The body's energy vault — and a hormone factory in its own right. Adipose tissue stores the surplus of every meal as triglyceride and reports its stores to the brain through leptin.
White adipose tissue is nearly pure storage: unilocular adipocytes with one giant lipid droplet, arranged in lobules with a capillary and nerve supply. Brown adipocyte tissue multiplies small droplets with mitochondria between them, built to burn rather than bank — thermogenesis through UCP1. Beige cells switch between programs on cold and adrenergic cue. Depot location matters as much as mass: visceral fat drains portal-ward and drives metabolic risk; subcutaneous fat is comparatively benign.
Metabolic Pathways
Lipogenesis after meals: insulin drives glucose uptake and fatty-acid synthesis — see fatty acid biosynthesis.
Lipolysis in fasting: the ATGL-HSL-MGL cascade releases fatty acids to blood.
Fatty-acid re-esterification and glyceroneogenesis let the tissue fine-tune release against re-storage hour by hour.
Regulation
Insulin stores, catecholamines and glucagon release — the same hormonal seesaw that runs liver.
Leptin and adiponectin report status to brain, liver, and muscle; obesity is leptin resistance, not leptin lack.
Cortisol and growth hormone reshape depot distribution over longer horizons.
Interactions
Fatty-acid flux to liver drives VLDL output and insulin resistance — the metabolic syndrome chain.
Brown fat consumes glucose and fat for heat in cold-exposed adults, visible on PET scans.
The tissue's macrophages and cytokine output link obesity to low-grade inflammation — see TNF.
Clinical Relevance
Obesity is adipose capacity exceeded: ectopic fat in liver, muscle, and pancreas follows.
Lipodystrophy — too little fat — causes the same metabolic syndrome by overflow elsewhere.
Cold-activated brown fat and UCP1 are drug targets that have stayed just out of reach.