Indexed on: 15 Aug '18Published on: 15 Aug '18Published in: European Journal of Clinical Investigation
Insulin resistance occurs in obesity, but also in lipodystrophy. Although adipose tissue controls metabolic fluxes and participates in inter-organ crosstalk, the role of energy metabolism within white adipose tissue for insulin resistance is less clear. A Medline search identified in vivo studies in humans on energy and lipid metabolism in subcutaneous (SAT) and visceral adipose tissue (VAT). Studies in adipocyte cultures and transgenic animal models were included for the better understanding of the link between abnormal energy metabolism in adipose tissue and insulin resistance. The current literature indicates that higher lipolysis and lower lipogenesis in VAT compared to SAT enhance portal delivery of lipid metabolites (glycerol, fatty acids) to the liver. Thus, the lower lipolysis and higher lipogenesis in SAT favor storage of excess lipids and allow for protection of insulin-sensitive tissues from lipotoxic effects. In insulin-resistant humans, enhanced lipolysis and impaired lipogenesis in adipose tissue lead to release of cytokines and lipid metabolites, which consecutively promote insulin resistance. Adipose tissue of insulin-resistant humans also displays lower expression of proteins involved in mitochondrial function. In turn, this leads to lower availability of mitochondria-derived energy sources for lipogenesis in adipose tissue. Abnormal mitochondrial function in human white adipose tissue likely contributes to the secretion of lipid metabolites and lactate, which are linked to insulin resistance in peripheral tissues. However, the relevance of adipose tissue energy metabolism for the regulation of human insulin sensitivity remains to be further elucidated. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.