Format

Send to

Choose Destination
Sci Rep. 2016 Dec 13;6:38887. doi: 10.1038/srep38887.

Endotoxins are associated with visceral fat mass in type 1 diabetes.

Lassenius MI1,2,3, Ahola AJ1,2,3, Harjutsalo V1,2,3,4, Forsblom C1,2,3, Groop PH1,2,3,5, Lehto M1,2,3.

Author information

1
Folkhälsan Institute of Genetics, Folkhälsan Research Center, Helsinki, Finland.
2
Abdominal Center Nephrology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.
3
Research Programs Unit, Diabetes and Obesity, University of Helsinki, Helsinki, Finland.
4
National Institute for Health and Welfare, Helsinki, Finland.
5
Baker IDI Heart &Diabetes Institute, Melbourne, Australia.

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.

PMID:
27958332
PMCID:
PMC5153626
DOI:
10.1038/srep38887
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center