Calcitriol and energy metabolism.
Calcitriol, a calcitrophic hormone that can be suppressed by high dietary calcium, favors fatty acid synthesis and inhibits lipolysis via non-genomic modulation of Ca(2+) influx. Calcitriol also suppresses UCP2 expression via the nVDR and thereby increases energy efficiency. Calcitriol exerts a dose-dependent impact on adipocyte apoptosis and regulates adipose tissue fat depot location and expansion by promoting glucocorticoid production and release. Recent data also demonstrate a pivotal role of calcitriol in the modulation of cytokines, with potential roles in energy metabolism in adipocytes, macrophages, and skeletal muscle.
The Department of Nutrition, The University of Tennessee, Knoxville, Tennessee 37996-1920, USA. mzemel@utk.edu
Michael B
MB
Zemel
Xiaocun
X
Sun
D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D002117:Calcitriol / Q000378:metabolism / Q000502:physiology*; D002136:Calcium, Dietary / Q000008:administration & dosage / Q000378:metabolism; D004734:Energy Metabolism / Q000187:drug effects* / Q000502:physiology*; D006801:Humans; D007473:Ion Channels / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D024101:Mitochondrial Proteins / Q000378:metabolism; D009765:Obesity / Q000378:metabolism* / Q000517:prevention & control; D000071246:Uncoupling Protein 2
D002136:Calcium, Dietary; D007473:Ion Channels; D024101:Mitochondrial Proteins; C000604389:UCP2 protein, human; D000071246:Uncoupling Protein 2; D002117:Calcitriol