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• W3026915437 endingPage "110226" @default.
• W3026915437 startingPage "110226" @default.
• W3026915437 abstract "• STZ-NA-induced diabetes mellitus (DM) progresses to hepatic lipotoxicity/injury. • DM-driven hepatic lipotoxicity is associated with increased HDAC activity. • SAT reverses HDAC activity and normalizes hepatic lipid and tissue integrity in DM rats. • SAT-led beneficial effects are associated with attenuated oxidative stress and proinflammation in DM rats. Hepatic lipid dysregulation with consequent lipotoxicity remains critical in the progression of non-alcoholic fatty liver disease, a rising prevalent complication of diabetes mellitus particularly type 2 diabetes. Diabetes-associated hepatic complications are among the leading causes of liver-related morbidity and mortality worldwide. Short chain fatty acids (SCFAs) have been demonstrated to regulate glycemic metabolism but its effect on diabetes-driven hepatic perturbation is unknown. This study is therefore designed to investigate the effect of SCFAs, acetate on diabetes-characterised hepatic lipotoxicity, and plausible involvement of histone deacetylase (HDAC) activity. Adult male Wistar rats (230−260 g) were allotted into groups (n = 6/group) namely: control (vehicle; p.o. ), sodium acetate (SAT)-treated (200 mg/kg), diabetic with/without SAT groups. Diabetes was induced by intraperitoneal injection of streptozotocin 65 mg/kg after a dose of nicotinamide 110 mg/kg. Data from diabetic animals showed increased fasting glycemia and insulinemia, decreased insulin sensitivity and body weight with increased relative hepatic mass. It also revealed increased hepatic lipid, serum/hepatic malondialdehyde, tissue necrosis factor-α, uric acid, aspartate transaminase, alanine aminotransferase and decreased glutathione content with elevated hepatic HDAC. Histologically, the hepatic tissue was characterised with disrupted architecture, inflammation of central vein and foci of periportal and sinusoidal cellular infiltration. However, these alterations were attenuated by sodium acetate. The study demonstrates that diabetes mellitus drives hepatic lipotoxicity, characterised with lipid accumulation, excessive lipid peroxidation, pro-inflammation, depleted glutathione content and accompanied by increased HDAC activity. Besides, the study suggests that acetate ameliorates diabetes-associated hepatic lipotoxicity through HDAC suppression and enhancement of insulin sensitivity." @default.
• W3026915437 created "2020-05-29" @default.
• W3026915437 creator A5040896735 @default.
• W3026915437 creator A5065719410 @default.
• W3026915437 date "2020-08-01" @default.
• W3026915437 modified "2023-10-18" @default.
• W3026915437 title "Sodium acetate-mediated inhibition of histone deacetylase alleviates hepatic lipid dysregulation and its accompanied injury in streptozotocin-nicotinamide-induced diabetic rats" @default.
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• W3026915437 doi "https://doi.org/10.1016/j.biopha.2020.110226" @default.
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