Swim training improves leptin receptor deficiency-induced obesity and lipid disorder by activating uncoupling proteins

Abstract

Leptin receptor deficiency causes morbid obesity and hyperlipidemia in mice. Since physical exercise enhances energy expenditure, it is an important part of successful weight-control regimens. We investigated the mechanism by which swim training regulates leptin receptor deficiency-induced obesity and lipid disorder in a mouse model of obesity (obese db/db mouse). Swim training for 6 weeks significantly decreased body weight gain and adipose tissue mass in both sexes of obese and lean mice, compared to their respective sedentary controls. These effects were particularly evident in obese mice. Swim training also caused significant decreases in serum levels of triglycerides, free fatty acids and total cholesterol in both obese and lean mice. In obese mice, swim training increased the levels of mRNAs and proteins encoding uncoupling protein 1 (UCP1), UCP2 and UCP3 in brown adipose tissue, white adipose tissue and skeletal muscle, respectively. In conclusion, these findings suggest that, in mice, swim training can effectively prevent body weight gain, adiposity and lipid disorders caused by leptin receptor deficiency, in part through activation of UCPs in adipose tissue and skeletal muscle, which may contribute to alleviating metabolic syndromes, such as obesity, hyperlipidemia and type 2 diabetes.

Effects of a semiochemical on feed conversion index and related indicators on fast-growing broilers housed during forty-two days

“…Thaxton et al (2006) found no influence on GLU, CHOL, and TRI on a stressing situation in overcrowded male broilers, whereas CS showed greater values compared with control. Our findings appear logical, because body fat content and concentration of TRI are linked (Oh et al, 2007). Indeed, a comparable TRI concentration between treatments reaches conclusions similar to those by Madec et al (2006), who observed no statistical differences in body fat between MHUSA and control.…”

Leptin impairs myogenesis in C2C12 cells through JAK/STAT and MEK signaling pathways

“…Additionally, lack of leptin receptors renders skeletal muscles more oxidative and fatigue resistant which is similar to skeletal muscle from aged mice [43]. Obviously, skeletal muscles of genetically obese mice did not respond to changes in body weight or activity [44], even though swim training improves leptin receptor deficiency-induced obesity by leptin-independent mechanism [45]. Physiologically, distinct leptin concentrations are evident in sexual dimorphism [46], whereas in pathology higher blood plasma leptin was found in cancer cachexia [14,15].…”

A combination of exercise and capsinoid supplementation additively suppresses diet-induced obesity by increasing energy expenditure in mice

“…UCP-1 has recently attracted attention as a target for suppressing obesity. CSNs and exercise have been reported to increase UCP-1 levels in interscapular BAT (31,37,38). Furthermore, exercise has been reported to induce browning in subcutaneous WAT (5).…”