PMID- 27325245 OWN - NLM STAT- MEDLINE DCOM- 20170517 LR - 20180614 IS - 1479-6805 (Electronic) IS - 0022-0795 (Linking) VI - 230 IP - 2 DP - 2016 Aug TI - Calcium reduces vitamin D and glucocorticoid receptors in the visceral fat of obese male rats. PG - 263-74 LID - 10.1530/JOE-16-0041 [doi] AB - Rats overfed during lactation show higher visceral adipose tissue (VAT) mass and metabolic dysfunctions at adulthood. As both vitamin D and glucocorticoids change adipogenesis, parameters related to metabolism and action of these hormones in the adipocyte can be altered in rats raised in small litters (SL). We also studied the antiobesity effects of high calcium diet since it decreases visceral fat in obesity models. On postnatal day (PN) 3, litter size was adjusted to 3pups/dam (SL) to induce overfeeding. Control litters (NL) remained with 10pups/dam until weaning. From PN120 to PN180, half of the SL rats were fed standard chow (SL) and the other half was fed a calcium-supplemented chow (SL-Ca, 10g CaCO3/kg). Both SL groups were heavier and hyperphagic when compared with the NL group; however, SL-Ca rats ate less than SL. SL-Ca rats had decreased VAT mass and adipocyte size, associated with lower hypothalamic NPY content, VAT fat acid synthase content and leptinemia. At PN120, SL rats had increased plasma 25(OH)D3, Cyp27b1 mRNA and glucocorticoid receptor (GR-alpha) in the VAT, but lower vitamin D receptor (Vdr) mRNA. At PN180, Cyp27b1 and GR-alpha remained higher, while Vdr normalized in SL rats. SL-Ca rats had normal VAT Cyp27b1 and GR-alpha, but lower Vdr Thus, higher body mass and glucocorticoid receptors in the VAT of SL rats are normalized by calcium-enriched diet, and Vdr expression in this tissue is reduced, suggesting a possible role of glucocorticoids and vitamin D in calcium action in the adipocyte. CI - (c) 2016 Society for Endocrinology. FAU - Conceicao, E P S AU - Conceicao EP AD - Laboratory of Endocrine PhysiologyDepartment of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, Brazil. FAU - Moura, E G AU - Moura EG AD - Laboratory of Endocrine PhysiologyDepartment of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, Brazil. FAU - Manhaes, A C AU - Manhaes AC AD - Laboratory of NeurophysiologyDepartment of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, Brazil. FAU - Carvalho, J C AU - Carvalho JC AD - Laboratory of Endocrine PhysiologyDepartment of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, Brazil. FAU - Nobre, J L AU - Nobre JL AD - Laboratory of Endocrine PhysiologyDepartment of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, Brazil. FAU - Oliveira, E AU - Oliveira E AD - Laboratory of Endocrine PhysiologyDepartment of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, Brazil. FAU - Lisboa, P C AU - Lisboa PC AD - Laboratory of Endocrine PhysiologyDepartment of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, Brazil pclisboa@uerj.br. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20160620 PL - England TA - J Endocrinol JT - The Journal of endocrinology JID - 0375363 RN - 0 (Receptors, Glucocorticoid) RN - 1406-16-2 (Vitamin D) RN - SY7Q814VUP (Calcium) SB - IM MH - Animals MH - Calcium/pharmacology/*therapeutic use MH - Dietary Supplements MH - Disease Models, Animal MH - Intra-Abdominal Fat/*drug effects/metabolism MH - Male MH - Obesity/etiology/metabolism/*prevention & control MH - Rats, Wistar MH - Receptors, Glucocorticoid/*metabolism MH - Vitamin D/*metabolism OTO - NOTNLM OT - NPY OT - calcium supplementation OT - corticosterone OT - overnutrition OT - vitamin D3 EDAT- 2016/06/22 06:00 MHDA- 2017/05/18 06:00 CRDT- 2016/06/22 06:00 PHST- 2016/05/26 00:00 [received] PHST- 2016/06/20 00:00 [accepted] PHST- 2016/06/22 06:00 [entrez] PHST- 2016/06/22 06:00 [pubmed] PHST- 2017/05/18 06:00 [medline] AID - JOE-16-0041 [pii] AID - 10.1530/JOE-16-0041 [doi] PST - ppublish SO - J Endocrinol. 2016 Aug;230(2):263-74. doi: 10.1530/JOE-16-0041. Epub 2016 Jun 20.