Rasekhi Hamid, Karandish Majid, Jalali Mohammad-Taha, Mohammadshahi Majid, Zarei Mehdi, Saki Azadeh, Shahbazian Hajieh
Nutrition and Metabolic Diseases Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Hyperlipidemia Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
J Diabetes Metab Disord. 2015 Jan 14;14(1):1. doi: 10.1186/s40200-014-0127-9. eCollection 2015.
Vitamin K, as a cofactor in the gamma carboxylation of certain glutamic acid (Gla) residues, has been related to glucose metabolism and insulin sensitivity. Osteocalcin, also known as bone γ-carboxyglutamic acid, increases β-cell proliferation as well as insulin and adiponectin secretion, which improve glucose tolerance and insulin sensitivity. Thus, the purpose of the present study was to examine the possible role of adiponectin as a mediator of glucose homeostasis following phylloquinone supplementation in premonopause women with prediabetes.
Eighty two women were randomized to consume vitamin k1 supplement (n = 39) or placebo (n = 43) for four weeks. Participants in vitamin K1 treatment group received one pearl softgel capsule containing 1000 micrograms phylloquinone while the placebo group received one placebo capsules daily for four weeks. The Blood samples were collected at baseline and after a four-week intervention to quantify osteocalcin, adiponectin, leptin and relevant variables.
Phylloquinone supplementation significantly increased serum adiponectin concentration (1.24 ± 1.90 compared with -0.27 ± 1.08 μg/ml), and did not alter total osteocalcin (0.50 ± 4.11 compared with 0.13 ± 1.85 ng/ml) and leptin (-0.29 ± 8.23 compared with -1.15 ± 5.25 ng/ml) compared with placebo. Adjustments for total osteocalcin and adiponectin using analysis of covariance (ANCOVA) did not affect the association of glycemic status with related variables.
In conclusion our study demonstrated that phylloquinone supplementation improved glycemic status in premonopausal prediabetic women independent of adiponectin.
This trial was registered in Iranian Registry of Clinical Trials with ID number of IRCT2013120915724N1.
维生素K作为某些谷氨酸(Gla)残基γ羧化反应中的一种辅助因子,与葡萄糖代谢及胰岛素敏感性有关。骨钙素,也称为骨γ-羧基谷氨酸,可增加β细胞增殖以及胰岛素和脂联素分泌,从而改善葡萄糖耐量和胰岛素敏感性。因此,本研究的目的是探讨在患有糖尿病前期的绝经前女性中补充叶绿醌后脂联素作为葡萄糖稳态调节因子的可能作用。
82名女性被随机分为两组,一组服用维生素K1补充剂(n = 39),另一组服用安慰剂(n = 43),为期四周。维生素K1治疗组的参与者每天服用一粒含1000微克叶绿醌的珍珠软胶囊,而安慰剂组每天服用一粒安慰剂胶囊,持续四周。在基线和四周干预后采集血样,以定量骨钙素、脂联素、瘦素及相关变量。
与安慰剂相比,补充叶绿醌显著提高了血清脂联素浓度(1.24±1.90 vs -0.27±1.08μg/ml),但未改变总骨钙素(0.50±4.11 vs 0.13±1.85ng/ml)和瘦素(-0.29±8.23 vs -1.15±5.25ng/ml)水平。使用协方差分析(ANCOVA)对总骨钙素和脂联素进行校正后,血糖状态与相关变量之间的关联未受影响。
总之,我们的研究表明,在绝经前糖尿病前期女性中,补充叶绿醌可改善血糖状态,且该作用与脂联素无关。
本试验已在伊朗临床试验注册中心注册,注册号为IRCT2013120915724N1。