Abstract
Jaboticaba peel powder (JPP) is rich in bioactive compounds, mainly soluble and insoluble polyphenols with great antioxidant properties. The aim of this study is to evaluate the effects of JPP supplementation on the oxidative stress and hepatic damage in a rat model of type 2 diabetes mellitus (T2DM). Diabetic rats received vehicle or JPP at 2.7 (JPP-I), 5.4 (JPP-II), or 10.8 (JPP-III) g/L in drinking water during 8 weeks. JPP-III attenuated hyperglycaemia and dyslipidemia increased by 86% the liver content of nonprotein thiol groups and by 90% the GSH/GSSG ratio by activating glutathione synthesis. Accordingly, JPP supplementation prevented the loss of activity of the sulfhydryl-dependent enzyme δ-aminolaevulinic acid dehydratase and attenuated hepatic injury assessed by the reduction of serum aspartate aminotransferase activity and liver hypertrophy. Our results support that JPP supplementation to T2DM rats decreases hepatic damage most likely by increasing glutathione synthesis and modulating the thiol/disulfide redox balance.
Highlights
Diabetes is a major public health problem that affected about 387 million persons worldwide in 2014. is figure is expected to reach 592 million by 2035 [1]
The accumulation of free fatty acids (FFA) in type 2 diabetes mellitus (T2DM) increases the hepatic production of very low-density lipoprotein (VLDL) and impairs insulin signalling [8]
Extractable polyphenols and anthocyanins were the main bioactive compounds found in Jaboticaba peel powder (JPP), and they have been associated to the improvement of oxidative stress, insulin resistance, and lipid profile in a rat model of obesity [14, 15, 44]
Summary
Diabetes is a major public health problem that affected about 387 million persons worldwide in 2014. is figure is expected to reach 592 million by 2035 [1]. E tripeptide glutathione is a major nonenzymatic antioxidant that plays a key role in the maintenance of hepatic redox balance and protection against diabetes-induced liver damage [6, 7]. The accumulation of free fatty acids (FFA) in T2DM increases the hepatic production of very low-density lipoprotein (VLDL) and impairs insulin signalling [8]. Such events contribute to the nonalcoholic fatty liver disease [4] and dyslipidemia, which increase the risk of cardiovascular disease in diabetic patients [9]
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