Abstract
Arazyme and extracts of soy leaves (ESLs) are used as ingredients for functional foods; however, their combined administration has not been studied. This study assessed the combined effect of Arazyme and ESLs in high-fat-diet (HFD)-induced obese C57BL/6J mice fed 2 mg/kg Arazyme, 50 mg/kg ESLs, or a combination of 2 mg/kg Arazyme and 50 mg/kg ESLs by oral gavage for 13 weeks. Individually, Arazyme and ESLs had no effect on the HFD-induced phenotypes. The combination of Arazyme and ESLs significantly suppressed body weight gain, improved glucose and insulin tolerance, and suppressed hepatic steatosis by reducing lipid synthesis and enhancing lipid utilization gene expression. Furthermore, the combination significantly reduced HFD-induced plasma bile acid reabsorption by suppressing bile acid transporter expression, including the ATP biding cassette subfamily B member 11 (Abcb11), solute carrier family 10 member 1 (Slc10a1), Slc10a2, Slc51a, and Slc51b in the liver and gut. Moreover, the combination of Arazyme and ESLs significantly prevented HFD-induced islet compensation in the pancreas. These results suggest that the incorporation of Arazyme combined with ESLs reduces HFD-induced body weight, hyperglycemia, and hepatic steatosis by regulating liver–gut bile acid circulation in HFD-fed mice. This combination can markedly reduce treatment doses and enhance their therapeutic effects, thereby reducing therapeutic healthcare costs.
Highlights
The incidence of non-alcoholic fatty liver disease (NAFLD), obesity, and type 2 diabetes is increasing globally
This study evaluated whether the combination treatment of Arazyme with extracts of soy leaves (ESLs), at lower doses than the previous effective single dosages, had enhanced effects on body weight gain, hyperglycemia, and hepatic steatosis in HFD-induced obese NAFLD-like mice
Glucose transporter 2 (Glut2) in the combination treatment group were the lowest among all experimental groups (Figure 6D). These results indicate that the reduced expression of insulin-synthesis- and β-cell function-related genes may be caused by reduced insulin requirements, which in turn was attributed to improved glucose homeostasis by the combination treatment of Arazyme and ESLs
Summary
The incidence of non-alcoholic fatty liver disease (NAFLD), obesity, and type 2 diabetes is increasing globally. Obesity and type 2 diabetes are important risk factors in the progression of NAFLD [1]. In chronic dietinduced obesity and NAFLD, hyperglycemia, hyperinsulinemia, and hyperlipidemia are observed, accompanied by enhanced de novo lipogenesis and cholesterogenesis through the activation of hepatic transcription factors, including sterol-regulatory element-binding transcription factor 1 (SREBP-1), SREBP-2, and MLX-interacting protein-like (MLXIPL, known as carbohydrate-responsive element-binding protein) [5,6]. Chronic diet-induced obesity and NAFLD-related physiology and pathology are associated with insulin resistance caused by hyperglycemia and hyperlipidemia. Hepatic fatty acids regulate important transcriptional factors controlling hepatic metabolism, including SREBPs, MLXIPL, peroxisome proliferator-activated receptors (PPARs), and forkhead box protein O1 [8]
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