CORRELATION BETWEEN GUT MICROBIOTA AND DEVELOPMENT OF GLUCOSE INTOLERANCE IN B6.V-Lepob/J LEPTIN DEFICIENT MICE

Research output: Contribution to conferencePosterResearch

Standard

CORRELATION BETWEEN GUT MICROBIOTA AND DEVELOPMENT OF GLUCOSE INTOLERANCE IN B6.V-Lepob/J LEPTIN DEFICIENT MICE. / Ellekilde, Merete; Hansen, Camilla Hartmann Friis; Nielsen, Dennis Sandris; Hufeldt, Majbritt Ravn; Vogensen, Finn Kvist; Hansen, Axel Jacob Kornerup.

2011. Poster session presented at Nature Mucosal Immunology konference, San Francisco, United States.

Research output: Contribution to conferencePosterResearch

Harvard

Ellekilde, M, Hansen, CHF, Nielsen, DS, Hufeldt, MR, Vogensen, FK & Hansen, AJK 2011, 'CORRELATION BETWEEN GUT MICROBIOTA AND DEVELOPMENT OF GLUCOSE INTOLERANCE IN B6.V-Lepob/J LEPTIN DEFICIENT MICE', Nature Mucosal Immunology konference, San Francisco, United States, 14/04/2011 - 16/04/2011.

APA

Ellekilde, M., Hansen, C. H. F., Nielsen, D. S., Hufeldt, M. R., Vogensen, F. K., & Hansen, A. J. K. (2011). CORRELATION BETWEEN GUT MICROBIOTA AND DEVELOPMENT OF GLUCOSE INTOLERANCE IN B6.V-Lepob/J LEPTIN DEFICIENT MICE. Poster session presented at Nature Mucosal Immunology konference, San Francisco, United States.

Vancouver

Ellekilde M, Hansen CHF, Nielsen DS, Hufeldt MR, Vogensen FK, Hansen AJK. CORRELATION BETWEEN GUT MICROBIOTA AND DEVELOPMENT OF GLUCOSE INTOLERANCE IN B6.V-Lepob/J LEPTIN DEFICIENT MICE. 2011. Poster session presented at Nature Mucosal Immunology konference, San Francisco, United States.

Author

Ellekilde, Merete ; Hansen, Camilla Hartmann Friis ; Nielsen, Dennis Sandris ; Hufeldt, Majbritt Ravn ; Vogensen, Finn Kvist ; Hansen, Axel Jacob Kornerup. / CORRELATION BETWEEN GUT MICROBIOTA AND DEVELOPMENT OF GLUCOSE INTOLERANCE IN B6.V-Lepob/J LEPTIN DEFICIENT MICE. Poster session presented at Nature Mucosal Immunology konference, San Francisco, United States.1 p.

Bibtex

@conference{0a8f460acd554e0e9b5be231aef072e2,
title = "CORRELATION BETWEEN GUT MICROBIOTA AND DEVELOPMENT OF GLUCOSE INTOLERANCE IN B6.V-Lepob/J LEPTIN DEFICIENT MICE",
abstract = "Life style associated diseases such as type 1 and 2 diabetes mellitus, atherosclerosis and inflammatory bowel disease originate form an adaptive immune response, which can be down regulated by a regulatory immune response and are under heavy stimulation from early life gut microbiota (GM). Today, a large proportion of laboratory animals are used to study such diseases, but inter-individual variation in these animal models leads to the need for larger group sizes to reach statistical significance and adequate power. By standardizing the microbial and immunological status of laboratory animals we may therefore be able to produce animals with a more standardized response and less variation. This would lead to more precise results and a reduced number of animals needed for statistical significance. The aim of the present study was to investigate if the composition of the GM of B6.V-Lepob/J leptin deficient mouse, a model of severe obesity and type 2 diabetes, was correlated with development of glucose intolerance. GM composition was analyzed by means of denaturing gradient gel electrophoresis (DGGE), a culture independent approach, separating PCR-derived DNA amplicons of bacterial 16S rRNA. Disease development was monitored by weekly weight and blood glucose measurements supplemented with measurements of oral glucose tolerance, HbA1c{\%}, plasma insulin and plasma cytokines. A significant correlation was demonstrated between GM composition and glucose intolerance. Also, a significant correlation was found between blood glucose, HbA1c{\%} and glucose intolerance and the pro-inflammatory cytokine IL-12, supporting the correlation found between gut and disease, as IL-12 is secreted after microbial stimulation of immunological cells – e.g. In the gut. Further investigations concerning the mechanisms of how the GM influences disease development is necessary, but based on these results it seems reasonable to assume, that by controlling the GM we may also influence disease development of type 2 diabetes in B6.V-Lepob/J leptin deficient mice, and thereby produce animals with less variation, which will provide the researchers better results and enable them to use smaller group sizes in the individual study.",
author = "Merete Ellekilde and Hansen, {Camilla Hartmann Friis} and Nielsen, {Dennis Sandris} and Hufeldt, {Majbritt Ravn} and Vogensen, {Finn Kvist} and Hansen, {Axel Jacob Kornerup}",
year = "2011",
month = "4",
language = "English",
note = "null ; Conference date: 14-04-2011 Through 16-04-2011",

}

RIS

TY - CONF

T1 - CORRELATION BETWEEN GUT MICROBIOTA AND DEVELOPMENT OF GLUCOSE INTOLERANCE IN B6.V-Lepob/J LEPTIN DEFICIENT MICE

AU - Ellekilde, Merete

AU - Hansen, Camilla Hartmann Friis

AU - Nielsen, Dennis Sandris

AU - Hufeldt, Majbritt Ravn

AU - Vogensen, Finn Kvist

AU - Hansen, Axel Jacob Kornerup

PY - 2011/4

Y1 - 2011/4

N2 - Life style associated diseases such as type 1 and 2 diabetes mellitus, atherosclerosis and inflammatory bowel disease originate form an adaptive immune response, which can be down regulated by a regulatory immune response and are under heavy stimulation from early life gut microbiota (GM). Today, a large proportion of laboratory animals are used to study such diseases, but inter-individual variation in these animal models leads to the need for larger group sizes to reach statistical significance and adequate power. By standardizing the microbial and immunological status of laboratory animals we may therefore be able to produce animals with a more standardized response and less variation. This would lead to more precise results and a reduced number of animals needed for statistical significance. The aim of the present study was to investigate if the composition of the GM of B6.V-Lepob/J leptin deficient mouse, a model of severe obesity and type 2 diabetes, was correlated with development of glucose intolerance. GM composition was analyzed by means of denaturing gradient gel electrophoresis (DGGE), a culture independent approach, separating PCR-derived DNA amplicons of bacterial 16S rRNA. Disease development was monitored by weekly weight and blood glucose measurements supplemented with measurements of oral glucose tolerance, HbA1c%, plasma insulin and plasma cytokines. A significant correlation was demonstrated between GM composition and glucose intolerance. Also, a significant correlation was found between blood glucose, HbA1c% and glucose intolerance and the pro-inflammatory cytokine IL-12, supporting the correlation found between gut and disease, as IL-12 is secreted after microbial stimulation of immunological cells – e.g. In the gut. Further investigations concerning the mechanisms of how the GM influences disease development is necessary, but based on these results it seems reasonable to assume, that by controlling the GM we may also influence disease development of type 2 diabetes in B6.V-Lepob/J leptin deficient mice, and thereby produce animals with less variation, which will provide the researchers better results and enable them to use smaller group sizes in the individual study.

AB - Life style associated diseases such as type 1 and 2 diabetes mellitus, atherosclerosis and inflammatory bowel disease originate form an adaptive immune response, which can be down regulated by a regulatory immune response and are under heavy stimulation from early life gut microbiota (GM). Today, a large proportion of laboratory animals are used to study such diseases, but inter-individual variation in these animal models leads to the need for larger group sizes to reach statistical significance and adequate power. By standardizing the microbial and immunological status of laboratory animals we may therefore be able to produce animals with a more standardized response and less variation. This would lead to more precise results and a reduced number of animals needed for statistical significance. The aim of the present study was to investigate if the composition of the GM of B6.V-Lepob/J leptin deficient mouse, a model of severe obesity and type 2 diabetes, was correlated with development of glucose intolerance. GM composition was analyzed by means of denaturing gradient gel electrophoresis (DGGE), a culture independent approach, separating PCR-derived DNA amplicons of bacterial 16S rRNA. Disease development was monitored by weekly weight and blood glucose measurements supplemented with measurements of oral glucose tolerance, HbA1c%, plasma insulin and plasma cytokines. A significant correlation was demonstrated between GM composition and glucose intolerance. Also, a significant correlation was found between blood glucose, HbA1c% and glucose intolerance and the pro-inflammatory cytokine IL-12, supporting the correlation found between gut and disease, as IL-12 is secreted after microbial stimulation of immunological cells – e.g. In the gut. Further investigations concerning the mechanisms of how the GM influences disease development is necessary, but based on these results it seems reasonable to assume, that by controlling the GM we may also influence disease development of type 2 diabetes in B6.V-Lepob/J leptin deficient mice, and thereby produce animals with less variation, which will provide the researchers better results and enable them to use smaller group sizes in the individual study.

M3 - Poster

ER -

ID: 35316725