Fat storage, or lipogenesis, is the essential physiological process where excess energy substrates, primarily derived from dietary intake, are converted into triglycerides and sequestered within adipocytes for long-term energy reserve. While a necessary survival mechanism, excessive or dysregulated fat storage, particularly visceral adiposity, is strongly linked to endocrine dysfunction and metabolic syndrome. Hormonal signals like insulin, cortisol, and leptin are the primary regulators of this energy partitioning process.
Origin
The concept of fat storage is fundamental to human and animal physiology, a core evolutionary mechanism for survival during periods of scarcity. The term is a direct description of the biological process, with its clinical relevance emerging alongside the understanding of endocrinology and metabolic disease in the 20th century. Research elucidating the adipocyte as an active endocrine organ, rather than a passive storage depot, profoundly shaped the modern clinical perspective on fat storage dynamics.
Mechanism
The primary mechanism is governed by insulin, which, when elevated, signals adipocytes to take up glucose and fatty acids and convert them into triglycerides, while simultaneously inhibiting lipolysis, the breakdown of stored fat. Cortisol, the stress hormone, promotes the redistribution of fat to the visceral depot via glucocorticoid receptors, especially when chronically elevated. Sex hormones also play a critical role, with declining testosterone and estrogen often correlating with increased central adiposity and a less favorable fat distribution pattern.
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