Inflammatory process in visceral adipose tissue

The inflammatory process in visceral adipose tissue refers to a complex cascade involving immune cell infiltration and activation within the fat depots surrounding internal organs. This chronic low-grade inflammation is driven by hypertrophic and dysfunctional adipocytes that secrete pro-inflammatory cytokines—such as TNF-alpha and IL‑6—and recruit various immune cells including macrophages, T cells, B cells, neutrophils, and others. The resulting local production of inflammatory mediators disrupts normal metabolic functions within the fat itself and systemically throughout the body. This state is closely linked with obesity-related complications such as insulin resistance, type 2 diabetes mellitus, cardiovascular disease risk factors like dyslipidemia and hypertension, ectopic lipid deposition in liver/muscle tissues ("metabolic syndrome"), fibrosis/remodeling of extracellular matrix proteins like collagen within fat depots ("pro-fibrotic phenotype"), increased cell death/apoptosis among adipocytes during expansion or aging ("inflammaging"), and overall systemic metabolic dysfunction.[1][2][3] This entry does not represent a single molecular target but rather describes an integrated pathophysiological mechanism involving multiple cellular players (adipocytes plus diverse immune populations) along with their secreted factors. As such it is not considered a canonical drug target like an enzyme or receptor but remains an area for therapeutic intervention through modulation of its components.[1][3]

Other names

Visceral adipose tissue inflammationVAT inflammationInflammation of visceral fatAdipose tissue inflammatory response (visceral)

Not applicable to a biological process; however, drugs that reduce pro-inflammatory cytokines or immune cell infiltration can attenuate this inflammatory state.