Which hormones drive cold-induced thermogenesis and what are their roles?

• A. Dopamine stimulates brown fat activation; cortisol decreases metabolic rate.
• B. Norepinephrine stimulates brown fat activation and lipolysis; thyroid hormones increase basal metabolic rate and amplify thermogenic gene expression.
• C. Serotonin stimulates brown fat; insulin increases metabolic rate.
• D. Insulin stimulates brown fat; growth hormone activates thermogenesis.

Answer: (B)

Cold-induced thermogenesis hinges on a coordinated hormonal response that ramps up heat production in brown adipose tissue. The immediate trigger is the sympathetic nervous system releasing norepinephrine, which binds to beta-adrenergic receptors on brown fat cells. This raises cAMP, activates PKA, and stimulates both lipolysis (providing fatty acids as fuel) and the transcription of thermogenic genes like UCP1. UCP1 uncouples oxidative phosphorylation from ATP production, releasing energy as heat instead. Thyroid hormones then step in as a powerful amplifier: they raise the overall metabolic rate and increase the tissue’s responsiveness to catecholamines, boosting both basal thermogenesis and the expression of thermogenic proteins. Together, norepinephrine initiates the heat-generating process, while thyroid hormones modulate and amplify the response.

Other hormones listed don’t drive the cold-activated brown fat pathway in the same direct way. They may influence metabolism in various contexts, but they are not the primary triggers for activating brown fat and fueling thermogenesis in the cold.