Abstract
Endurance exercise has been shown to improve metabolic outcomes in obesity and type 2 diabetes; however, the physiological and molecular mechanisms for these benefits are not completely understood. Although endurance exercise has been shown to decrease lipogenesis, promote fatty acid oxidation (FAO), and increase mitochondrial biosynthesis in adipose tissue, muscle, and liver, its effects on intestinal lipid metabolism remain unknown. The absorptive cells of the small intestine, enterocytes, mediate the highly efficient absorption and processing of nutrients, including dietary fat for delivery throughout the body. We investigated how endurance exercise altered intestinal lipid metabolism in obesity and type 2 diabetes using Otsuka Long‐Evans Tokushima Fatty (OLETF) rats. We assessed mRNA levels of genes associated with intestinal lipid metabolism in nonhyperphagic, sedentary Long‐Evans Tokushima Otsuka (LETO) rats (L‐Sed), hyperphagic, sedentary OLETF rats (O‐Sed), and endurance exercised OLETF rats (O‐EndEx). O‐Sed rats developed hyperphagia‐induced obesity (HIO) and type 2 diabetes compared with L‐Sed rats. O‐EndEx rats gained significantly less weight and fat pad mass, and had improved serum metabolic parameters without change in food consumption compared to O‐Sed rats. Endurance exercise resulted in dramatic up‐regulation of a number of genes in intestinal lipid metabolism and mitochondrial content compared with sedentary rats. Overall, this study provides evidence that endurance exercise programs intestinal lipid metabolism, likely contributing to its role in improving metabolic outcomes in obesity and type 2 diabetes.
Highlights
The obesity epidemic is associated with the overconsumption of energy-dense dietary fat, higher calorie intake, and a sedentary lifestyle in developed countries (Hedley et al 2004; Cordain et al 2005; Matthews et al 2008)
Relative mRNA levels for genes associated with lipid anabolism including CM synthesis and secretion (Mtp and Cd36), cytoplasmic lipid droplets (CLDs) formation (Plin2 and perilipin 3 (Plin3)), and fatty acid and TAG synthesis (Dgat1, diacylglycerolO-acyltransferase 2 (Dgat2), monoacylglycerol-Oacyltransferase 2 (Mgat2), Srebp1c, liver X receptor a (Lxra), acetyl-CoA carboxylase 1 (Acc1), and Acsl5) were determined in intestinal mucosa
While O-Sed rats had higher mRNA level of perilipin 2 (Plin2), a gene involved in CLD formation, than L-Sed rats, O-Endurance exercise (EndEx) rats had even greater mRNA levels of Plin2 and Plin3 compared with L-Sed rats and O-Sed rats (P < 0.05; Fig. 2B)
Summary
The obesity epidemic is associated with the overconsumption of energy-dense dietary fat, higher calorie intake, and a sedentary lifestyle in developed countries (Hedley et al 2004; Cordain et al 2005; Matthews et al 2008). The beneficial effects of EndEx include weight loss (Cuff et al 2003), improved insulin sensitivity and glucose metabolism (O’Hagan et al 2013), ameliorated postprandial triglyceridemic response (Merrill et al 1989), and increased rate of fat oxidation (Bordenave et al 2008). It remains unclear how EndEx training may affect lipid metabolism in the small intestine.
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