The pathophysiology of visceral adipose tissues in cardiometabolic diseases.
Level 5 - mechanism / opinion, no new human data
Narrative review summarizing pathophysiological mechanisms without systematic search methodology or new human empirical data
PubMed 38460909 · doi:10.1016/j.bcp.2024.116116
What was done
This narrative review summarizes depot-specific metabolic and endocrine properties of adipose tissue, focusing on the cellular mechanisms (adipocyte hypertrophy, cell death, hypoxia, inflammation, and fibrosis) underlying visceral fat remodeling, the portal hypothesis, and the effects of various weight loss interventions on cardiometabolic outcomes.
What was found
The abstract reports no numerical findings, effect sizes, or statistical results. It qualitatively describes the sequence whereby dysfunctional visceral adipose tissue secretes elevated levels of free fatty acids, glycerol, and proinflammatory/profibrotic cytokines directly into the portal circulation, inducing hepatic steatosis, hepatic insulin resistance, and systemic metabolic derangements.
Why it matters
This synthesis outlines the biological mechanisms linking intra-abdominal adiposity directly to liver pathology and systemic cardiometabolic risk, highlighting potential mechanistic targets for metabolic therapies.
Limits
This is a narrative review without a systematic search protocol, formal inclusion/exclusion criteria, or quantitative data synthesis. The abstract provides no primary human data, sample sizes, or quantitative comparisons among different weight loss interventions.
Cited by
- supports Adipose tissue becomes pro-inflammatory when it exceeds a certain threshold.