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1,25-dihydroxyvitamin D3 modulation of adipocyte glucocorticoid function
Kristin L Morris1, Michael B Zemel
1Department of Nutrition, University of Tennessee, Room 229, Jessie Harris Building, 1215 West Cumberland Avenue, Knoxville, TN 37996, USA.
Obesity Research
|May 18, 2005
Summary
1,25-dihydroxyvitamin D3 regulates local cortisol production in fat cells by increasing 11beta-HSD 1 expression. This finding may explain how high-calcium diets reduce visceral fat and adiposity.
Area of Science:
- Endocrinology
- Metabolic Research
Background:
- 1,25-dihydroxyvitamin D3 increases intracellular calcium in human adipocytes.
- Dietary calcium influences 1,25-dihydroxyvitamin D3 levels, impacting adiposity and fat distribution.
- Adipocyte glucocorticoid metabolism, particularly cortisol production via 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD 1), is linked to visceral adiposity.
Purpose of the Study:
- To investigate the role of 1,25-dihydroxyvitamin D3 in modulating adipocyte glucocorticoid metabolism.
- To determine if 1,25-dihydroxyvitamin D3 affects the expression of 11beta-HSD 1 in human adipocytes.
Main Methods:
- Human adipocytes were treated with 1,25-dihydroxyvitamin D3 or angiotensin II.
- Cortisol production was measured in the presence of cortisone (substrate).
- Gene expression of 11beta-HSD 1, angiotensin II receptor type 1 (AT1), and AT2 receptor was analyzed using real-time RT-PCR.
Main Results:
- 1,25-dihydroxyvitamin D3 significantly augmented cortisol production in a dose-dependent manner (2- to 6-fold).
- 1,25-dihydroxyvitamin D3 increased 11beta-HSD 1 expression up to 2-fold.
- 1,25-dihydroxyvitamin D3 decreased AT1 expression by 30% to 50%.
Conclusions:
- 1,25-dihydroxyvitamin D3 directly regulates 11beta-HSD 1 expression in adipocytes.
- This regulation influences local cortisol levels within adipose tissue.
- The findings suggest a mechanism by which high-calcium diets may promote preferential loss of visceral fat.