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
[21]  
MORRISSEY RL, 1975, P SOC EXP BIOL MED, V149, P56
[22]   THE VITAMIN-D ENDOCRINE SYSTEM - STEROID-METABOLISM, HORMONE RECEPTORS, AND BIOLOGICAL RESPONSE (CALCIUM-BINDING PROTEINS) [J].
NORMAN, AW ;
ROTH, J ;
ORCI, L .
ENDOCRINE REVIEWS, 1982, 3 (04) :331-366
[23]   INFLUENCE OF VITAMIN-D STATUS ON INSULIN-SECRETION AND GLUCOSE-TOLERANCE IN THE RABBIT [J].
NYOMBA, BL ;
BOUILLON, R ;
DEMOOR, P .
ENDOCRINOLOGY, 1984, 115 (01) :191-197
[24]   INSULIN RECEPTORS OF SKELETAL-MUSCLE - SPECIFIC INSULIN BINDING-SITES AND DEMONSTRATION OF DECREASED NUMBERS OF SITES IN OBESE RATS [J].
OLEFSKY, J ;
BACON, VC ;
BAUR, S .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1976, 25 (02) :179-191
[25]  
PIKE JW, 1981, J STEROID BIOCHEM, V16, P385
[26]  
RAO KV, 1994, BIOSTATISTICS MANUAL, V2
[27]   PREVENTIVE EFFECT OF BETA-ALANYL-L-HISTIDINATO ZINC ON BONE METABOLISM IN RATS FED ON LOW-CALCIUM AND VITAMIN-D-DEFICIENT DIETS [J].
SEGAWA, Y ;
TSUZUIKE, N ;
TAGASHIRA, E ;
YAMAGUCHI, M .
RESEARCH IN EXPERIMENTAL MEDICINE, 1992, 192 (03) :213-219
[28]  
STANBURY SW, 1980, VITAMIN D MOL BIOL C, V2, P251
[29]   BIOLOGICAL ACTIVITY OF 25-HYDROXYERGOCALCIFEROL IN RATS [J].
SUDA, T ;
DELUCA, HF ;
TANAKA, Y .
JOURNAL OF NUTRITION, 1970, 100 (09) :1049-&
[30]   Development of non-insulin-dependent diabetes mellitus in the double knockout mice with disruption of insulin receptor substrate-1 and beta cell glucokinase genes - Genetic reconstitution of diabetes as a polygenic disease [J].
Terauchi, Y ;
Iwamoto, K ;
Tamemoto, H ;
Komeda, K ;
Ishii, C ;
Kanazawa, Y ;
Asanuma, N ;
Aizawa, T ;
Akanuma, Y ;
Yasuda, K ;
Kodama, T ;
Tobe, K ;
Yazaki, Y ;
Kadowaki, T .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 99 (05) :861-866