HOPE Cardiometabolic Research Team & Department of Physiology, Faculty of Basic Medical Sciences, University of Ilorin, Ilorin, Nigeria.
HOPE Cardiometabolic Research Team & Department of Physiology, Faculty of Basic Medical Sciences, University of Ilorin, Ilorin, Nigeria; Department of Physiology, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria.
Environ Toxicol Pharmacol. 2020 Nov;80:103452. doi: 10.1016/j.etap.2020.103452. Epub 2020 Jun 28.
High fructose intake has been associated with perturbed lipid, uric acid and lactate homeostasis. However, consumption of fructose-sweetened beverages is not usually regulated during pregnancy. The effect of short-chain fatty acid (acetate) on the metabolic effects of high fructose intake during pregnancy is not known. We hypothesized that acetate prevents gestational fructose-induced hepatic triglyceride (TG) accumulation by suppressing uric acid and lactate production. Pregnant Wistar rats were randomly separated into three groups (n = 6/group) receiving drinking water (CON), 10 % (w/v) fructose drink (FRU) and 10 % (w/v) fructose with 200 mg/kg (w/w; p.o.) sodium acetate (FRU + ACE) daily for nineteen days. Fructose intake resulted in increased body weight gain, liver weight, fluid intake, visceral fat, insulin resistance, fasting blood glucose, insulin, plasma and hepatic TG, total cholesterol, free fatty acid, lipid peroxidation, adenosine deaminase, xanthine oxidase, uric acid, lactate, lactate dehydrogenase, and liver injury marker enzymes. However, gestational high fructose intake led to depressed plasma and hepatic glucose-6-phosphate dehydrogenase (G6PD)-dependent antioxidant barrier, adenosine and food intake. All these effects except water intake and food intake were abated by sodium acetate. These results demonstrate that maternal fructose-enriched drink would cause hepatic TG accumulation that is associated with perturbed glucose, uric acid, lactate homeostasis, and G6PD-dependent antioxidant barrier. These results also demonstrate that acetate protects the liver against gestational fructose-induced TG accumulation by inhibiting uric acid and lactate production. Thus, acetate may be useful in the treatment of hyperuricemia- and hyperlactatemia-related disorders.
高果糖摄入与脂质、尿酸和乳酸稳态失调有关。然而，在怀孕期间，通常不会对果糖甜味饮料的摄入量进行调节。短链脂肪酸（醋酸盐）对怀孕期间高果糖摄入的代谢影响尚不清楚。我们假设醋酸盐通过抑制尿酸和乳酸的产生来防止妊娠果糖诱导的肝甘油三酯（TG）积累。将怀孕的 Wistar 大鼠随机分为三组（每组 n = 6），分别给予饮用水（CON）、10%（w/v）果糖饮料（FRU）和 10%（w/v）果糖加 200 mg/kg（w/w；口服）醋酸钠（FRU + ACE），共 19 天。果糖摄入导致体重增加、肝重、液体摄入、内脏脂肪、胰岛素抵抗、空腹血糖、胰岛素、血浆和肝 TG、总胆固醇、游离脂肪酸、脂质过氧化、腺苷脱氨酶、黄嘌呤氧化酶、尿酸、乳酸、乳酸脱氢酶和肝损伤标志物酶增加。然而，妊娠高果糖摄入导致血浆和肝葡萄糖-6-磷酸脱氢酶（G6PD）依赖性抗氧化屏障、腺苷和食物摄入降低。除了水摄入和食物摄入外，醋酸钠减轻了所有这些影响。这些结果表明，母体富含果糖的饮料会导致肝 TG 积累，这与葡萄糖、尿酸、乳酸稳态失调和 G6PD 依赖性抗氧化屏障有关。这些结果还表明，醋酸盐通过抑制尿酸和乳酸的产生来保护肝脏免受妊娠果糖引起的 TG 积累。因此，醋酸盐可用于治疗高尿酸血症和高乳酸血症相关疾病。
