Muscle development and obesity

Abstract

The formation of skeletal muscle from the epithelial somites involves a series of events triggered by temporally and spatially discrete signals resulting in the generation of muscle fibers which vary in their contractile and metabolic nature. The fiber type composition of muscles varies between individuals and it has now been found that there are differences in fiber type proportions between lean and obese animals and humans. Amongst the possible causes of obesity, it has been suggested that inappropriate prenatal environments may 'program' the fetus and may lead to increased risks for disease in adult life. The characteristics of muscle are both heritable and plastic, giving the tissue some ability to adapt to signals and stimuli both pre and postnatally. Given that muscle is a site of fatty acid oxidation and carbohydrate metabolism and that its development can be changed by prenatal events, it is interesting to examine the possible relationship between muscle development and the risk of obesity.

Gut microbiota can transfer fiber characteristics and lipid metabolic profiles of skeletal muscle from pigs to germ-free mice

“…During the past decade, it has been increasingly identified that skeletal muscle development and metabolism are closely associated with obesity46. There are differences in the fiber type proportions between lean and obese animals2147.…”

“…In humans, skeletal muscle represents approximately 40% of the body weight and constitutes the largest organ in our body 45 . During the past decade, it has been increasingly identified that skeletal muscle development and metabolism are closely associated with obesity 46 . There are differences in the fiber type proportions between lean and obese animals 21 47 .…”

Genetic Dissection of the Physiological Role of Skeletal Muscle in Metabolic Syndrome

“…In sedentary life style-induced conditions such as obesity, metabolic syndrome, and type 2 diabetes, it has been assumed that skeletal muscle would present a similar type of physiological changes as observed in the unweighted muscle, fostering the development of skeletal muscle insulin resistance. This assumption has been verified in reports showing that conditions including insulin resistance, type 2 diabetes, and obesity in humans are associated with reduction in SO muscle fibers and/or oxidative metabolism [31][32][33][34][35][36][37][38][39][40][41][42]. Furthermore, molecular level studies have demonstrated that, in humans with insulin resistance and type 2 diabetes, expression of oxidative metabolism genes is significantly reduced in a coordinated manner [43][44][45].…”

The Link between Fetal Programming, Inflammation, Muscular Strength, and Blood Pressure

“…The deficit in body size or “somatic capital” in the low birth weight neonate is almost entirely accounted for by lower fat-free mass [ 59 ] and a positive association between birth weight and fat-free mass is a highly consistent finding [ 60 ] observed across the lifecycle. Muscle fiber number and type are set in-utero and experimentally induced fetal undernutrition in animals is associated with lower muscle fiber number [ 61 ]. In humans, LBW is also associated with alterations in muscle morphology [ 62 ] and deficits in muscle signaling proteins [ 63 ], alterations that negatively affect muscle glucose and fat metabolism and may precede metabolic abnormalities and increase susceptibility to obesity and comorbidities.…”