Department of Toxicology, Tianjin Centers for Disease Control and Prevention, No. 6, Huayue Road, Hedong District, Tianjin, China.
Endocr Metab Immune Disord Drug Targets. 2021;21(12):2260-2272. doi: 10.2174/1871530321666210809152555.
The incidence and mortality of hyperlipidemia are increasing year by year, showing a younger trend. At present, the treatment of hyperlipidemia is mainly dependent on western medicine, but its side effects on liver and kidney function are common in clinics. Therefore, it is necessary to study the treatment of hyperlipidemia by augmenting effective dietary nutrition supplements. Vitamin B6 (VitB6), as an essential cofactor for enzymes, participates in lipid metabolism. The effects of VitB6 on hyperlipidemia, however, have not been reported until now.
The present study was to investigate the influence of VitB6 on hepatic lipid metabolism in hyperlipidaemia rats induced by a High-Fat Diet (HFD).
Male Sprague-Dawley rats were kept on HFD for two weeks to establish the hyperlipidemia model. The rats in low-dosage and high-dosage groups were received 2.00 and 3.00 mg/kg/- day of VitB6 for eight weeks, respectively.
The results showed that both doses of VitB6 reduced HFD-induced hepatic Low-Density Lipoprotein Cholesterol (LDL-C); decreased blood cholesterol (TC), triglycerides, LDL-C, atherogenic index (AI), Atherogenic Index of Plasma (AIP), apolipoprotein B (ApoB) and ApoB/apolipoprotein A-1(ApoA1) ratio; increased liver High-Density Lipoprotein Cholesterol (HDL-C) and serum ApoA1; reduced hepatic steatosis and triglyceride accumulation, lowered fat storage, and recovered heart/body and brain/body ratio to a normal level. In addition, VitB6 supplementation markedly decreased HMGR level, increased the mRNA abundance of LDLR and CYP7A1, and protein expression of SIRT1, following the downregulation of SREBP-1 and PPARγ protein expression in the liver of hyperlipidemia rats.
In summary, oral VitB6 supplementation can ameliorate HFD-induced hepatic lipid accumulation and dyslipidemia in SD rats by inhibiting fatty acid and cholesterol synthesis, promoting fatty acid decomposition and cholesterol transport.
高血脂的发病率和死亡率逐年上升，呈年轻化趋势。目前，高血脂的治疗主要依赖于西药，但临床常见对肝肾功能有副作用。因此，有必要研究通过增加有效的膳食营养补充剂来治疗高血脂。维生素 B6（VitB6）作为酶的必需辅助因子，参与脂代谢。然而，目前尚未有关于 VitB6 对高血脂影响的报道。
本研究旨在探讨 VitB6 对高脂饮食（HFD）诱导的高血脂大鼠肝脂代谢的影响。
雄性 Sprague-Dawley 大鼠高脂饮食喂养 2 周建立高血脂模型。低剂量组和高剂量组分别给予 2.00 和 3.00mg/kg/d VitB6 干预 8 周。
结果表明，两种剂量的 VitB6 均降低了 HFD 诱导的肝 LDL-C；降低了血胆固醇（TC）、甘油三酯、LDL-C、致动脉粥样硬化指数（AI）、血浆致动脉粥样硬化指数（AIP）、载脂蛋白 B（ApoB）和 ApoB/载脂蛋白 A-1（ApoA1）比值；增加了肝 HDL-C 和血清 ApoA1；减轻了肝脂肪变性和甘油三酯堆积，降低了脂肪储存，使心体比和脑体比恢复到正常水平。此外，VitB6 补充显著降低了 HMGR 水平，增加了 LDLR 和 CYP7A1 的 mRNA 丰度，下调了 SREBP-1 和 PPARγ 蛋白表达，同时上调了 SIRT1 蛋白表达，改善了高血脂大鼠肝脏中脂质的积累和血脂异常。
综上所述，口服 VitB6 补充剂可通过抑制脂肪酸和胆固醇合成、促进脂肪酸分解和胆固醇转运，改善 HFD 诱导的 SD 大鼠肝脏脂质堆积和血脂异常。
