Publications by authors named "Surekha Mullapudi Venkata"

3 Publications

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Vitamin A deficiency increases the oleic acid (C18:1) levels in the kidney of high fructose diet-fed rats.

Indian J Med Res 2019 12;150(6):620-629

Divisions of Lipid Biochemistry, ICMR-National Institute of Nutrition, Hyderabad, Telangana, India.

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.

Methods: 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.

Results: 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.
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http://dx.doi.org/10.4103/ijmr.IJMR_1574_17DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7038806PMC
December 2019

Vitamin A deficiency suppresses high fructose-induced triglyceride synthesis and elevates resolvin D1 levels.

Biochim Biophys Acta 2016 Mar 18;1861(3):156-65. Epub 2015 Nov 18.

Lipid Biochemistry Division, National Institute of Nutrition, Jamai Osmania, Hyderabad 500007, India. Electronic address:

Background/aims: Vitamin A and its metabolites are known to regulate lipid metabolism. However so far, no study has assessed, whether vitamin A deficiency per se aggravates or attenuates the development of non-alcoholic fatty liver disease (NAFLD). Therefore, here, we tested the impact of vitamin A deficiency on the development of NAFLD.

Methods: Male weanling Wistar rats were fed one of the following diets; control, vitamin A-deficient (VAD), high fructose (HFr) and VAD with HFr (VADHFr) of AIN93G composition, for 16weeks, except half of the VAD diet-fed rats were shifted to HFr diet (VAD(s)HFr), at the end of 8(th) week.

Results: Animals fed on VAD diet with HFr displayed hypotriglyceridemia (33.5mg/dL) with attenuated hepatic triglyceride accumulation (8.2mg/g), compared with HFr diet (89.5mg/dL and 20.6mg/g respectively). These changes could be partly explained by the decreased activity of glycerol 3-phosphate dehydrogenase (GPDH) and the down-regulation of stearoyl CoA desaturase 1 (SCD1), both at gene and protein levels, the key determinants of triglyceride biosynthesis. On the other hand, n-3 long chain polyunsaturated fatty acid, docosahexaenoic acid and its active metabolite; resolvin D1 (RvD1) levels were elevated in the liver and plasma of VAD diet-fed groups, which was negatively associated with triglyceride levels. All these factors confer vitamin A deficiency-mediated protection against the development of hepatic steatosis, which was also evident from the group shifted from VAD to HFr diet.

Conclusions: Vitamin A deficiency attenuates high fructose-induced hepatic steatosis, by regulating triglyceride synthesis, possibly through GPDH, SCD1 and RvD1.
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http://dx.doi.org/10.1016/j.bbalip.2015.11.005DOI Listing
March 2016

Wound healing: a new perspective on glucosylated tetrahydrocurcumin.

Drug Des Devel Ther 2015 13;9:3579-88. Epub 2015 Jul 13.

Ashian Herbex Ltd, Hyderabad, AP, India.

Wound healing represents a dynamic set of coordinated physiological processes observed in response to tissue injury. Several natural products are known to accelerate the process of wound healing. Tetrahydrocurcumin (THC), an in vivo biotransformed product/metabolite of curcumin, is known to exhibit a wide spectrum of biological activities similar to those of native curcuminoids. The poor bioavailability of these curcuminoids limits their clinical applications. The present study highlights the percutaneous absorption and wound healing activity of glucosyl-conjugated THC (glucosyl-THC) in male Wistar rats. A high plasma concentration of glucosyl-THC (4.35 μg/mL) was found in rats 3 hours after application. A significant enhanced wound healing activity and reduced epithelialization time were observed in rats that received glucosyl-THC. This may have been due to the improved bioavailability of the glucosyl compound. The nonstaining and lack of skin-sensitive side effects render the bioconjugated glucosyl-THC a promising therapeutic compound in the management of excision wounds and in cosmetic applications, in the near future.
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http://dx.doi.org/10.2147/DDDT.S85041DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4507491PMC
April 2016
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