Abstract
Cajanolactone A (CLA) is a stilbenoid isolated from Cajanus canjan (L.) Millsp with the potential to prevent postmenopausal obesity. In this study, the effect of CLA on high-fat diet (HFD)-induced obesity in female C57BL/6 mice was investigated. It was found that, treatment with CLA reduced the energy intake and effectively protected the mice from HFD-induced body weight gain, fat accumulation within the adipose tissues and liver, and impairment in energy metabolism. Further investigation revealed that CLA significantly down-regulated the expression of ORX, ORXR2, pMCH, and Gal in the hypothalamus and antagonized HFD-induced changes in the expression of UCP1, Pgc-1α, Tfam, and Mfn1 in the inguinal white adipose tissue (iWAT); Caveolin-1, MT and UCP3 in the perigonadal white adipose tissue (pWAT); and Pdhb, IRS2, Mttp, Hadhb, and Cpt1b in the liver. CLA also protected the pWAT and liver from HFD-induced mitochondrial damage. However, neither HFD nor CLA showed an effect on the mass of brown adipose tissue (BAT) or the expression of UCP1 in the BAT. In summary, our findings suggest that CLA is a potential drug candidate for preventing diet-induced obesity, at least in females. CLA works most likely by suppressing the hypothalamic expression of orexigenic genes, which leads to reduced energy intake, and subsequently, reduced fat accumulation, thereby protecting the adipose tissues and the liver from lipid-induced mitochondrial dysfunction.
Highlights
Obesity is one of the most dangerous factors in triggering insulin resistance, non-alcoholic fatty liver disease, type II diabetes, etc. (Reaven, 2002; Després and Lemieux, 2006; Meldrum et al, 2017)
Compared to mice in the high-fat diet (HFD) group, mice in the Cajanolactone A (CLA) group grew obviously slower (Figures 1A,B) and accumulated less visceral and subcutaneous fat (Figures 1C–F, 1H–I), indicating that treatment with CLA effectively prevented HFD-induced weight gain and development of obesity in female mice with normal ovarian function, may have the potential to prevent premenopausal obesity induced by hyperphagia
Due to the unbalanced mass gain between the White adipose tissue (WAT) and brown adipose tissue (BAT) (Figure 1), it is feasible to attribute the HFD-induced decrease of the metabolic rate to the excessively accumulated visceral and subcutaneous white fat, and the CLA-increased metabolic rate to the reduced fat mass gain
Summary
Obesity is one of the most dangerous factors in triggering insulin resistance, non-alcoholic fatty liver disease, type II diabetes, etc. (Reaven, 2002; Després and Lemieux, 2006; Meldrum et al, 2017). Long-term diet control is difficult to achieve for people who love good food, especially in a society where food is plentiful. Medications such as Liraglutide (Lin et al, 2020) and Qsymia (Cohen and Gadde, 2019), which suppress the appetite, have roles to play in people suffering from overweight. On the other hand, preventing the absorption of high-calorie food in the gastrointestinal tract is an effective way to reduce energy intake and storage, which can be accomplished via Orlistat. Orlistat inactivates the CLA Prevents HFD-Induced Obesity lipases in the gut by binding to them to prevent the lipasecatalyzed hydrolysis of triglycerides and the consequent absorption of the hydrolysates (free fatty acids and monoglycerides) (Curran and Scott, 2004)
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