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This study describes neuromedin B (NB) and NB receptor as new regulators of skeletal muscle mitochondrial function. The white skeletal muscle mitochondrial oxidative phosphorylation capacity was increased by NB receptor genetic disruption in female mice. These findings may contribute to the resistance to diet-induced obesity, previously found in these mice, which requires future studies. Thus, investigations are necessary to clarify if blockade of NB receptor may be an approach to develop drugs to combat obesity.

The endocannabinoid system (ECS) increases food intake, appetite for fat and lipogenesis, while decreases energy expenditure (thermogenesis), contributing to metabolic dysfunctions. We demonstrated that maternal high-fat diet (HFD) alters cannabinoid signaling in brown adipose tissue (BAT) of neonate and weanling male rat offspring, which have increased adiposity but also higher energy expenditure in adulthood. In this study, the main objective was to investigate the ECS expression in thermogenic tissues as BAT and skeletal muscle of adult rats programmed by maternal HFD. We hypothesized that maternal HFD would modulate ECS and energy metabolism markers in BAT and skeletal muscle of adult male offspring.Female rats received standard diet (9.4 % of calories as fat) or isocaloric HFD (28.9 % of calories as fat) for 8 weeks premating and throughout gestation and lactation. Male offspring were weaned on standard diet and euthanatized in adulthood.Maternal HFD increased body weight, adiposity, glycemia, leptinemia while decreased testosterone levels in adult offspring. Maternal HFD did not change cannabinoid receptors in BAT or skeletal muscle as hypothesized but increased the content of uncoupling protein and tyrosine hydroxylase (thermogenic markers) in parallel to changes in mitochondrial morphology in skeletal muscle of adult offspring.In metabolic programming models, the ECS modulation in the BAT and skeletal muscle may be more important early in life to adapt energy metabolism during maternal dietary insult, and other mechanisms are possibly involved in muscle metabolism long-term regulation.

Obesity is associated with bioenergetic dysfunction of peripheral muscles; however, little is known regarding the impact of obesity on the diaphragm. We hypothesized that obesity would be associated with diaphragm dysfunction attributable to mitochondrial oxygen consumption and structural and ultrastructural changes. Wistar rat litters were culled to 3 pups to induce early postnatal overfeeding and consequent obesity. Control animals were obtained from unculled litters. From