Glucoregulatory Effect of Butyrate is Associated with Elevated Circulating VEGF and Reduced Cardiac Lactate in High Fructose Fed Rats

Overview

Journal Heliyon

Specialty Social Sciences

Date 2023 Nov 30

PMID 38034766

Authors

Adewumi Oluwafemi Oyabambi

Olubayode Bamidele

Aindero Blessing Boluwatife

Lawrence Dayo Adedayo

Affiliations

Soon will be listed here.

Abstract

Background: High fructose diet has been linked with impaired body metabolism and cardiovascular diseases. Sodium butyrate (NaB) was documented to improve glucoregulation and cardiometabolic problems associated with high fructose diet (HFrD) but the mechanisms behind it are unclear. As a result, the purpose of this study was to look into the effects of NaB on VEGF and cardiac lactate in HFrD-induced dysmetabolism.

Methods: Twenty male Wistar rats of weight 130-140 g were assigned randomly after a week of acclimation into four groups: Control diet (CTR), High fructose drink (HFrD); 10 % (w/v), NaB (200 mg/kg bw), and HFrD + NaB (200 mg/kg bw). The animals were induced to be unconscious with 50 mg/kg of pentobarbital sodium intraperitoneally, blood samples were taken via cardiac puncture and cardiac tissue homogenates were obtained for Fasting Blood Sugar (FBS) and plasma insulin, cardiac glycogen, plasma and cardiac glycogen synthase, plasma and cardiac nitric oxide as well as vascular endothelial growth factor (VEGF).

Result: HFrD resulted in statistical elevation body and cardiac weight, plasma glucose, plasma insulin, cardiac lactate, glycogen and decreased nitric oxide level (NO) when compared with the control group. Administration of NaB reduced cardiac weight, blood glucose, plasma insulin, cardiac lactate while nitric oxide and glycogen increased (P < 0.05). NaB increased plasma glycogen synthase in normal rats, plasma and cardiac circulating VEGF in HFrD administered rats (P < 0.05) while no change was produced in plasma and cardiac glycogen synthase level of HFrD treated rats.

Conclusion: Sodium butyrate improves glucoregulation by reducing cardiac lactate and increasing circulating VEGF in HFrD-treated rats.

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