Classification of hormone receptor locations:

• Androgens are lipophilic steroid hormones that readily diffuse across the plasma membrane and bind intracellular androgen receptors (AR) in the cytoplasm/nucleus.
• Estrogens are lipophilic steroid hormones that bind intracellular estrogen receptors (ER$\alpha$/ER$\beta$).
• Progestins (progesterone) are lipophilic steroid hormones that bind intracellular progesterone receptors (PR) to modulate transcription.
• Insulin is a large peptide hormone that cannot cross the hydrophobic lipid bilayer; it binds an extracellular cell-surface receptor tyrosine kinase (RTK).

Hypothalamic control of appetite and energy homeostasis:

• Glucagon acts primarily on hepatic glycogenolysis and gluconeogenesis.
• Adiponectin promotes fatty acid oxidation and insulin sensitivity primarily in muscle and liver.
• Ghrelin binds GHSR on NPY/AgRP neurons to stimulate NPY release and promote hunger.
• Circulating insulin (along with leptin) crosses the blood-brain barrier to bind insulin receptors on orexigenic NPY/AgRP neurons in the arcuate nucleus of the hypothalamus, hyperpolarizing them and inhibiting the expression and release of orexigenic neuropeptide Y (NPY), thereby suppressing appetite as an anorexigenic signal.

Hypothalamic-pituitary-thyroid axis dynamics:

• Statement (I) is correct: Hypothyroidism is by definition the clinical and biochemical state resulting from insufficient production and secretion of thyroid hormones ($T_4$ and $T_3$) by the thyroid gland.
• Statement (II) is incorrect: In primary hypothyroidism (which constitutes $\gt 95\%$ of clinical cases in animals), circulating levels of free $T_4$ and $T_3$ are low, which relieves negative feedback inhibition on the anterior pituitary gland; consequently, the pituitary secretes markedly elevated (above normal) concentrations of Thyroid-Stimulating Hormone (TSH) in an attempt to stimulate the failing thyroid gland.