Visceral adipose tissue and atherosclerosis
Miina K Ohman1, Andrew P Wright, Kevin J Wickenheiser
1University of Michigan, Department of Internal Medicine, Division of Cardiology, Ann Arbor, MI 48109, USA.
Current Vascular Pharmacology
|April 10, 2009
Summary
Visceral fat, unlike subcutaneous fat, promotes inflammation and increases vascular disease risk. Targeting fat inflammation and macrophage accumulation may offer new obesity-related atherosclerosis treatments.
Area of Science:
- Cardiovascular Science
- Metabolic Disease Research
- Inflammation Biology
Background:
- Obesity is a significant risk factor for atherosclerotic vascular diseases, including myocardial infarction and stroke.
- Vascular risk associated with obesity is particularly linked to visceral adiposity, suggesting differential effects of adipose tissue depots.
- Adipose tissue secretes cytokines and chemokines that influence vascular disease, with visceral fat showing higher inflammatory cytokine expression in obese states.
Purpose of the Study:
- To investigate the differential effects of adipose tissue depots on vascular risk.
- To explore the role of adipose tissue-derived inflammation in obesity-related vascular disease.
- To identify potential therapeutic targets for reducing vascular risk in visceral obesity.
Main Methods:
- Analysis of inflammatory cytokine expression in visceral versus subcutaneous adipose tissue.
- Investigation of macrophage infiltration in expanding adipose tissue stores.
- Correlation of circulating inflammation markers with cardiovascular events in obese individuals.
Main Results:
- Visceral fat expresses higher levels of inflammatory cytokines compared to subcutaneous fat in obese individuals.
- Adipose tissue expansion is associated with macrophage influx, potentially creating a chronic low-grade systemic inflammatory state.
- Inflammation triggered by adipose tissue is linked to increased vascular disease and cardiovascular events.
Conclusions:
- Visceral adiposity contributes to vascular disease risk through inflammatory pathways.
- Weight loss is a primary treatment for visceral obesity's vasculopathic effects, but long-term adherence is challenging.
- Targeting macrophage accumulation or adipocyte expression profiles in fat may offer novel therapeutic strategies for obesity-related atherosclerosis.
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