One previous study reported that patients with asthma rarely developed diabetes mellitus. Recently, a Science paper has reported in an animal study that helminth-induced adipose tissue eosinophilia enhanced glucose tolerance. It was hypothesized that eosinophil might take an active part in the pathogenesis of T2D. In the present study, we investigated the association of peripheral eosinophil percentage with T2D, impaired glucose regulation and insulin resistance in a community-based Chinese population. To the best of our knowledge, this is the first report on the association between peripheral eosinophil percentage and impaired glucose metabolism and insulin resistance in a large population. We found that high eosinophil percentage associated with a decreased risk of T2D and IGR, and lower risk of insulin resistance in NGT participants. A meta-analysis about WBC count and T2D showed that total WBC count was significantly associated with T2D, even WBC count in the normal range. Vozarova B et al found that a high WBC count was associated with a decline in insulin sensitivity. In the present study, we used the factorial design to do the analysis of variance and the result showed no interaction between WBC and eosinophil percentage on insulin resistance. Our findings are in line with several previous experimental studies that showed a relationship between diabetes and eosinophil. High risk of diabetes was associated with decreased allergic inflammation which can be reflected by eosinophil. It has been found that antigen-evoked eosinophil AbMole Aristolochic-acid-A accumulation in pleural appeared significantly reduced in rats rendered diabetic 72 hr after alloxan. In our study, we also found that eosinophil percentage in T2D was significantly lower than those with NGT or IGR. However, Kim et al found that with the accumulation of the total WBC count and differential WBC counts, the frequencies of diabetes, hypertension, obesity, dyslipidemia and metabolic syndrome increased in a Korea population. Gulcan E et al evaluated the glucose tolerance status in patients with asthma bronchiale and suggested that disturbance of the glucose metabolism may occur in asthmatic patients and that the risk of diabetes mellitus may increase in these individuals. Our results are not consistent with those of the two studies. The possibility may be the different study design and compositions of study subjects. Our study is based on general population in the community, whereas Kim enrolled participants who came for medical check-up and Gulcan E included asthmatic patients. The pre-existing factors involved in asthma pathogenesis may influence the association of glucose metabolism with eosinophil. The mechanism of the relationship between eosinophil percentage and glucose metabolism has not been clarified. Some studies explained that decreased insulin level inhibited the recruitment of eosinophil. However, we found that fasting serum insulin was significantly higher in T2D than those without T2D.
There may be other mechanism for the decreased eosinophil in T2D
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