by Gigi
(Italy)
Hi, Wray!
What do You here think about the follower abstract???
Role of Calcitriol and Cortisol on Human
Adipocyte Proliferation and Oxidative and
Inflammatory Stress: A Microarray Study
Xiaocun Sun
a
Kristin L. Morris
b
Michael B. Zemel
a
a
University of Tennessee, Knoxville, Tenn. and
b
Mead-Johnson Nutritionals, Evansville, Ind. , USA
Abstract
Dietary calcium inhibits adiposity, and a key underlying
mechanism is suppression of calcitriol, which modulates
Ca 2+ signaling and mitochondrial uncoupling in adipocytes.
We demonstrated that calcitriol directly regulates adipocyte
11 -HSD-1 expression and cortisol production in human adipocytes in vitro and dietary calcium inhibits visceral adipose tissue 11 -HSD-1 expression in mice, indicating an interaction of calcitriol and cortisol in obesity. Consequently,
we have evaluated the gene expression profile of human
subcutaneous adipocytes treated with calcitriol and/or cortisone. Data analysis demonstrated significant calcitriol
modulation of gene expression toward inhibition of the adipocyte apoptosis (e.g., VEGF and STC-2) and promotion of
adipocyte proliferation (e.g., IGF-1 and IGF-1R). Calcitriol also
up-regulated oxidative stress and inflammatory genes such
as NOX-4 and TLR-3. The calcitriol/cortisone combination resulted in significant additional up-regulation of 11 -HSD-1
and down-regulation of adiponectin expression, while cortisone exerted little independent effect in the absence of
calcitriol. Overall, calcitriol stimulated a pattern of adipocyte
gene expression which favored adipocyte proliferation, oxidative and inflammatory stress and visceral adiposity, andthese effects were amplified in the presence of cortisone;
however, this conclusion must be tempered by the adipocyte source (subcutaneous) and requires confirmation in visceral adipocytes. Copyright © 2007 S. Karger AG, Basel
Comments for Vitamin D and Visceral Fat
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