Abstract
Simple SummaryBeetroot is one of the most consumable plants across the world. Previous studies have shown many health benefits of beetroot, with evidence of having potent hypoglycemic, antioxidant, and anti-inflammatory effects. The data obtained from this study further confirmed this effect in streptozotocin-diabetic animals. They showed the ability of methanolic beetroot extract to prevent the associated hepatic oxidative stress, inflammation, steatosis, and dyslipidaemia. However, the protection mechanisms involve, at least, upregulation of endogenous antioxidants, anti-apoptotic Bcl2, and PPARα.The present study examined if methanolic beetroot extract (BE) could prevent dyslipidemia and hepatic steatosis and damage in a type-2 diabetes mellitus (T2DM) rat model and studied some mechanisms of action. T2DM was induced in adult male Wistar rats by a low single dose of streptozotocin (STZ) (35 mg/kg, i.p) and a high-fat diet (HFD) feeding for 5 weeks. Control or T2DM rats then continued on standard or HFDs for another 12 weeks and were treated with the vehicle or BE (250 or 500 mg/kg). BE, at both doses, significantly improved liver structure and reduced hepatic lipid accumulation in the livers of T2DM rats. They also reduced body weight gain, serum glucose, insulin levels, serum and hepatic levels of cholesterol, triglycerides, free fatty acids, and serum levels of low-density lipoproteins in T2DM rats. In concomitant, they significantly reduced serum levels of aspartate and alanine aminotransferases, hepatic levels of malondialdehyde, tumor-necrosis factor-α, interleukin-6, and mRNA of Bax, cleaved caspase-3, and SREBP1/2. However, both doses of BE significantly increased hepatic levels of total glutathione, superoxide dismutase, and mRNA levels of Bcl2 and PPARα in the livers of both the control and T2DM rats. All of these effects were dose-dependent and more profound with doses of 500 mg/kg. In conclusion, chronic feeding of BE to STZ/HFD-induced T2DM in rats prevents hepatic steatosis and liver damage by its hypoglycemic and insulin-sensitizing effects and its ability to upregulate antioxidants and PPARα.
Highlights
Type-2 diabetes mellitus is a chronic disorder that results mainly from the ineffectiveness of insulin peripheral action or resistance [1]
A significant increase in the final body weights, fasting glucose and insulin levels, and values of HOMA-insulin resistance (IR) were seen in type-2 diabetes mellitus (T2DM)-induced rats when compared to control rats, which were significantly reduced in T2DM, and treated with beetroot extract (BE) at doses of 250 or 500 mg/kg (Table 2)
The reduction in all of these parameters was more significant in T2DM + BE (500 mg/kg)-treated rats when compared to T2DM + BE (250 mg/kg)-treated rats, levels that were not significantly different when compared to control rats (Table 2)
Summary
Type-2 diabetes mellitus is a chronic disorder that results mainly from the ineffectiveness of insulin peripheral action or resistance [1]. Hepatic oxidative stress and inflammation, mainly due to the co-existence of peripheral insulin resistance (IR), are the key pathological mechanisms leading to hepatic damage in NAFLD patients by acting in a vicious cycle [4,5,6]. Within this view, the influx of free fatty acids (FAs) and inflammatory cytokines/adipokines is highly increased to the liver, causing a state of inflammation, stimulating the generation of reactive oxygen species (ROS) by activating the Kupffer cells, increasing macrophage infiltration, damaging the mitochondria, activating lipogenesis, and promoting endoplasmic reticulum stress [4,7,8,9,10]. ROS and inflammatory cytokines cause hepatic IR, stimulate de novo lipogenesis, and promote hepatocyte damage and fibrosis by impairing insulin signaling and activating several lipogenic, apoptotic, and fibrotic signaling pathways [4,5,6,7,9,11]
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