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Release of TNF‐α From In Vitro ‐Stimulated Monocytes is Negatively Associated with Serum Levels of Apolipoprotein B in Patients with Type 2 Diabetes
Author(s) -
Zykova S. N.,
Svartberg J.,
Seljelid R.,
Iversen H.,
Lund Å.,
Svistounov D. N.,
Jenssen T. G.
Publication year - 2004
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.0300-9475.2004.01509.x
Subject(s) - endocrinology , medicine , apolipoprotein b , tumor necrosis factor alpha , diabetes mellitus , type 2 diabetes , cytokine , lipopolysaccharide , inflammation , alpha (finance) , immune system , diabetic retinopathy , cholesterol , immunology , construct validity , nursing , patient satisfaction
Impaired course of inflammation is a likely mechanism behind a number of diabetic complications. The present study was undertaken to investigate lipopolysaccharide‐induced production of tumour necrosis factor (TNF)‐α in monocytes from patients with type 2 diabetes and to assess its relationship with diabetes‐associated metabolic abnormalities. Monocytic TNF‐α mRNA production was lower in the diabetic participants compared to their corresponding controls. Diabetic subjects who had been receiving simvastatin treatment had TNF‐α mRNA production similar to that of the healthy participants. The release of TNF‐α from diabetic cells correlated negatively with serum levels of apolipoprotein B (apoB) ( R = −0.755, P = 0.001), total plasma cholesterol ( R = − 0.702, P = 0.002) and the presence of retinopathy ( R = −0.572, P = 0.021). No such associations were found in the control subjects. In a multiple linear regression model, only the level of apoB and diabetes duration demonstrated significant effects on the release of TNF‐α, with apoB alone accounting for 57% of the variation. We conclude that production of TNF‐α mRNA in response to the bacterial stimulant is compromised in poorly controlled type 2 diabetes. Lipid abnormalities are associated with the observed defect. Impaired cytokine production represents a significant defect in the functioning of the immune system and may contribute to aberrations in the course of inflammation in the diabetic state.