Structure and function of adipose tissue, adrenals, bone, gonads, hypothalamus, parathyroids, pituitary, and thyroid

Adipose tissue as an endocrine organ

Adipose tissue functions as an active endocrine organ (not simply energy storage), secreting hormones (leptin, adiponectin) that signal to the hypothalamus to regulate appetite and energy balance - the hypothalamus integrates these peripheral signals with central neural inputs to control hunger, satiety, and metabolic rate
Foundational physiology underlying understanding of obesity, appetite regulation, and the mechanism of several weight-management pharmacotherapies

Leptin, secreted proportional to fat mass, signals energy sufficiency to the hypothalamus, normally suppressing appetite as fat stores increase - obesity is typically associated with leptin resistance (elevated leptin levels that fail to produce the expected appetite-suppressing effect) rather than leptin deficiency, explaining why leptin itself is not an effective weight-loss treatment in typical obesity (as opposed to the rare cases of true congenital leptin deficiency, where replacement is dramatically effective)
Adiponectin, in contrast, is reduced in obesity and has insulin-sensitising, anti-inflammatory effects - lower adiponectin in obesity contributes to the associated insulin resistance

Not routinely tested clinically in standard obesity assessment, but understanding this pathway explains the mechanism and rationale of specific pharmacotherapy and the distinction between typical obesity and rare monogenic obesity syndromes (e.g. congenital leptin deficiency, melanocortin-4 receptor deficiency)
GLP-1 receptor agonists exploit a related but distinct gut-hypothalamic signalling pathway (incretin-mediated satiety and appetite suppression) rather than the leptin-adiponectin axis directly, explaining their efficacy despite leptin resistance being present in typical obesity
Rare monogenic obesity syndromes (leptin deficiency, MC4R deficiency) may respond to pathway-specific targeted therapy where available, unlike typical polygenic obesity

Leptin resistance in typical obesity (a key mechanistic concept), monogenic obesity syndromes (leptin deficiency, MC4R deficiency - rare but mechanistically illustrative), GLP-1 receptor agonist mechanism as a distinct pathway
Leptin resistance, not leptin deficiency, characterises typical obesity - most patients with obesity have elevated, not low, leptin levels, which is why leptin replacement therapy is not an effective weight-loss treatment outside the rare specific cases of true congenital leptin deficiency, where it is dramatically effective

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