like at synapses, but it's distinct. Paracrine's local effect distinguishes it, critical for short-range coordination, unlike self, systemic, or neural mechanisms.

Correct Answer: C

Rationale: Follicle-stimulating hormone (FSH) from the anterior pituitary stimulates spermatogenesis in male testes' Sertoli cells and follicle growth in female ovaries monthly, driving gamete production. Luteinizing hormone (LH) triggers testosterone in males and ovulation/oestradiol in females, not sperm/follicle initiation. Somatostatin inhibits hormone release (e.g., GH), not stimulating reproduction. Thymosin, from the thymus, boosts immunity, not gonadal function. FSH's dual reproductive role distinguishes it, key to fertility, unlike ovulation, inhibition, or immune hormones.