[27] found that resistance exercise activity, click here at least once a week, was associated with a lower proportion of subjects with NAFLD, independently of BMI, nutritional factors, insulin resistance, and some circulating adipokines, such as adiponectin and resistin. The underlying mechanisms by which exercise, particularly resistance training, may reduce hepatic fat content are not entirely understood. They probably include changes in energy balance, circulatory lipids, fat

oxidation, and insulin sensitivity.[24] In our study, we were careful to avoid a hypocaloric diet or dietary changes during the exercise intervention. Thus, the mild weight loss we observed in both groups is attributable to the effects of exercise and is actually a proof of patients’ compliance with Olaparib mw the training protocol. Although transferring the results

of randomized clinical trials, like ours, to “real-world” settings is not always easy, we believe that our data are clinically important, as they support a beneficial effect of exercise per se for the treatment of NAFLD in type 2 diabetic patients, which can be an adjunct to caloric restriction. Moreover, the finding that resistance exercise is as effective as aerobic exercise in improving hepatic steatosis provides a useful alternative in patients in whom aerobic training may not be accessible, as the high cardiorespiratory demand characteristic of this type of exercise is associated with fatigue and discomfort. Another interesting and MCE novel finding of our study is the close association between changes in hepatic fat content and changes in SSAT and DSAT. In multivariate regression analysis, the absolute reduction in hepatic fat content was best predicted by baseline hepatic fat content and changes in SSAT and DSAT. Whereas the relation between baseline hepatic fat content and its change after exercise intervention could be an expected finding, the independent and opposite associations between the absolute reduction in hepatic fat content and changes in SSAT and DSAT are intriguing. Evidence

indicates that these two subcutaneous fat depots differ in terms of structure and pathophysiology.[28] Interestingly, whereas VAT and DSAT correlate negatively with whole-body insulin sensitivity, SSAT does not.[29] Moreover, SSAT correlates with a more favorable cardiometabolic risk profile in type 2 diabetic patients, whereas DSAT behaves as a VAT depot.[30] Based on these findings, it was hypothesized that higher energy storage in SSAT might exert protective effects by decreasing fat deposition in the liver as well as in other ectopic fat depots. Our data further support this hypothesis, showing that the lower the reduction in SSAT following exercise-induced energy burning, the higher the reduction in hepatic fat content.