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Blood coagulation and metabolic profiles in middle-aged male and female ob/ob mice

Ohkura, Naokia; Oishi, Katsutakab,c; Atsumi, Gen-ichia

Blood Coagulation & Fibrinolysis: July 2015 - Volume 26 - Issue 5 - p 522–526
doi: 10.1097/MBC.0000000000000267
Original Articles

Obese and diabetic states in humans are associated with an increased incidence of thrombotic diseases caused by various coagulation abnormalities. Genetically obese ob/ob mice produce metabolic abnormalities similar to those associated with type 2 diabetes. However, little is known about their coagulation features or sex differences. The present study aimed to determine the effects of obese and diabetic complications on blood coagulation and vascular diseases by exploring correlations between blood coagulation and metabolic profiles in middle-aged male and female ob/ob mice. Plasma levels of plasminogen activator inhibitor 1 (PAI-1) were significantly increased, whereas those that of platelet factor-4 (PF-4) was slightly, but significantly increased in male and female ob/ob mice compared with lean counterparts. Prothrombin time (PT) was significantly shortened in female ob/ob mice and activated partial thrombin time (APTT) significantly differed between male and female ob/ob mice. Plasma levels of antithrombin (AT) were significantly increased in male and female ob/ob mice. None of the other coagulation and fibrinolytic factors examined significantly differed between ob/ob mice and lean counterparts. On the contrary, factors such as body weight and cholesterol levels significantly differed between ob/ob and lean mice, whereas glucose, fructosamine and insulin levels significantly differed only in one sex of each strain. These results provided fundamental information about blood coagulation and metabolic features for exploring the function of altered blood coagulation states in ob/ob mice.

aMolecular Physiology and Pathology, School of Pharma-Sciences, Teikyo University, Tokyo

bBiological Clock Research Group, Biomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Ibaraki

cDepartment of Medical Genome Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Chiba, Japan

Correspondence to Naoki Ohkura, Molecular Physiology and Pathology, School of Pharma-Sciences, Teikyo University, 2-11-1 Kaga, Itabashi, Tokyo 173-8605, Japan Tel: +81 3 3964 8216; fax: +81 3 3964 8226; e-mail: n-ohkura@pharm.teikyo-u.ac.jp

Received 17 September, 2014

Revised 9 December, 2014

Accepted 5 January, 2015

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