Vitamin K2alleviates type 2 diabetes in rats by induction of osteocalcin gene expression

• Published in: Nutrition (Burbank, Los Angeles County, Calif.) Vol. 47; p. 33
• Main Authors: Hussein, Atef G, Mohamed, Randa H, Shalaby, Sally M, Dalia M Abd El Motteleb
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier Limited 01.03.2018
• Subjects: Adiponectin; Biocompatibility; Cell growth; Cell proliferation; Cyclin D2; Diabetes; Diabetes mellitus; Diabetes mellitus (non-insulin dependent); Drug dosages; Energy expenditure; Energy metabolism; Fasting; Gene expression; Glucose; Glucose metabolism; Hemoglobin; Insulin; Insulin resistance; Metabolism; Nutrition research; Osteocalcin; Plasma; Polymerase chain reaction; Rats; Rodents; Uncertainty analysis; Vitamin K; Vitamins; United States > US
• ISSN: 0899-9007; 1873-1244
• DOI: 10.1016/j.nut.2017.09.016

ObjectivesThe biological mechanisms behind the association between vitamin K (Vit K) and glucose metabolism are uncertain. We aimed to analyze the expression of insulin 1 (Ins 1), insulin 2 (Ins 2) andcyclin D2, the expression ofadiponectinand UCP-1 . In addition, we aimed to estimate the doses of Vit K2 able to affect various aspects of glucose and energy metabolism in type 2 diabetes.MethodsThirty adult male rats were allocated equally into five groups: control group, diabetes mellitus group, and groups 3, 4, and 5, which received Vit K2at three daily dose levels (10, 15, and 30 mg/kg, respectively) for 8 wk. At the end of the study, blood samples were collected to quantify total osteocalcin, fasting plasma glucose, fasting insulin, and relevant variables. The expression ofOC,Ins 1,Ins 2,cyclin D2,adiponectin,UCP-1genes was analyzed by real-time polymerase chain reaction.ResultsAfter administration of Vit K2, a dose-dependent decrease in fasting plasma glucose, hemoglobin A1c and homeostatic model assessment method insulin resistance, and a dose-dependent increase in fasting insulin and homeostatic model assessment method β cell function levels, when compared with diabetes mellitus rats, were detected. There was significant upregulation ofOC,Ins 1,Ins 2, orcyclin D2gene expression in the three treated groups in a dose-dependent manner when compared with the diabetic rats. However, expression ofadiponectinandUCP-1were significantly increased at the highest dose (30 mg/kg daily) only.ConclusionsVit K2administration could improve glycemic status in type 2 diabetic rats by induction ofOCgene expression. Osteocalcin could increase β-cell proliferation, energy expenditure, andadiponectinexpression. Different concentrations of Vit K2were required to affect glucose metabolism and insulin sensitivity.