Sedentary time and markers of chronic low-grade inflammation in a high risk population

PLoS One. 2013 Oct 29;8(10):e78350. doi: 10.1371/journal.pone.0078350. eCollection 2013.

Abstract

Background: Sedentary behaviour has been identified as a distinct risk factor for several health outcomes. Nevertheless, little research has been conducted into the underlying mechanisms driving these observations. This study aimed to investigate the association of objectively measured sedentary time and breaks in sedentary time with markers of chronic low-grade inflammation and adiposity in a population at a high risk of type 2 diabetes mellitus.

Methods: This study reports data from an ongoing diabetes prevention programme conducted in Leicestershire, UK. High risk individuals were recruited from 10 primary care practices. Sedentary time (<25 counts per 15 s) was measured using Actigraph GT3X accelerometers (15 s epochs). A break was considered as any interruption in sedentary time (≥25 counts per 15 s). Biochemical outcomes included interleukin-6 (IL-6), C-reactive protein (CRP), leptin, adiponectin and leptin:adiponectin ratio (LAR). A sensitivity analysis investigated whether results were affected by removing participants with a CRP level >10 mg/L, as this can be indicative of acute inflammation.

Results: 558 participants (age = 63.6±7.7 years; male = 64.7%) had complete adipokine and accelerometer data. Following adjustment for various confounders, sedentary time was detrimentally associated with CRP (β = 0.176±0.057, p = 0.002), IL-6 (β = 0.242±0.056, p = <0.001), leptin (β = 0.146±0.043, p = <0.001) and LAR (β = 0.208±0.052, p = <0.001). Associations were attenuated after further adjustment for moderate-to-vigorous physical activity (MVPA) with only IL-6 (β = 0.231±0.073, p = 0.002) remaining significant; this result was unaffected after further adjustment for body mass index and glycosylated haemoglobin (HbA1c). Similarly, breaks in sedentary time were significantly inversely associated with IL-6 (β = -0.094±0.047, p = 0.045) and leptin (β = -0.075±0.037, p = 0.039); however, these associations were attenuated after adjustment for accelerometer derived variables. Excluding individuals with a CRP level >10 mg/L consistently attenuated the significant associations across all markers of inflammation.

Conclusion: These novel findings from a high risk population recruited through primary care suggest that sedentary behaviour may influence markers associated with inflammation, independent of MVPA, glycaemia and adiposity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adiponectin / metabolism
  • Adiposity / physiology
  • Biomarkers / metabolism*
  • Body Mass Index
  • C-Reactive Protein / metabolism
  • Diabetes Mellitus, Type 2 / metabolism
  • Diabetes Mellitus, Type 2 / physiopathology*
  • Female
  • Glycated Hemoglobin A / metabolism
  • Humans
  • Inflammation / metabolism*
  • Inflammation / pathology*
  • Interleukin-6 / metabolism
  • Leptin / metabolism
  • Male
  • Middle Aged
  • Motor Activity / physiology*
  • Risk Factors
  • Sedentary Behavior

Substances

  • Adiponectin
  • Biomarkers
  • Glycated Hemoglobin A
  • Interleukin-6
  • Leptin
  • C-Reactive Protein

Grant support

The research was supported by The National Institute for Health Research Collaboration for Leadership in Applied Health Research and Care - Leicestershire, Northamptonshire and Rutland (NIHR CLAHRC – LNR) (http://www.clahrc-lnr.nihr.ac.uk/index.php/walking-away-from-diabetes), the University of Leicester Clinical Trials Unit and the NIHR Leicester-Loughborough Diet, Lifestyle and Physical Activity Biomedical Research Unit which is a partnership between University Hospitals of Leicester NHS Trust, Loughborough University and the University of Leicester (http://www.ll.dlpa.bru.nihr.ac.uk/). The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health. C-reactive protein and adipokine analysis was carried out and funded by Unilever Discover, UK. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.