Abstract

Bacterial lipopolysaccharides (LPS), potent inducers of inflammation, have been associated with chronic metabolic disturbances. Obesity is linked to dyslipidemia, increased body adiposity, and endotoxemia. We investigated the cross-sectional relationships between serum LPS activity and body adiposity as well as inflammation in 242 subjects with type 1 diabetes. Body fat distribution was measured by DXA and serum LPS activity by the limulus amebocyte lysate end-point assay. Since no interaction between visceral fat mass and sex was observed, data were pooled for the subsequent analyses. LPS was independently associated with visceral fat mass, when adjusted for traditional risk factors (age, sex, kidney status, hsCRP, insulin sensitivity). In the multivariate analysis, serum LPS activity and triglyceride concentrations had a joint effect on visceral fat mass, independent of these factors alone. A combination of high LPS and high hsCRP concentrations was also observed in those with the largest visceral fat mass. In conclusion, high serum LPS activity levels were associated with visceral fat mass in subjects with type 1 diabetes strengthening its role in the development of central obesity, inflammation and insulin resistance.

Highlights

  • Bacterial lipopolysaccharides (LPS), potent inducers of inflammation, have been associated with chronic metabolic disturbances

  • Endotoxins are redistributed towards VLDL and LDL particles especially in conditions of lower HDL cholesterol concentrations, like in atherosclerosis and insulin resistance[1,2]

  • Toll-like receptor 4 (TLR4) expression is up-regulated in the adipose tissue of obese subjects[3]

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Summary

Introduction

Bacterial lipopolysaccharides (LPS), potent inducers of inflammation, have been associated with chronic metabolic disturbances. We investigated the cross-sectional relationships between serum LPS activity and body adiposity as well as inflammation in 242 subjects with type 1 diabetes. High serum LPS activity levels were associated with visceral fat mass in subjects with type 1 diabetes strengthening its role in the development of central obesity, inflammation and insulin resistance. A low dose LPS infusion induces insulin resistance and potentiates the expression of inflammatory markers in adipose tissue[5]. Studies in non-diabetic children and obese adults, have shown an adverse association between endotoxin levels, central adiposity and insulin resistance[6,7]. Our aim was to investigate the association between serum LPS activity and visceral fat mass, measured by dual-energy x-ray absorptiometry (DXA), in subjects with type 1 diabetes

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