Does 11β-HSD1 Associate with the Development of Visceral Adiposity in Maternal Mg Restricted Wistar/NIN Rat Offspring?Kalashikam Rajender Rao1,2*, Inagadapa Padmavathi2, Lagishetty Venu2,3 and Manchala Raghunath2
- corresponding Author:
- Kalashikam Rajender Rao
National Center for Laboratory Animal sciences
National Institute of Nutrition
Jamai Osmania P O, Hyderabad - 500 007, India
E-mail: [email protected]
Received Date: January 02, 2012; Accepted Date: February 07, 2012; Published Date: February 09, 2012
Citation: Rajender Rao K, Padmavathi I, Venu L, Raghunath M (2012) Does 11β-HSD1 Associate with the Development of Visceral Adiposity in Maternal Mg Restricted Wistar/NIN Rat Offspring? Endocrinol Metabol Syndrome S7:002. doi: 10.4172/2161-1017.S7-002
Copyright: © 2012 Rajender Rao K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Maternal magnesium restriction irreversibly increased body fat %, specially the visceral adiposity in WNIN rat offspring. We have now investigated whether the increased visceral adiposity was associated with increased adipogenesis and glucocorticoid stress. Female, weanling WNIN rats were fed for 12 weeks, a control (AIN 93G) diet (MgC) or the same with 70% restriction of Mg (MgR) and mated with control males. Some of the pregnant MgR dams were rehabilitated from parturition and their pups weaned on to control diet (MgRP). At weaning half of the pups from MgR dams were shifted to control diet (MgRW) while the other half continued on Mg restriction (MgR). mRNA expression for fatty acid synthase (FAS) and 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) was significantly higher in MgR adipose tissue offspring. However leptin mRNA expression was comparable among different groups. Both the rehabilitation regimes corrected the expression of 11β-HSD1 but not that of FAS. Maternal Mg restriction predisposed the offspring to increased glucocorticoid stress (11β-HSD1) that could underlie the increased body fat %/central adiposity.