Abstract
Galangin is a natural flavonoid. In this study, we evaluated whether galangin could alleviate signs of metabolic syndrome (MS) and cardiac abnormalities in rats receiving a high-fat (HF) diet. Male Sprague–Dawley rats were given an HF diet plus 15% fructose for four months, and they were fed with galangin (25 or 50 mg/kg), metformin (100 mg/kg), or a vehicle for the last four weeks. The MS rats exhibited signs of MS, hypertrophy of adipocytes, impaired liver function, and cardiac dysfunction and remodeling. These abnormalities were alleviated by galangin (p < 0.05). Interleukin-6 and tumor necrosis factor-α concentrations and expression were high in the plasma and cardiac tissue in the MS rats, and these markers were suppressed by galangin (p < 0.05). These treatments also alleviated the low levels of adiponectin and oxidative stress induced by an HF diet in rats. The downregulation of adiponectin receptor 1 (AdipoR1) and cyclooxygenase-2 (COX-2) and the upregulation of nuclear factor kappa B (NF-κB) expression were recovered in the galangin-treated groups. Metformin produced similar effects to galangin. In conclusion, galangin reduced cardiometabolic disorders in MS rats. These effects might be linked to the suppression of inflammation and oxidative stress and the restoration of AdipoR1, COX-2, and NF-κB expression.
Highlights
Metabolic syndrome (MS) is comprised of a set of cardiometabolic risk factors such as dyslipidemia, insulin resistance, central obesity, and hypertension
We evaluated whether galangin could alleviate the signs of MS, cardiac alterations, oxidative damage, and inflammation induced by an HF diet in rats
MS rats showed significant increases in the ratio of retroperitoneal fat pads/body weight and epididymal fat pads/body weight compared to the control group (p < 0.05) (Table 1.)
Summary
Metabolic syndrome (MS) is comprised of a set of cardiometabolic risk factors such as dyslipidemia, insulin resistance, central obesity, and hypertension. It is well documented that excessive caloric intake is the major cause of obesity and metabolic syndrome in humans [2]. Obesity has been proposed to be the cause of adverse effects on the metabolic system, dyslipidemia, and hyperglycemia. In a rat model of MS, HF diet-induced metabolic disturbances have been associated with signs of MS and cardiovascular alterations in humans [4]. Several studies have demonstrated that rats that received an HF diet had hyperglycemia, an impaired oral glucose tolerance test (OGTT), hyperinsulinemia, dyslipidemia, visceral fat pad accumulation, and hypertension [5,6]. Fructose supplementation in rats can induce signs of MS, as Antioxidants 2021, 10, 769.
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