Oyabambi Adewumi Oluwafemi, Michael Olugbenga Samuel, Areola Emmanuel Damilare, Saliu Salam Babatunde, Olatunji Lawrence Aderemi
Department of Physiology, Faculty of Basic Medical Sciences, College of Health Sciences, University of Ilorin, P.M.B. 1515, Ilorin, 240001, Nigeria.
Cardiometabolic, Microbiome and Applied Physiology Laboratory, Physiology Program, College of Health Sciences, Bowen University, Iwo, Nigeria.
Naunyn Schmiedebergs Arch Pharmacol. 2021 Jul;394(7):1425-1435. doi: 10.1007/s00210-021-02058-6. Epub 2021 Feb 27.
Pregnancy is an insulin-resistant condition especially at near term predisposing maternal kidneys to hyperinsulinemia-induced oxidative stress. The impact of fructose on renal metabolic dysregulation and oxidative stress in pregnancy requires elucidation. Short-chain fatty acids (SCFAs) are known for protective roles in oxidative stress conditions. Therefore, the study aimed at investigating fructose-induced glucose dysregulation and renal oxidative stress in pregnant and non-pregnant rats and the possible preventive role of SCFA, acetate. Thirty female Wistar rats were grouped (n = 5/group). Three groups were made pregnant (P); the other three remained non-pregnant (NP). Both pregnant and non-pregnant rats received drinking water (control), 10% fructose (w/v) (NP+F or P+F), and 10% (w/v) fructose plus sodium acetate (200 mg/kg) (NP+F+A or P+F+A) for 3 weeks. Renal and plasma glutathione antioxidant index (GSH/GSSG), G6PDH, and adenosine were significantly lower in NP+F and P+F groups compared with control while renal and plasma adenosine deaminase (ADA), xanthine oxidase (XO), uric acid (UA), lactate dehydrogenase (LDH), and malonaldehyde (MDA) were significantly elevated in NP+F and P+F groups compared with controls. HOMA-IR showed marked impairment in both NP+F and P+F groups. The P+F group revealed greater suppression in plasma and renal G6PDH-dependent antioxidant index, adenosine, and aggravation of LDH, MDA compared with the NP+F group (p < 0.05). Sodium acetate reduces plasma and renal surrogate oxidative stress markers, improved G6PD-dependent antioxidant index, and HOMA-IR in NP+F and P+F groups. Pregnancy exacerbates fructose-induced insulin resistance and renal oxidative stress whereas acetate ameliorated fructose-induced redox and glucose dysregulation in pregnant and non-pregnant rats.
妊娠是一种胰岛素抵抗状态，尤其是在孕晚期，会使母体肾脏易受高胰岛素血症诱导的氧化应激影响。果糖对妊娠期间肾脏代谢失调和氧化应激的影响尚需阐明。短链脂肪酸（SCFAs）在氧化应激条件下具有保护作用。因此，本研究旨在调查果糖诱导的妊娠和非妊娠大鼠的葡萄糖失调及肾脏氧化应激，以及SCFA（乙酸盐）可能的预防作用。将30只雌性Wistar大鼠分组（每组n = 5）。其中三组使其怀孕（P）；另外三组保持未怀孕（NP）。怀孕和未怀孕的大鼠均接受饮用水（对照）、10%果糖（w/v）（NP+F或P+F）以及10%（w/v）果糖加醋酸钠（200 mg/kg）（NP+F+A或P+F+A），持续3周。与对照组相比，NP+F组和P+F组的肾脏和血浆谷胱甘肽抗氧化指数（GSH/GSSG）、葡萄糖-6-磷酸脱氢酶（G6PDH）及腺苷显著降低，而NP+F组和P+F组的肾脏和血浆腺苷脱氨酶（ADA）、黄嘌呤氧化酶（XO）、尿酸（UA）、乳酸脱氢酶（LDH）及丙二醛（MDA）显著升高。稳态模型评估的胰岛素抵抗（HOMA-IR）在NP+F组和P+F组均显示出明显受损。与NP+F组相比，P+F组的血浆和肾脏G6PDH依赖性抗氧化指数、腺苷受到更大抑制，LDH、MDA加重（p < 0.05）。醋酸钠可降低NP+F组和P+F组的血浆和肾脏替代氧化应激标志物，改善G6PD依赖性抗氧化指数及HOMA-IR。妊娠会加剧果糖诱导的胰岛素抵抗和肾脏氧化应激，而醋酸盐可改善妊娠和非妊娠大鼠果糖诱导的氧化还原和葡萄糖失调。
