Which hormone pair is implicated in obesity-associated sleep apnea and satiety regulation?

Which hormone pair is implicated in obesity-associated sleep apnea and satiety regulation?

• A. Leptin and ghrelin
• B. Insulin and cortisol
• C. Thyroxine and TSH
• D. Adiponectin and resistin

Answer: (A)

Satiety and sleep–breathing disorders in obesity are tightly linked to two opposing signals that communicate energy status to the brain: leptin and ghrelin. Leptin, produced by fat tissue, signals fullness and helps limit appetite; ghrelin, released primarily from the stomach, increases hunger. In obesity, the brain can become less responsive to leptin (leptin resistance), so satiety signaling is blunted. At the same time, poor sleep or sleep disturbance—common in sleep apnea—can raise ghrelin and lower or dysregulate leptin, promoting increased appetite and further weight gain. This dynamic ties together obesity, sleep apnea, and regulation of food intake, making the leptin–ghrelin pair central to satiety regulation in this context. Insulin and cortisol influence metabolism and stress responses but are not the primary pair governing short-term satiety signals. Thyroxine and TSH control metabolic rate rather than appetite signaling. Adiponectin and resistin affect insulin sensitivity and inflammation more than direct acute satiety control.

Satiety and sleep–breathing disorders in obesity are tightly linked to two opposing signals that communicate energy status to the brain: leptin and ghrelin. Leptin, produced by fat tissue, signals fullness and helps limit appetite; ghrelin, released primarily from the stomach, increases hunger. In obesity, the brain can become less responsive to leptin (leptin resistance), so satiety signaling is blunted. At the same time, poor sleep or sleep disturbance—common in sleep apnea—can raise ghrelin and lower or dysregulate leptin, promoting increased appetite and further weight gain. This dynamic ties together obesity, sleep apnea, and regulation of food intake, making the leptin–ghrelin pair central to satiety regulation in this context.

Insulin and cortisol influence metabolism and stress responses but are not the primary pair governing short-term satiety signals. Thyroxine and TSH control metabolic rate rather than appetite signaling. Adiponectin and resistin affect insulin sensitivity and inflammation more than direct acute satiety control.