Abstract
Obesity is a major driver of metabolic diseases such as nonalcoholic fatty liver disease, certain cancers, and insulin resistance. However, there are no effective drugs to treat obesity. Betaine is a nontoxic, chemically stable and naturally occurring molecule. This study shows that dietary betaine supplementation significantly inhibits the white fat production in a high-fat diet (HFD)-induced obese mice. This might be due to betaine preventing the formation of new white fat (WAT), and guiding the original WAT to burn through stimulated mitochondrial biogenesis and promoting browning of WAT. Furthermore, dietary betaine supplementation decreases intramyocellular lipid accumulation in HFD-induced obese mice. Further analysis shows that betaine supplementation reduced intramyocellular lipid accumulation might be associated with increasing polyunsaturated fatty acids (PUFA), fatty acid oxidation, and the inhibition of fatty acid synthesis in muscle. Notably, by performing insulin-tolerance tests (ITTs) and glucose-tolerance tests (GTTs), dietary betaine supplementation could be observed for improvement of obesity and non-obesity induced insulin resistance. Together, these findings could suggest that inhibiting WAT production, intramyocellular lipid accumulation and inflammation, betaine supplementation limits HFD-induced obesity and improves insulin resistance.
Highlights
White adipose tissue (WAT) is mainly located in the subcutaneous fat (SAT) and visceral fat, which is an important secretory and energy metabolizing organ [1]
Previous studies suggested that consumption of a high-fat diet (HFD) rapidly reprograms systemic metabolism and, causes obesity [38,39]
Further analysis showed that HFD-fed mice gained more inguinal fat (Figure 1D), gonadal fat (Figure 1E) and perirenal fat (Figure 1F), all of which were significantly increased when compared to normal chow (NCW)-fed mice, as reported by Jeffery et al [40]
Summary
White adipose tissue (WAT) is mainly located in the subcutaneous fat (SAT) and visceral fat, which is an important secretory and energy metabolizing organ [1]. A large body of work indicates that SAT is the largest and least harmful adipose depot to store excess lipids. Adipocytes can secrete a large number of disease-promoting exosomes that contain special microRNAs, proteins and mRNAs to establish a distant pro-metastatic niche [8,9,10]. Ikrame et al [11] reported that mature adipocyte-derived exosomes promote melanoma aggressiveness through fatty acid oxidation. Deng et al [12] suggested that adipose tissue exosome-like vesicles mediate activation of macrophage-induced insulin resistance. Cheng et al [13] found that perivascular adipose tissue-conditioned medium induced adventitial fibroblast migration, which may be associated with the pathogenesis of neointimal formation
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