Abstract
The present study examined the effects of Wasabi leaf (WL) on 45% Kcal high-fat diet (HFD)-fed mild diabetic obese mice. In particular, the hepatoprotective (i.e., liver weight, histopathology of liver, serum aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyltransferase) effects of 12 weeks of continuous oral administration of 250 mg/kg metformin, and 200, 100, or 50 mg/kg WL were investigated. In addition, the hypolipidemic (i.e., serum triglyceride, total cholesterol, high-density lipoprotein-cholesterol, and low-density lipoprotein levels), hypoglycemic (i.e., glycated hemoglobin, blood glucose and insulin levels, pancreatic weight, and immunohistochemical-histopathological analysis of the pancreas), and anti-obesity effects (i.e., body weight, mean food consumption, total and abdominal body fat mass, periovarian fat weight, and histopathology of the periovarian and abdominal wall adipocytes) were monitored. The liver and general antioxidant defense systems were also assessed by lipid metabolism-related gene expression. All diabetes manifestations and related complications, including obesity and non-alcoholic fatty liver disease (NAFLD), were dose-dependently reduced after 84 days of oral treatment with metformin or each of the three dosages of WL. In particular, 50 mg/kg WL showed effective suppression effects against HFD-induced diabetes and related complications of obesity, NAFLD, and hyperlipidemia, comparable to the effects of metformin.
Highlights
The increasing incidence of obesity worldwide is highly correlated with a metabolic syndrome known as type II diabetes, which results from high-calorie intake and physical inactivity [1]
We investigated the efficacy of Wasabi leaf (WL) in 45% Kcal high-fat diet (HFD)-fed mice, compared with metformin treatment, a representative anti-diabetic and anti-obesity drug used to treat type II diabetes
The body weight changes during administration period decreased in a significant (p < 0.01) and dose-dependent manner in mice that received any WL treatment, as well as in metformin group, compared with changes in HFD control group
Summary
The increasing incidence of obesity worldwide is highly correlated with a metabolic syndrome known as type II diabetes, which results from high-calorie intake and physical inactivity [1]. Excessive consumption of fatty acids induced the accumulation of triglycerides (TGs) in fat tissue, where lipolysis increases. High levels of fatty acids, related with elevated lipolysis in insulin-resistant adipocytes, lead to an excess of fatty acids in non-adipose tissues (e.g., muscle, liver, and pancreas). Augmented levels of tissue fatty acid transport and binding proteins in non-adipose and adipose tissues facilitate uptake in insulin-resistant individuals. Prolonged exposure of the pancreas to free fatty acids impairs insulin release through a lipotoxic mechanism [5]. High free fatty acid concentrations in the liver cause insulin resistance through enhanced glucose output by the liver [6]. The increase of TGs in the liver caused by high concentrations of free fatty acids results in non-alcoholic fatty liver disease (NAFLD)
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