Divisions of Lipid Biochemistry, ICMR-National Institute of Nutrition, Hyderabad, Telangana, India.
Divisions of Pathology, ICMR-National Institute of Nutrition, Hyderabad, Telangana, India.
Indian J Med Res. 2019 Dec;150(6):620-629. doi: 10.4103/ijmr.IJMR_1574_17.
BACKGROUND & OBJECTIVES: Stearoyl-CoA desaturase 1 (SCD1) is a key lipogenic enzyme responsible for endogenous synthesis of monounsaturated fatty acids (MUFA) and plays a key role in various pathophysiology, including fatty liver diseases. In this experimental study the impact of vitamin A deficiency was assessed on SCD1 regulation in relation to kidney biology, under high fructose (HFr) diet-fed condition in rats.
Forty male weanling (21 day old) Wistar rats were divided into four groups control, vitamin A-deficient (VAD), HFr, VAD with HFr consisting of eight rats each, except 16 for the VAD group. The groups received one of the following diets: control, VAD, HFr and VAD with HFr for 16 wk, except half of the VAD diet-fed rats were shifted to HFr diet, after eight week period.
Feeding of VAD diet (alone or with HFr) significantly reduced the kidney retinol (0.51, 0.44 μg/g vs. 2.1 μg/g; P < 0.05), while increased oleic (C18:1) and total MUFA levels (23.3, 22.2% and 27.3, 25.4% respectively vs. 14.7 and 16.6%; P < 0.05) without affecting the SCD1, both at protein and mRNA levels, when compared with HFr. Comparable, immunohistological staining for SCD1 was observed in the distal convoluted tubules. Despite an increase in MUFA, morphology, triglyceride content and markers of kidney function were not affected by VAD diet feeding.
INTERPRETATION & CONCLUSIONS: Feeding of VAD diet either alone or under HFr condition increased the kidney oleic acid (C18:1) levels and thus total MUFA, which corroborated with elevated SCD1 activity index, without affecting its expression status. However, these changes did not alter the kidney morphology and function. Thus, nutrient-gene regulation in kidney biology seems to be divergent.
硬脂酰辅酶 A 去饱和酶 1（SCD1）是一种关键的脂肪生成酶，负责内源性合成单不饱和脂肪酸（MUFA），并在各种病理生理学中发挥关键作用，包括脂肪肝疾病。在这项实验研究中，评估了维生素 A 缺乏对 SCD1 调节的影响，这与高脂肪果糖（HFr）饮食喂养条件下大鼠的肾脏生物学有关。
40 只雄性断奶（21 天大）Wistar 大鼠分为四组：对照组、维生素 A 缺乏组（VAD）、HFr 组和 VAD 加 HFr 组，每组 8 只，除了 VAD 组有 16 只。这些组接受以下饮食中的一种：对照组、VAD、HFr 和 VAD 加 HFr，共 16 周，除了一半的 VAD 饮食喂养的大鼠在 8 周后转换为 HFr 饮食。
单独或与 HFr 一起喂养 VAD 饮食（0.51、0.44 μg/g 与 2.1 μg/g；P < 0.05）显著降低了肾脏视黄醇水平，而增加了油酸（C18:1）和总 MUFA 水平（23.3、22.2%和 27.3、25.4%，分别与 14.7 和 16.6%；P < 0.05），而 SCD1 蛋白和 mRNA 水平均不受影响。类似地，在远曲小管中观察到 SCD1 的免疫组织化学染色。尽管 MUFA 增加，但 VAD 饮食喂养并未影响肾脏形态、甘油三酯含量和肾功能标志物。
单独或在 HFr 条件下喂养 VAD 饮食会增加肾脏油酸（C18:1）水平，从而增加总 MUFA，这与 SCD1 活性指数升高相符，而不影响其表达状态。然而，这些变化并未改变肾脏形态和功能。因此，肾脏生物学中的营养-基因调节似乎存在分歧。
