Subcutaneous fat cell lipolysis independent contributor to variations in plasma lipids
Subcutaneous Adipocyte Lipolysis Contributes to Circulating Lipid LevelsLiterature - Rydén M and Arner P - Arterioscler Thromb Vasc Biol. 2017 Jun 29, Epub ahead of print
- Correlations between various circulating lipids levels and lipolysis were significant, but weak (r2<0.05). However, basal lipolysis was significantly negatively and strongly correlated with HDL-c and positively and strongly with plasma triglycerides. In contrast, insulin sensitivity was positively correlated with HDL-c and negatively with triglycerides.
- The relationships between basal lipolysis with HDL-c or triglycerides were stronger in nonobese individuals (HDL-c nonobese r=-0.27, P<0.0001, obese r=-0.10, P=0.012 and triglycerides nonobese r=0.27, P<0.0001, obese r=0.12, P=0.0035). Insulin sensitivity vs HDL-c or triglyceride were equally strong in obese and nonobese individuals.
- Removing type 2 diabetes patients and individuals on antihyperlipidemic treatment from the analyses generated similar results. Similarly, there was no sex interaction in the relationship between basal lipolysis or insulin sensitivity and HDL-c or triglycerides.
- The relationships were still highly significant after correction for intrinsic/extrinsic cofactors known to influence circulating lipid levels (cofactors: sex, age, BMI, waist circumference, waist-to-hip ratio, nicotine use, treatment of type 2 diabetes, hypertension or hyperlipidemia and fat cell size).
- Combining factors revealed an adjusted r2 of 0.14 between insulin sensitivity and basal lipolysis together and both triglycerides and HDL-c (both P<0.0001). Combining all cofactors and correlate this, r2 values were 0.28 (HDL-c) and 0.17 (triglycerides, both P<0.0001). Pooling all cofactors and insulin sensitivity and basal lipolysis, r2 for HDL-c was 0.36 and for triglycerides was 0.29 (both P<0.0001).
In this study, resistance to the antilipolytic effect of insulin and a high rate of basal lipolysis are associated with low HDL-c and high triglyceride levels. This was independent of classical risk factors influencing plasma lipids. Moreover, antilipolytic insulin sensitivity and basal lipolytic activity together explained 14% of variations in plasma triglycerides or HDL-c, thereby suggesting clinical importance for dyslipidemia.