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Articles by K Kotani
Total Records ( 2 ) for K Kotani
  A Gugliucci , K Kotani , E Kinugasa , R Hermo , R Caccavello and S. Kimura
  Background

Studies regarding aspirin metabolism can be important in patients with renal failure who have an increased risk of cardiovascular diseases. We undertook this study to assess the aspirin esterase (AE) status in end-stage renal disease (ESRD) patients.

Methods

A total of 42 patients on long-term haemodialysis (HD) with a mean dialysis course of 6.1 y were recruited.

Results

Serum AE levels were 44% lower and cholinesterase (ChE) levels were 22% lower in ESRD patients before dialysis as compared with control subjects (P = 0.0001). A very strong correlation was found between AE and ChE levels. AE levels increased on average 28% after dialysis with adjustments for age, gender, total cholesterol, triglyceride and high-density lipoprotein cholesterol (P = 0.002). In addition, ChE levels were significantly increased (48%) after dialysis (P = 0.0001). Changes in AE activity were significantly and positively correlated with those of ChE (r = 0.427, P = 0.005). When we adjusted for several confounders, we found that the changes in AE activity operated by dialysis are significant independently of age, gender, aspirin (ASA) intake, cholesterol, triglycerides, high-density lipoprotein cholesterol and ChE.

Conclusions

We report that serum AE activity is significantly lower in ESRD and that treatment by HD results in an increase of activity. We confirm that AE is associated with lipid parameters and ChE. Our results show variations in ASA catabolism between the dialysis sessions, suggesting an oscillating pattern in ASA disposal in these patients. The mechanisms for reduced AE activity in uraemia and the effects of HD need further investigation.

  Y Fukatsu , T Noguchi , T Hosooka , T Ogura , K Kotani , T Abe , T Shibakusa , K Inoue , M Sakai , K Tobimatsu , K Inagaki , T Yoshioka , M Matsuo , J Nakae , Y Matsuki , R Hiramatsu , K Kaku , H Okamura , T Fushiki and M. Kasuga
 

Physical exercise ameliorates metabolic disorders such as type 2 diabetes mellitus and obesity, but the molecular basis of these effects remains elusive. In the present study, we found that exercise up-regulates heparin-binding epidermal growth factor-like growth factor (HB-EGF) in skeletal muscle. To address the metabolic consequences of such gain of HB-EGF function, we generated mice that overexpress this protein specifically in muscle. The transgenic animals exhibited a higher respiratory quotient than did wild-type mice during indirect calorimetry, indicative of their selective use of carbohydrate rather than fat as an energy substrate. They also showed substantial increases in glucose tolerance, insulin sensitivity, and glucose uptake by skeletal muscle. These changes were accompanied by increased kinase activity of Akt in skeletal muscle and consequent inhibition of Forkhead box O1-dependent expression of the pyruvate dehydrogenase kinase 4 gene. Furthermore, mice with a high level of transgene expression were largely protected from obesity, hepatic steatosis, and insulin resistance, even when maintained on a high-fat diet. Our results suggest that HB-EGF produced by contracting muscle acts as an insulin sensitizer that facilitates peripheral glucose disposal.

 
 
 
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