menatetrenone and Weight-Gain

Osteoporosis is a common complication of anorexia nervosa (AN). Although weight recovery and resumption of menses are important goals in AN treatment, they are often achieved only after a prolonged period of recovery. Therefore, it becomes important to find therapies with the potential to prevent further decreases in bone mineral density (BMD). We conducted a non-randomized study of the effects of menatetrenone (vitamin K2) on bone loss in patients with AN. Lumbar BMD was longitudinally measured by Dual Energy X-ray Absorptiometry (DXA) in 10 patients with AN who chose to receive menatetrenone treatment (MED+ group) and 11 patients who did not (MED- group). During the mean 0.9-year follow-up period, the BMD of the lumbar vertebrae of the MED+ group decreased significantly less than that of the MED- group (-2.8% and -6.9%, respectively). Among bone metabolism markers, gamma-carboxyglutamic acid osteocalcin significantly increased (128.6% and 28.3%, respectively) and urine deoxypyridinoline significantly decreased (-44.5% and -13.7%, respectively) more in the MED+ group than in the MED- group. These differences in BMD and bone metabolism markers may be attributable to menatetrenone treatment. The results suggest that menatetrenone may be beneficial in the prevention of bone loss in patients with AN. Randomized placebo-controlled studies are needed to confirm these findings.

Topics: Adult; Anorexia Nervosa; Blood Chemical Analysis; Bone Density; Female; Follow-Up Studies; Hemostatics; Humans; Male; Osteoporosis; Urinalysis; Vitamin K 2; Weight Gain

Previous studies have shown that α-tocopherol intake lowers phylloquinone (PK) concentration in some extrahepatic tissues in rats. The study's aim was to clarify the effect of α-tocopherol intake on vitamin K concentration in bone, as well as the physiological action of vitamin K. Male Wistar rats were divided into 4 groups. Over a 3-mo period, the K-free group was fed a vitamin K-free diet with 50 mg RRR-α-tocopherol/kg, the E-free group was fed a diet containing 0.75 mg PK/kg without vitamin E, the control group was fed a diet containing 0.75 mg PK/kg with 50 mg RRR-α-tocopherol/kg, and the E-excess group was fed a diet containing 0.75 mg PK/kg with 500 mg RRR-α-tocopherol/kg. PK concentration in the liver was higher in E-excess rats than in E-free rats, was lower in the tibias of control rats than in those of E-free rats, and was lower in E-excess rats than in control rats. Menaquinone-4 (MK-4) concentration in the liver was higher in E-excess rats than in E-free and control rats. However, MK-4 concentrations in the tibias of E-free, control, and E-excess rats were almost the same. Blood coagulation activity was lower in K-free rats than in the other rats but was not affected by the level of α-tocopherol intake. Additionally, dietary intake of PK and α-tocopherol did not affect uncarboxylated-osteocalcin concentration in the serum, femur density, or expression of the genes related to bone resorption and formation in the femur. These results suggest that α-tocopherol intake decreases PK concentration in bone but does not affect bone metabolism in rats.

Topics: alpha-Tocopherol; Animals; Biomarkers; Bone and Bones; Bone Density; Bone Development; Diet; Dietary Supplements; Energy Metabolism; Gene Expression Regulation, Developmental; Liver; Male; Organ Specificity; Osteocalcin; Rats, Wistar; Specific Pathogen-Free Organisms; Tibia; Vitamin K 1; Vitamin K 2; Vitamin K Deficiency; Vitamin K Deficiency Bleeding; Weight Gain