• Mooli Raja Gopal Reddy, Manchiryala Sravan Kumar, Vani Acharya, Surekha Mullapudi Venkata, Uday Kumar Putcha, and Shanmugam Murugaiha Jeyakumar.
• Divisions of Lipid Biochemistry, ICMR-National Institute of Nutrition, Hyderabad, Telangana, India.
• Indian J Med Res. 2019 Dec 1; 150 (6): 620-629.

Background & ObjectivesStearoyl-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.MethodsForty 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.ResultsFeeding 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 & ConclusionsFeeding 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.

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