Impaired glucose tolerance in vitamin D deficiency can be corrected by calcium

被引:24
作者
Ismail, A [1 ]
Namala, R [1 ]
机构
[1] Indian Council Med Res, Natl Inst Nutr, Dept Endocrinol & Metab, Hyderabad 500007, Andhra Pradesh, India
关键词
vitamin D-3; 25-hydroxyvitamin D-3 (25-OH-D-3); glucose tolerance; insulin tolerance; area under the curve (AUC);
D O I
10.1016/S0955-2863(99)00090-X
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Vitamin D-3, via its active metabolite 1 alpha,25-dihydroxyvitamin D-3, helps maintain normal calcium levels in the body Apart from the maintenance of calcium homeostasis, the active form of vitamin D-3 is now known to be involved in a number of other functions including that of pancreatic beta cells. Low serum insulin levels and impaired glucose tolerance in a vitamin D-deficient state have been reported in experimental animals Hypocalcemia is a major consequence of vitamin D deficiency Whether the impairment observed is due to vitamin D deficiency per se or is secondary to low calcium is still a matter of controversy. The present study was conducted to delineate the roles of vitamin D and calcium in glucose intolerance associated with vitamin D deficiency in vivo. It was found that supplementation with either vitamin D-3 or high calcium alone to vitamin D-deficient rats could correct the defects. In addition, insulin sensitivity was found to be enhanced in the vitamin D-deficient group compared with vitamin D control or calcium-supplemented groups. Hence the present study demonstrates that calcium per se in the absence of vitamin D increases insulin secreation and normalizes intolerance to glucose seen in vitamin D deficiency. (C) Elsevier Science Inc. 2000. All rights reserved.
引用
收藏
页码:170 / 175
页数:6
相关论文
共 36 条
[11]   SIMPLIFIED COMPETITIVE-PROTEIN-BINDING ASSAY FOR 25-HYDROXYCALCIFEROL [J].
GARCIAPASCUAL, B ;
PEYTREMANN, A ;
COURVOISIER, B ;
LAWSON, DEM .
CLINICA CHIMICA ACTA, 1976, 68 (02) :99-105
[12]  
GAVIN JR, 1974, P NATL ACAD SCI USA, V71, P84, DOI 10.1073/pnas.71.1.84
[13]  
GIBALDI M, 1982, PHARMACOKINETICS, P1
[14]  
GOLDFINE ID, 1973, BIOCHEM BIOPH RES CO, V53, P852, DOI 10.1016/0006-291X(73)90171-X
[15]   1,25-DIHYDROXYCHOLECALCIFEROL STIMULATES OSTEOCLASTS IN RAT BONES IN THE ABSENCE OF PARATHYROID-HORMONE [J].
HOLTROP, ME ;
COX, KA ;
CLARK, MB ;
HOLICK, MF ;
ANAST, CS .
ENDOCRINOLOGY, 1981, 108 (06) :2293-2301
[16]   DEMONSTRATION THAT THE VITAMIN-D METABOLITE 1,25(OH)2-VITAMIN-D3 AND NOT 24R,25(OH)2-VITAMIN-D3 IS ESSENTIAL FOR NORMAL INSULIN-SECRETION IN THE PERFUSED RAT PANCREAS [J].
KADOWAKI, S ;
NORMAN, AW .
DIABETES, 1985, 34 (04) :315-320
[17]   STUDIES ON THE MODE OF ACTION OF VITAMIN-D .52. DIETARY VITAMIN-D IS ESSENTIAL FOR NORMAL INSULIN-SECRETION FROM THE PERFUSED RAT PANCREAS [J].
KADOWAKI, S ;
NORMAN, AW .
JOURNAL OF CLINICAL INVESTIGATION, 1984, 73 (03) :759-766
[18]  
KAPLAN MM, 1972, GASTROENTEROLOGY, V62, P452
[19]   INCREASED INSULIN ACTION IN RATS WITH MILD INSULIN DEFICIENCY INDUCED BY NEONATAL STREPTOZOTOCIN [J].
KERGOAT, M ;
GUERREMILLO, M ;
LAVAU, M ;
PORTHA, B .
AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 260 (04) :E561-E567
[20]  
Laron Z, 1970, Horm Metab Res, V2, P121