Aims: Chronic inflammation is linked to type 2 diabetes (T2DM), so we investigated correlations between obesity, blood glucose levels, and inflammation in T2DM patients.
Methods: Peripheral blood mononuclear cells (PBMCs) were collected from 40 T2DM patients (27 men, 13 women; mean age 49.63 years), and 10 non-diabetic controls (all men; mean age 38.60 years). Inflammation was measured as DNA-binding activity of nuclear factor kappaB (NF-kappaB), a key transcription factor in inflammation. Protein levels of NF-kappaB subunit p65, and NF-kappaB inhibitor IkappaBalpha were assessed by Western blot. Transcript levels for p65, IkappaBalpha, and the NF-kappaB target genes TNF-alpha, MMP-9, IL-6, IL-8, and IL-18 were measured by real-time PCR. Body mass index (BMI) and glycohemoglobin were measured for all the subjects.
Results: NF-kappaB DNA-binding activity, p65 and IkappaBalpha protein levels, and expression of IL-6, TNFalpha and MMP-9 were significantly higher in PBMCs from T2DM patients, than from non-diabetic controls. NF-kappaB binding was significantly positively associated with both BMI and homeostasis model assessment of insulin resistance (HOMA-IR).
Conclusions: Inflammation was observed in PBMCs in T2DM patients in a Chinese population, and correlated independently with obesity and blood glucose levels. Lack of correlation with glycohemoglobin suggested that moderate-term blood glucose control did not mitigate inflammation.