Subcutaneous Adipocyte Lipolysis Contributes to Circulating Lipid Levels
Objective—Fatty acids released via fat cell lipolysis can affect circulating lipid levels. However, the contribution of different lipolysis measures in adipose tissue is unknown and was presently examined in isolated subcutaneous adipocytes.
Approach and Results—One thousand and sixty-six men and women were examined for lipolysis regulation in subcutaneous abdominal fat cells. Results were compared with fasting plasma levels of total cholesterol, high-density lipoprotein (HDL) cholesterol (HDL-C) and triglycerides. Spontaneous (basal) lipolysis and the effects of the major hormones stimulating (catecholamines and natriuretic peptides) and inhibiting lipolysis (insulin) were examined. Several statistically significant (P<0.0001) correlations between the different lipolysis parameters and plasma lipids were observed. However, physiologically relevant correlations (adjusted r2≥0.05) were only evident between basal or insulin-inhibited lipolysis and plasma triglycerides or HDL-C. Together, these lipolysis measures explained 14% of the variation in triglycerides or HDL-C, respectively. In comparison, a combination of established factors associated with variations in plasma lipids, that is, age; body mass index; waist circumference; waist-to-hip ratio; sex; nicotine use; fat cell volume; and pharmacotherapy against diabetes mellitus; hypertension; or hyperlipidemia explained 17% and 28%, respectively, of the variations in plasma triglycerides and HDL-C.
Conclusions—Subcutaneous fat cell lipolysis is an important independent contributor to interindividual variations in plasma lipids. High spontaneous lipolysis activity and resistance to the antilipolytic effect of insulin associate with elevated triglyceride and low HDL-C concentrations. Thus, although several other factors also play a role, subcutaneous adipose tissue may have a causal influence on dyslipidemia.
- Received June 1, 2017.
- Accepted June 21, 2017.
- © 2017 The Authors.
Arteriosclerosis, Thrombosis, and Vascular Biology is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.