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Physical inactivity, insulin resistance, and the oxidative-inflammatory loop
Abstract
Epidemiological data indicate that physical inactivity, a main factor of global energetic imbalance, is involved in the worldwide epidemic of obesity and metabolic disorders such as insulin resistance. Although the complex pathogenesis of insulin resistance is not fully understood, literature data accumulated during the past decades clearly indicate that the activation of the oxidative-inflammatory loop plays a major role. By activating the oxidative-inflammatory loop in insulin-sensitive tissues, fat gain and adipose tissue dysfunction likely contribute to induce insulin resistance during chronic and prolonged physical inactivity. However, in the past years, evidence has emerged showing that early insulin resistance also occurs after very short-term exposure to physical inactivity (1-7 days) without any fat gain or energetic imbalance. The possible role of liver disturbances or endothelial dysfunction is suggested, but further studies are necessary to really conclude. Inactive skeletal muscle probably constitutes the primary triggering tissue for the development of early insulin resistance. In the present review, we discuss on the current knowledge about the effect of physical inactivity on whole-body and peripheral insulin sensitivity, and how local inflammation and oxidative stress arising with physical inactivity could potentially induce insulin resistance. We assume that early muscle insulin resistance allows the excess nutrients to shift in the storage tissues to withstand starvation through energy storage. We also consider when chronic and prolonged, physical inactivity over an extended period of time is an underestimated contributor to pathological insulin resistance and hence indirectly to numerous chronic diseases.
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In the citing paper
“Sedentary lifestyles, characterised by inactive skeletal muscle, sarcopenia and adipose tissue accumulation, are associated with moderate-to-high levels of reactive oxygen species, which can deplete antioxidant defences resulting in oxidation of proteins, lipids and DNA (Bjork et al. 2012; Derbre et al. 2014; Gratas-Delamarche et al. 2014; Le Lay and Simard 2014).”
From Is immunosenescence influenced by our lifetime “dose” of exercise? (2016) · cites this paper as Gratas-Delamarche et al. 2014
In the citing paper
“Regular moderate-intensity exercise stimulates optimal reactive oxygen species production above resting values, but not to the levels associated with chronic sedentary behaviour (Bjork et al. 2012; Derbre et al. 2014; Gratas-Delamarche et al. 2014; Le Lay and Simard 2014).”
From Is immunosenescence influenced by our lifetime “dose” of exercise? (2016) · cites this paper as Gratas-Delamarche et al. 2014
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Metadata
- Authors
- Gratas-Delamarche, A., Derbré, F., Vincent, S., & Cillard, J.
- Affiliations
- École Normale Supérieure Paris-Saclay (FR)
- Corresponding author
- Derbré, F.
- ORCID
- Derbré, F.
- Venue
- Free Radical Research
- Publisher
- Informa UK Limited
- Published
- 2013-10-17
- Volume
- 48
- Issue
- 1
- Pages
- 93-108
- ISSN
- 1029-2470 (ISSN-L)
- 1071-5762
- OpenAlex
- W2154187478
- Cited by
- 99
- References
- 202
- Citations by year
- 2026: 3 · 2025: 9 · 2024: 7 · 2023: 10 · 2022: 6 · 2021: 11 · 2020: 8 · 2019: 11 · 2018: 9 · 2017: 6 · 2016: 8 · 2015: 6 · 2014: 3 · 2013: 2
- FWCI
- 0.75
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Free Radical Research (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › Exercise and Physiological Responses
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- physical inactivity, insulin resistance, oxidative stress, inflammation, skeletal muscle insulin sensitivity, adipose tissue dysfunction, obesity, energy imbalance, endothelial dysfunction, liver dysfunction, energy storage
- MeSH terms
- Animals, Humans, Inflammation, Insulin Resistance, Motor Activity, Oxidation-Reduction, Sedentary Behavior
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