Adipose tissue hypertrophy is enhanced when fatty acids and glucose are preferentially channeled to adipose tissue rather than to other tissues, and particularly to muscle, where their main metabolic fate is oxidation. Two important players in nutrient partitioning between fat and muscle are LPL and GLUT4, both of which are highly expressed in the two tissues. Disregulation or imbalances of these two activities in muscle and adipose tissue may contribute to obesity, or may even cause it. Muscle LPL activity is inversely correlated with percentage body fat and body mass index in humans,60,61 and moderate overexpression of LPL selectively in skeletal muscle prevents the development of diet-induced obesity in transgenic mice.62 In mice, transgenic overexpression of GLUT4 in adipose tissue results in an obese phenotype,63,64 whereas lack of GLUT4 in adipose tissue (through tissue-specific knockout) results in reduced adiposity.65
LPL activity in adipose tissue changes during the day according to the nutritional state: it decreases during short-term fasting, by means of a post-
translational mechanism,66 and recovers upon refeeding. Failure to decrease adipose tissue LPL activity in the post-absorptive state may contribute to increased fat deposition in obesity,66 as suggested by the finding of a higher LPL activity in adipose tissue during fasting in obese subjects compared with lean controls.67 LPL activity in adipose tissue is affected not only by the nutritional state, but also by specific nutrients: it is stimulated by glucose, by post-transcriptional mechanisms,57 and inhibited by fatty acids and high-fat diets, which however induce the transcription of the LPL gene in adipo-cytes.68,69 GLUT4 expression is also subject to dietary modulation: it increases with high-fat diets more in adipose tissue than in muscle, whereas in the unfed state it is markedly down-regulated in adipose tissue and up-regulated in muscle (reviewed in reference 70).
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