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Vitamin K for Diabetes Prevention

 

    Impaired insulin sensitivity and glucose intolerance play a major role in the development of diabetic pathophysiology. Vitamin K is well known for its function in blood coagulation. The beneficial role of vitamin K supplementation in improving insulin sensitivity and glucose tolerance, preventing insulin resistance, and reducing the risk of type 2 diabetes had been reported (1).

   

    Vitamin K is a fat-soluble vitamin occurring in two forms: phylloquinone and menaquinones. Phylloquinone (vitamin K1), the most common form, is present in green, leafy vegetables and certain vegetable oils, such as soybean, cottonseed, canola, and olive oils. Menaquinones (vitamin K2) occur in animal products such as meat, eggs, and cheese (2).

 

    Dietary intake data from a prospective study in 38,094 Dutch men and women 20-70 years of age were analyzed to investigate whether dietary vitamin K intake was related to the risk of type 2 diabetes. During 10.3 years of follow-up, 918 cases of diabetes were documented. Vitamin K1 intake tended to be associated (p=0.08) with a reduced risk of type 2 diabetes with a 19% reduced risk for the highest quartile vs the lowest quartile of dietary intake levels. For vitamin K2, there was a significant lowered 7% risk of type 2 diabetes with each 10 microgram increment in dietary intake. In this study population, the vitamin K1 intake was 200 ± 98 micrograms per day and vitamin K2 intake was 31± 7 micrograms per day. Vegetables contributed 78% of vitamin K1 intake, whereas cheese contributed 53%, milk products 19%, and meat 17% of vitamin K2 intake. This study showed that both vitamin K1 and K2 intakes were associated with a reduced risk of type 2 diabetes (3).

 

    A study in 2719 American men and women (1247 men and 1472 women) 26-81 years of age reported that the vitamin K1 dietary intake ranged from 10 to 1975 micrograms per day in that population (4). People in the highest vitamin K1 intake quintile were more likely to be women than men, to use multivitamin supplements and were less likely to be current smokers. This study found that higher vitamin K1 intake was associated with greater insulin sensitivity, as measured by 2-hour post Oral Glucose Tolerance Test (OGTT: a standard 75-g oral glucose load test after an overnight fast), insulin and insulin sensitivity index (ISI at 0, 2 hour), and better glycemic status by 2-hour post-OGTT glucose concentrations. The ISI reflects peripheral insulin resistance, glucose disposal and β-cell response to an energy load. It is a complex assessment of insulin sensitivity that accounts for the β-cell response to glucose loading, peripheral and hepatic insulin sensitivity, and glucose disposal (4). 

 

    These population studies suggested that high vitamin K intake might have a beneficial effect on glucose homeostasis, or it could be a potential surrogate marker for a healthy dietary pattern, as characterized by higher intakes of fruit, vegetables, fish, dietary fiber, and lower intakes of saturated fat. Since green leafy vegetables are also rich in other components (e.g. dietary fiber and potassium) which have been reported to improve insulin sensitivity, vitamin K1 intake may be tracking components in green leafy vegetables that may be beneficial to insulin sensitivity and glycemic status.

 

    Whether Vitamin K supplementation can improve insulin sensitivity and glycemic status or not was tested in human studies. In a randomized, double-blind controlled study, older nondiabetic men and women (n=355; aged 60–80 years; 60% women) were given vitamin K1 supplementation at 500 micrograms per day. After 3 years of daily supplementation of vitamin K1, insulin sensitivity was significantly improved in older non-diabetic men with insulin 0.49 microU/ml lowered in the vitamin K-supplemented group from their baseline level (5).   

 

    Women with prediabetes were randomized to consume vitamin K1 supplement 1000 microgram per day (n=39) or placebo (n=43) for 4 weeks. Glycemic status was assessed using OGTT. The vitamin K1 treated group had significantly lowered glucose and insulin levels at 2-hour post-OGTTs than those of the control group. Compared the values from the end of 4-week treatment to those of the baseline, the placebo group had increased glucose and insulin levels at 2-hour post-OGTT with 1.2% and 5.9%, respectively, whereas the vitamin K1-supplemented group had decreased glucose and insulin levels at 2-hour post-OGTT with 10.9% and 17.5%, respectively. This study demonstrated that vitamin K1 supplementation at 1000 micrograms per day improved glycemic status in women with pre-diabetes (6).

   

    As demonstrated by these studies, supplement vitamin K1 could improve insulin sensitivity and glycemic status. Leafy green vegetables contain many nutritional factors including vitamin K. Eating more leafy greens is a good dietary strategy for diabetes prevention.

References:

  1. Manna PKalita J. Beneficial role of vitamin K supplementation on insulin sensitivity, glucose metabolism, and the reduced risk of type 2 diabetes: A review. Nutrition. 2016. 32(7-8):732-9.

  2. Booth SLSuttie JW. Dietary intake and adequacy of vitamin K. J Nutr. 1998. 128(5):785-8.

  3. Beulens JWvan der A DLGrobbee DESluijs ISpijkerman AMvan der Schouw YT. Dietary phylloquinone and menaquinones intakes and risk of type 2 diabetes. Diabetes Care. 2010. 33(8):1699-705.

  4. Yoshida MBooth SLMeigs JBSaltzman EJacques PF. Phylloquinone intake, insulin sensitivity, and glycemic status in men and women. Am J Clin Nutr. 2008. 88(1):210-5.

  5. Yoshida MJacques PFMeigs JBSaltzman EShea MKGundberg CDawson-Hughes BDallal GBooth SL. Effect of vitamin K supplementation on insulin resistance in older men and women. Diabetes Care. 2008. 31(11):2092-6.

  6. Rasekhi HKarandish MJalali MTMohammadshahi MZarei MSaki AShahbazian H. Phylloquinone supplementation improves glycemic status independent of the effects of adiponectin levels in premenopausal women with prediabetes: a double-blind randomized controlled clinical trial. J Diabetes Metab Disord. 2015. 201(1):1

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