Abstract
B lymphocytes are involved in inflammation and are related to insulin resistance in obesity and type 2 diabetes (T2D). This study investigated the phenotype and frequency of B-lymphocyte subsets in subjects recently diagnosed with T2D (n = 60), impaired glucose regulation (IGR, n = 73), and normal glucose tolerance (NGT, n = 169) by flow cytometry. T2D subjects had an increased percentage of CD19+CD23+ (B-2) cells and a decreased percentage of CD19+CD23− (B-1) cells attributing to CD19+CD23−CD5− (B-1b) cells, but not CD19+CD23−CD5+ (B-1a) cells, compared to NGT and IGR subjects. The proportion of CD19+CD5+CD1dhi (B10) cells did not differ between the IGR or T2D group and NGT controls. Of note, HbA1c and triglyceride showed a positive correlation with B-2 cells but an inverse correlation with B-1 and B-1b cells, which were independently associated with the presence of T2D by logistic regression models. In summary, this study shows an unbalanced proinflammatory phenotype of B-cell subsets correlated with glycemia and lipidemia in patients with T2D. Our data provide new insight into chronic activation of the immune system and subclinical inflammation in T2D. Further prospective studies are warranted to confirm our observations.
Highlights
The natural history of diabetes is characterized by a progressive deterioration of glucose metabolism status from euglycemia through prediabetes to type 2 diabetes (T2D) [1]
A fresh fasting venous blood sample was obtained for determination of glycemia, fasting C-peptide (FCP), total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C)
There was a gradual increase in the FPG but a gradual decrease in the HDL-C level from normal glucose tolerance (NGT) controls via individuals with impaired glucose regulation (IGR) to T2D
Summary
The natural history of diabetes is characterized by a progressive deterioration of glucose metabolism status from euglycemia through prediabetes to type 2 diabetes (T2D) [1]. Chronic systemic inflammation is an important link between obesity, insulin resistance, and T2D [4]. Elevated proinflammatory cytokines are linked with decreased insulin sensitivity, while antiinflammatory cytokine expressions are associated with better glucose status [4,5,6,7]. Components of the immune system including macrophages, T cells, neutrophils, and eosinophils have been implicated in adipose tissue inflammation and insulin resistance [8,9,10,11]. Accumulating evidence demonstrated that B lymphocytes are recruited to adipose tissue in diet-induced obese (DIO) mice and facilitate insulin resistance through proinflammatory T cells and production of pathogenic IgG antibodies [14]. B cells support T cell-mediated inflammation in subjects with obesity and T2D [16]
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