Sodium butyrate aggravates glucose dysregulation and dyslipidemia in high fat-fed Wistar rats

Abstract

Sodium butyrate (NaB), a short chain fatty acid (SCFA) has been shown to improve metabolic, glucose and lipid signaling. High fat diet elicits increased risk of cardiometabolic disease due to dysmetabolism, altered endothelial function and elevated oxidant activities. This study aims at evaluating the effect of NaB on high fat diet-fed female Wistar rats, and the possible role of vascular endothelial growth factor (VEGF). Twenty female Wistar rats with mean weight of 120 ± 5 g were divided randomly after one week of acclimatization into four groups: Control diet (CTR), High fat diet (HFD), NaB (200 mg/kg), and HFD + NaB. After six weeks of the experimental procedure, blood samples were collected by cardiac puncture. Data were analyzed and expressed in mean ± SEM and p-values <0.05 were accepted as significant. Data showed that HFD increased lactate dehydrogenase (LD) and free fatty acid (FFA), but not triglyceride (TG) and total cholesterol (TC). It also led to insulin resistance (elevated fasting blood glucose, insulin and homeostasis model assessment for insulin resistance). These effects of HFD were accompanied by increased lipid peroxidation (malondialdehyde and 4-hydroxynonenal). Sodium butyrate significantly decreased circulating nitric oxide (NO) and LD while increasing FFA, TG, insulin resistance, aggravated lipid peroxidation and increased VEGF in HFD rats (P < 0.05). We speculated therefore, that NaB aggravated glucose dysregulation and dyslipidemia, which is accompanied by increased VEGF.