Regular exercise leads to fat breakdown (lipolysis) by lowering insulin and increasing PPARg-2

  • Exercise helps you stay slim by "oxidising" (burning) fat and carbohydrates in the muscles. However, it can also help you slim down via numerous other mechanisms, two of which are described in this paper conducted in Japan.
  • Specifically, in experiments on mice the Japanese researchers found that regular exercise increases ATGL, a lipolytic (fat-releasing) enzyme found in fat cells, whose purpose is to break down fat, thereby helping reduce fat accumulation in the fat cells.
  • Adipose triglyceride lipase (ATGL) levels in fat cells increase with regular exercise, partially due to an increase in a protein called PPARg2 but also due to a reduction in circulating insulin
  • Insulin is well-known as the most important inhibitor of lipolysis and high levels of this hormone can lead to an almost complete shut down of lipolysis. By controlling insulin via regular exercise, we allow ATGL to break down fat and release it into the bloodstream for oxidation (burning) in the muscles, liver and organs.
  • Source: Higher Levels of ATGL Are Associated with Exercise-Induced Enhancement of Lipolysis in Rat Epididymal Adipocytes
  • Abstract: BACKGROUND: In adipose cells, adipose triglyceride lipase (ATGL) catalyzes the first step in adipocyte triacylglyceride hydrolysis, thereby regulating both basal and hormone-stimulated lipolysis. However, little is known about the molecular mechanism(s) underlying habitual exercise-induced adaptive modulation of ATGL in white adipocytes via alteration in transcription regulator and lipolytic cofactors. METHODOLOGY/PRINCIPAL RESULTS:
    Male Wistar rats were randomly divided into 2 groups a sedentary control group (CG) and a habitual exercise group (EG). The EG was subjected to running on a treadmill set at 5 days per week for 9 weeks. The CG was not subjected to running on a treadmill. In the EG, levels of ATGL mRNA and protein were elevated with a significant increase in lipolysis compared with the CG, accompanied by a significant increase in associations of CGI-58 with ATGL protein. Under these conditions, an upregulation of peroxisome proliferation-activated receptorg-2 (PPARg-2) was observed. In the EG, the addition of rosiglitazone further significantly increased the levels of ATGL protein compared with the CG. However, attenuated levels of the ATGL protein in adipocytes were obtained by the addition of insulin, which is known to inhibit the expression of ATGL, in both types of groups. Actually, levels of plasma insulin were significantly reduced in the EG compared with the CG. CONCLUSIONS: These data suggest that elevated levels of ATGL are involved in the exercise-induced enhancement of lipolysis in primary adipocytes. The exact mechanism(s) underlying this phenomenon is associated, at least in part, with upregulated transcriptional activation of PPARg-2. In addition, exercise-induced lower circulation levels of insulin also correlate with habitual exercise-induced higher levels of ATGL in primary adipocytes.