Cited by 260Exercise and Physiological ResponsesAdipokines, Inflammation, and Metabolic DiseasesPhysical Activity and Health

Exercise and type 2 diabetes: focus on metabolism and inflammation

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Karstoft, Kristian, Pedersen, Bente Klarlund·2016·Immunology & Cell Biology

Abstract

Type 2 diabetes mellitus (T2DM) is associated with metabolic dysregulation and chronic inflammation, and regular exercise may provide a strong stimulus for improving both. In this review, we first discuss the link between inflammation and metabolism. Next, we give an update on the clinical metabolic effects of exercise in T2DM patients with special focus on which parameters to consider for optimizing metabolic improvements. We then discuss the mechanisms whereby exercise exerts its anti-inflammatory and related metabolic effects. Evidence exists that interleukin (IL)-1β is involved in pancreatic β-cell damage, whereas tumor necrosis factor (TNF)-α appears to be a key molecule in peripheral insulin resistance. Mechanistic studies in humans suggest that moderate acute elevations in IL-6, as provoked by exercise, exert direct anti-inflammatory effects by an inhibition of TNF-α and by stimulating IL-1ra (IL-1 receptor antagonist), thereby limiting IL-1β signaling. In addition, IL-6 has direct impact on glucose and lipid metabolism. Moreover, indirect anti-inflammatory effects of exercise may be mediated via improvements in, for example, body composition. While waiting for the outcome of long-term randomized clinical training studies with hard end points, it should be emphasized that physical activity represents a natural strong anti-inflammatory and metabolism-improving strategy with minor side effects.

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  • Physical inactivity is associated with low-grade chronic inflammation, especially when associated with obesity.

    “Physical inactivity is associated with low-grade chronic inflammation, not least when a physical inactive lifestyle is associated with obesity (29, 142, 144, 145, 207-210).”

    From Muscle–Organ Crosstalk: The Emerging Roles of Myokines (2020) · cites this paper as [144]

  • Physical activity suppresses cytokines by increasing IL-6, which decreases TNF-alpha and IL-1 signaling.

    “PA suppresses these cytokines by increasing levels of IL-6, which decrease TNF-alpha and IL-1 signaling.”
  • Utilizing excess calories prevents accumulation of pro-inflammatory visceral fat.

    “Utilizing excess calories also prevents the accumulation of pro-inflammatory visceral fat.”
  • Elevated blood glucose damages vasculature and releases inflammatory markers such as CRP, TNF-alpha, and IL-1, worsening inflammation and progression of type 2 diabetes.

    “Elevated blood glucose levels damage vasculature and release inflammatory markers such as C-reactive protein (CRP), tumor necrosis factor-alpha (TNFalpha), interleukin (IL)-1 within the bloodstream, furthering inflammation and progression of DM2.”

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References 65 · Cited by 260

Authors
Karstoft, K., & Pedersen, B. K.
Affiliations
University of Copenhagen (DK)
Corresponding author
Pedersen, Bente Klarlund
Venue
Immunology & Cell Biology
Publisher
Wiley
Published
2015-12
Volume
94
Issue
2
Pages
146-150
ISSN
  • 0004-945X (ISSN-L)
  • 0818-9641
  • 1440-1711
OpenAlex
W2183649177
Cited by
260
References
65
Citations by year
2026: 8 · 2025: 16 · 2024: 20 · 2023: 39 · 2022: 36 · 2021: 47 · 2020: 34 · 2019: 12 · 2018: 14 · 2017: 19 · 2016: 14 · 2015: 1
FWCI
2.22
Type
journal article
Language
en
Open access
Locations
  • Immunology and Cell Biology (publishedVersion)
  • PubMed (publishedVersion)
  • Research at the University of Copenhagen (University of Copenhagen) (publishedVersion)
Funders
Centre for Physical Activity Research
Topics
  • Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology › Physical Activity and Health
Keywords
type 2 diabetes, physical activity, inflammation, metabolism, insulin resistance, interleukin-6, IL-1β, TNF-α, interleukin-1 receptor antagonist, pancreatic beta-cell damage, glucose metabolism, lipid metabolism, body composition
MeSH terms
Animals, Diabetes Mellitus, Type 2, Exercise Therapy, Humans, Inflammation, Tumor Necrosis Factor-alpha, Exercise, Interleukin-1beta, Interleukin 1 Receptor Antagonist Protein

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