Chronic exercise provides renal-protective effects with upregulation of fatty acid oxidation in the kidney of high fructose-fed rats
Chronic exercise provides renal-protective effects with upregulation of fatty acid oxidation in the kidney of high fructose-fed rats
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DOI：
10.1152/ajprenal.00444.2019
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发表时间：
2020-03-01
影响因子：
4.2
通讯作者：
Ito, Osamu
中科院分区：
文献类型：
--
作者：
Hu, Gaizun;Xu, Lusi;Ito, Osamu
摄入过多果糖会导致代谢综合征和肾脏脂质蓄积，导致肾功能障碍和损害。运动（Ex）可以改善脂质调节，但肾脏的机制尚不清楚。在本研究中，雄性 Sprague-Dawley 大鼠被分配到对照组或高果糖 (HFr) 饮食组。每组部分大鼠接受有氧跑步机Ex训练12周。在最后 4 周内对 HFr 饮食喂养的大鼠进行非诺贝特灌胃的药物治疗。肾功能、组织学变化。并评估了参与脂肪酸（FA）代谢的调节因子的表达。在 CON 饮食喂养组中，Ex 不影响肾功能或组织学，并且显着增加 FA β 氧化调节剂的肾表达，包括酰基辅酶 A 脱氢酶 (CAD)、酰基辅酶 A 氧化酶、过氧化物酶体增殖物激活受体 (PPAR)-α 和 PPAR-γ 共激活剂 (PGC)-1 α 以及脂肪生成因子，包括乙酰辅酶 A 羧化酶 (ACC α)、FA 合酶(FAS) 和甾醇调节元件结合蛋白 1c。 HFr 引起蛋白尿、脂质蓄积和肾脏病理组织学变化，Ex 可以减弱这些变化，但非诺贝特则不能。 HFr 降低了中链和短链 CAD 和 PPAR-α 的肾脏表达，并增加了 ACC α、FAS 和甾醇调节元件结合蛋白 1c 的肾脏表达。 Ex 增加了 CAD 的表达。 HFr 饮食喂养的大鼠中，I 型肉碱棕榈酰转移酶、酰基辅酶 A 氧化酶、PPAR-α 和 PGC-1 α 以及 ACC α 和 FAS 的肾表达降低。 Ex 诱导的 FA 代谢改变与非诺铅矿治疗组相似。总之，本研究表明 Ex 增强了肾脏 FA 代谢，这可能在脂质失调疾病中保护肾脏。
Excessive fructose intake causes metabolic syndrome and lipid accumulation in the kidney and leads to renal dysfunction and damage. Exercise (Ex) improves lipids regulation, but the mechanisms are unclarified in the kidney. In the present study, male Sprague-Dawley rats were allocated to groups fed with control or high-fructose (HFr) diet. Part of rats in each group underwent aerobic treadmill Ex for 12 wk. Drug treatment was performed as the fenofibrate gavage during the last 4 wk on HFr diet-fed rats. Renal function, histological changes. and expression of regulators involved in fatty acid (FA) metabolism were assessed. In CON diet-fed groups, Ex did not affect renal function or histology and significantly increased renal expression of FA beta-oxidation regulators including acyl-CoA dehydrogenases (CADs), acyl-CoA oxidase, peroxisome proliferator-activated receptor (PPAR)-alpha, and PPAR-gamma coactivator (PGC)-1 alpha and lipogenic factors including acetyl-CoA carboxylase (ACC alpha), FA synthase (FAS), and sterol regulatory element-binding protein 1c. HFr caused albuminuria, lipid accumulation, and renal pathohistological changes, which were attenuated by Ex but not by fenofibrate. HFr decreased renal expression of medium- and shortchain CADs and PPAR-alpha and increased renal expression of ACC alpha, FAS, and sterol regulatory element-binding protein 1c. Ex increased expression of CADs. carnitine palmitoyltransferase type I, acyl-CoA oxidase, PPAR-alpha, and PGC-1 alpha and decreased renal expression of ACC alpha and FAS in HFr diet-fed rats. The Ex-induced FA metabolism alteration was similar to that in the fenolibnite-treated group. In conclusion, the present study indicates that Ex enhanced renal FA metabolism, which might protect the kidney in lipid dysregulation diseases.