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.
Zemel
Michael B
MB
The Department of Nutrition, The University of Tennessee, Knoxville, Tennessee 37996-1920, USA. mzemel@utk.edu
Sun
Xiaocun
X
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