Associations of serum 25-hydroxyvitamin D and components of the metabolic syndrome in obese adolescent females.

Associations of serum 25-hydroxyvitamin D and components of the metabolic syndrome in obese adolescent females.
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DOI:
10.1038/oby.2011.110
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发表时间:
2011-11
期刊:
Obesity (Silver Spring, Md.)
影响因子:
--
通讯作者:
McCormick KL
McCormick KL
中科院分区:
其他
文献类型:
--
作者:
Ashraf AP;Alvarez JA;Gower BA;Saenz KH;McCormick KL

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缺乏维生素D可能会增加患代谢综合征的风险。我们测定了肥胖青春期女性血清25-羟基维生素D(25(OH)D)与代谢综合征成分的关系,并评估了维生素D治疗是否纠正了代谢紊乱。对80名绝经后青少年(53名非裔美国人(AA)和27名高加索裔美国人(CA))进行了血压和空腹25(OH)D、血脂、C反应蛋白、丙氨酸氨基转移酶(ALT)和天冬氨酸转氨酶(ALT)的测定,并进行了口服葡萄糖耐量试验。在维生素D治疗后,对维生素D缺乏受试者的亚组(n=14)进行了重新评估。在所有受试者中,25(OH)D与空腹血糖呈负相关(r=LDL0.28,P=0.02),与低密度脂蛋白胆固醇呈正相关(r=0.31,P=0.008),与种族和−无关。在校正体重指数的RACE分析中,25(OH)D与CA的空腹胰岛素呈负相关(r=−0.42,P=0.03),而与AA的空腹胰岛素无关(r=0.11,P=0.43);25(OH)D与AA的ALT呈正相关,但与CA的ALT无关(r=0.29,P=0.04vs.r=−0.21,P=0.32)。维生素D治疗组空腹血糖改善(从89.07±8.3 mg/dl降至84.34±8.4 mg/dl,P=0.05)。在排除了4名血清25(OH)D2在治疗后没有改善的受试者后,空腹血糖仍有改善的趋势(P=0.12)。综上所述,血清25(OH)D与空腹血糖呈负相关,维生素D治疗对空腹血糖有一定的改善作用。25(OH)D与空腹胰岛素和丙氨酸氨基转移酶的关系具有种族特异性。与低密度脂蛋白和丙氨酸氨基转移酶呈正相关,提示维生素D可能有不良影响。
Vitamin D deficiency may increase the risk for metabolic syndrome. We determined the relationship of serum 25-hydroxyvitamin D (25(OH)D) with metabolic syndrome components in obese adolescent females and assessed whether vitamin D treatment corrects metabolic disturbances. Eighty postmenarchal adolescents (53 African American (AA) and 27 Caucasian American (CA)) were evaluated with blood pressures and fasting measurements of serum 25(OH)D, lipid profile, C-reactive protein, alanine transaminases (ALTs) and aspartate transaminases followed by an oral glucose tolerance test. A subgroup (n = 14) of vitamin D deficient subjects were re-evaluated following vitamin D treatment. Among all subjects, 25(OH)D was inversely associated with fasting glucose (r = −0.28, P = 0.02) and positively associated with low-density lipoprotein (LDL) cholesterol (r = 0.31, P = 0.008), independent of race and BMI. In analyses by race, adjusted for BMI, 25(OH)D was inversely associated with fasting insulin in CA (r = −0.42, P = 0.03) but not AA (r = 0.11, P = 0.43) whereas 25(OH)D was positively associated with ALT in AA, but not CA (r = 0.29, P = 0.04 vs. r = −0.21, P = 0.32). Fasting glucose improved in vitamin D treated subgroup (from 89.07 ± 8.3 mg/dl to 84.34 ± 8.4 mg/dl, P = 0.05). A trend toward improvement in fasting glucose remained after exclusion of four subjects whose serum 25(OH)D2 did not improve following treatment (P = 0.12). In conclusion, serum 25(OH)D was inversely associated with fasting glucose, and vitamin D treatment had beneficial effects on fasting glucose. Relationships of 25(OH)D with fasting insulin and ALT were ethnic specific. The positive relationship with LDL and ALT were suggestive of possible adverse influences of vitamin D.
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