What physiological response does B adrenergic receptors stimulate in adipose tissue?

The stimulation of β-adrenergic receptors in adipose tissue primarily leads to lipolysis, which is the breakdown of stored triglycerides into free fatty acids and glycerol. When catecholamines, such as epinephrine and norepinephrine, bind to these receptors, they activate adenylate cyclase via G protein signaling. This process increases the levels of cyclic AMP (cAMP) within the adipocytes.

Elevated cAMP activates protein kinase A (PKA), which then phosphorylates hormone-sensitive lipase and perilipin. This cascade of events promotes the hydrolysis of triglycerides and the release of fatty acids into the bloodstream, making them available for energy production, especially during periods of increased energy demand, such as exercise or fasting.

In contrast, the other options involve different physiological processes. Glycogenolysis primarily occurs in the liver and muscles and is regulated by other hormonal mechanisms, mainly involving glucagon and epinephrine but not directly through β-adrenergic stimulation in adipose tissue. Insulin secretion is primarily stimulated by elevated blood glucose levels and is not related to the action of β-adrenergic receptors on adipose tissue. Glucagon secretion is primarily a response initiated by low blood glucose levels