Association of changes in inflammation with variation in glycaemia, insulin resistance and secretion based on the KORA study

IMI DIRECT Consortium, Tonia de las Heras Gala, Christian Herder, Femke Rutters, Maren Carstensen-Kirberg, Cornelia Huth, Coen D. A. Stehouwer, Giel Nijpels, Casper Schalkwijk, Allan Flyvbjerg, Paul W. Franks, Jacqueline Dekker, Christa Meisinger, Wolfgang Koenig, Michael Roden, Wolfgang Rathmann, Annette Peters, Barbara Thorand

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Aims: Subclinical systemic inflammation may contribute to the development of type 2 diabetes, but its association with early progression of glycaemic deterioration in persons without diabetes has not been fully investigated. Our primary aim was to assess longitudinal associations of changes in pro-inflammatory (leukocytes, high-sensitivity C-reactive protein (hsCRP)) and anti-inflammatory (adiponectin) markers with changes in markers that assessed glycaemia, insulin resistance, and secretion (HbA1c, HOMA-IR, and HOMA-ß). Furthermore, we aimed to directly compare longitudinal with cross-sectional associations. Materials and methods: This study includes 819 initially nondiabetic individuals with repeated measurements from the Cooperative Health Research in the Region of Augsburg (KORA) S4/F4 cohort study (median follow-up: 7.1 years). Longitudinal and cross-sectional associations were simultaneously examined using linear mixed growth models. Changes in markers of inflammation were used as independent and changes in markers of glycaemia/insulin resistance/insulin secretion as dependent variables. Models were adjusted for age, sex, major lifestyle and metabolic risk factors for diabetes using time-varying variables in the final model. Results: Changes of leukocyte count were positively associated with changes in HbA1c and HOMA-ß while changes in adiponectin were inversely associated with changes in HbA1c. All examined cross-sectional associations were statistically significant; they were generally stronger and mostly directionally consistent to the longitudinal association estimates. Conclusions: Adverse changes in low-grade systemic inflammation go along with glycaemic deterioration and increased insulin secretion independently of changes in other risk factors, suggesting that low-grade inflammation may contribute to the development of hyperglycaemia and a compensatory increase in insulin secretion.
LanguageEnglish
Article numbere3063
JournalDiabetes/Metabolism Research and Reviews
Volume34
Issue number8
DOIs
Publication statusPublished - 2018

Cite this

@article{c9f9949e957545cbb64574cb12a33c27,
title = "Association of changes in inflammation with variation in glycaemia, insulin resistance and secretion based on the KORA study",
abstract = "Aims: Subclinical systemic inflammation may contribute to the development of type 2 diabetes, but its association with early progression of glycaemic deterioration in persons without diabetes has not been fully investigated. Our primary aim was to assess longitudinal associations of changes in pro-inflammatory (leukocytes, high-sensitivity C-reactive protein (hsCRP)) and anti-inflammatory (adiponectin) markers with changes in markers that assessed glycaemia, insulin resistance, and secretion (HbA1c, HOMA-IR, and HOMA-{\ss}). Furthermore, we aimed to directly compare longitudinal with cross-sectional associations. Materials and methods: This study includes 819 initially nondiabetic individuals with repeated measurements from the Cooperative Health Research in the Region of Augsburg (KORA) S4/F4 cohort study (median follow-up: 7.1 years). Longitudinal and cross-sectional associations were simultaneously examined using linear mixed growth models. Changes in markers of inflammation were used as independent and changes in markers of glycaemia/insulin resistance/insulin secretion as dependent variables. Models were adjusted for age, sex, major lifestyle and metabolic risk factors for diabetes using time-varying variables in the final model. Results: Changes of leukocyte count were positively associated with changes in HbA1c and HOMA-{\ss} while changes in adiponectin were inversely associated with changes in HbA1c. All examined cross-sectional associations were statistically significant; they were generally stronger and mostly directionally consistent to the longitudinal association estimates. Conclusions: Adverse changes in low-grade systemic inflammation go along with glycaemic deterioration and increased insulin secretion independently of changes in other risk factors, suggesting that low-grade inflammation may contribute to the development of hyperglycaemia and a compensatory increase in insulin secretion.",
keywords = "Glycemic deterioration, HbA1c, Inflammation, Insulin resistance, {\ss}-cell function",
author = "{IMI DIRECT Consortium} and {de las Heras Gala}, Tonia and Christian Herder and Femke Rutters and Maren Carstensen-Kirberg and Cornelia Huth and Stehouwer, {Coen D. A.} and Giel Nijpels and Casper Schalkwijk and Allan Flyvbjerg and Franks, {Paul W.} and Jacqueline Dekker and Christa Meisinger and Wolfgang Koenig and Michael Roden and Wolfgang Rathmann and Annette Peters and Barbara Thorand",
year = "2018",
doi = "10.1002/dmrr.3063",
language = "English",
volume = "34",
journal = "Diabetes/Metabolism Research and Reviews",
issn = "1520-7552",
number = "8",

}

Association of changes in inflammation with variation in glycaemia, insulin resistance and secretion based on the KORA study. / IMI DIRECT Consortium.

In: Diabetes/Metabolism Research and Reviews, Vol. 34, No. 8, e3063, 2018.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - Association of changes in inflammation with variation in glycaemia, insulin resistance and secretion based on the KORA study

AU - IMI DIRECT Consortium

AU - de las Heras Gala, Tonia

AU - Herder, Christian

AU - Rutters, Femke

AU - Carstensen-Kirberg, Maren

AU - Huth, Cornelia

AU - Stehouwer, Coen D. A.

AU - Nijpels, Giel

AU - Schalkwijk, Casper

AU - Flyvbjerg, Allan

AU - Franks, Paul W.

AU - Dekker, Jacqueline

AU - Meisinger, Christa

AU - Koenig, Wolfgang

AU - Roden, Michael

AU - Rathmann, Wolfgang

AU - Peters, Annette

AU - Thorand, Barbara

PY - 2018

Y1 - 2018

N2 - Aims: Subclinical systemic inflammation may contribute to the development of type 2 diabetes, but its association with early progression of glycaemic deterioration in persons without diabetes has not been fully investigated. Our primary aim was to assess longitudinal associations of changes in pro-inflammatory (leukocytes, high-sensitivity C-reactive protein (hsCRP)) and anti-inflammatory (adiponectin) markers with changes in markers that assessed glycaemia, insulin resistance, and secretion (HbA1c, HOMA-IR, and HOMA-ß). Furthermore, we aimed to directly compare longitudinal with cross-sectional associations. Materials and methods: This study includes 819 initially nondiabetic individuals with repeated measurements from the Cooperative Health Research in the Region of Augsburg (KORA) S4/F4 cohort study (median follow-up: 7.1 years). Longitudinal and cross-sectional associations were simultaneously examined using linear mixed growth models. Changes in markers of inflammation were used as independent and changes in markers of glycaemia/insulin resistance/insulin secretion as dependent variables. Models were adjusted for age, sex, major lifestyle and metabolic risk factors for diabetes using time-varying variables in the final model. Results: Changes of leukocyte count were positively associated with changes in HbA1c and HOMA-ß while changes in adiponectin were inversely associated with changes in HbA1c. All examined cross-sectional associations were statistically significant; they were generally stronger and mostly directionally consistent to the longitudinal association estimates. Conclusions: Adverse changes in low-grade systemic inflammation go along with glycaemic deterioration and increased insulin secretion independently of changes in other risk factors, suggesting that low-grade inflammation may contribute to the development of hyperglycaemia and a compensatory increase in insulin secretion.

AB - Aims: Subclinical systemic inflammation may contribute to the development of type 2 diabetes, but its association with early progression of glycaemic deterioration in persons without diabetes has not been fully investigated. Our primary aim was to assess longitudinal associations of changes in pro-inflammatory (leukocytes, high-sensitivity C-reactive protein (hsCRP)) and anti-inflammatory (adiponectin) markers with changes in markers that assessed glycaemia, insulin resistance, and secretion (HbA1c, HOMA-IR, and HOMA-ß). Furthermore, we aimed to directly compare longitudinal with cross-sectional associations. Materials and methods: This study includes 819 initially nondiabetic individuals with repeated measurements from the Cooperative Health Research in the Region of Augsburg (KORA) S4/F4 cohort study (median follow-up: 7.1 years). Longitudinal and cross-sectional associations were simultaneously examined using linear mixed growth models. Changes in markers of inflammation were used as independent and changes in markers of glycaemia/insulin resistance/insulin secretion as dependent variables. Models were adjusted for age, sex, major lifestyle and metabolic risk factors for diabetes using time-varying variables in the final model. Results: Changes of leukocyte count were positively associated with changes in HbA1c and HOMA-ß while changes in adiponectin were inversely associated with changes in HbA1c. All examined cross-sectional associations were statistically significant; they were generally stronger and mostly directionally consistent to the longitudinal association estimates. Conclusions: Adverse changes in low-grade systemic inflammation go along with glycaemic deterioration and increased insulin secretion independently of changes in other risk factors, suggesting that low-grade inflammation may contribute to the development of hyperglycaemia and a compensatory increase in insulin secretion.

KW - Glycemic deterioration

KW - HbA1c

KW - Inflammation

KW - Insulin resistance

KW - ß-cell function

UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85054309122&origin=inward

UR - https://www.ncbi.nlm.nih.gov/pubmed/30114727

U2 - 10.1002/dmrr.3063

DO - 10.1002/dmrr.3063

M3 - Article

VL - 34

JO - Diabetes/Metabolism Research and Reviews

T2 - Diabetes/Metabolism Research and Reviews

JF - Diabetes/Metabolism Research and Reviews

SN - 1520-7552

IS - 8

M1 - e3063

ER -