Diet-induced obesity alters signalling pathways and induces atrophy and apoptosis in skeletal muscle in a prediabetic rat model: Diet-induced obesity and skeletal muscle
Open accessAbstract
Pro-inflammatory and stress-activated signalling pathways are important role players in the pathogenesis of obesity and insulin resistance. Obesity and type II diabetes are associated with chronic, low-grade inflammation and elevated tumour necrosis factor-α (TNF-α) levels. There is increasing evidence that TNF-α may play a critical role in skeletal muscle atrophy. However, the effects of obesity-induced insulin resistance on these signalling pathways are poorly understood in skeletal muscle. Therefore, the present study addressed the effects of obesity-induced insulin resistance on the activity of the ubiquitin ligases, nuclear factor-B, p38 MAPK and phosphoinositide 3-kinase signalling pathways in the gastrocnemius muscle and compared these with muscle of standard chow-fed control rats. Male Wistar rats were randomly allocated to a control diet group (standard commercial chow; 60% carbohydrates, 30% protein and 10% fat) or a cafeteria diet group (65% carbohydrates, 19% protein and 16% fat) for 16 weeks. Blood analysis was conducted to determine the impact of the model of obesity on circulating insulin, glucose, free fatty acids, TNF-α and angiotensin II concentrations. The experimental animals were 18% heavier and had 68% greater visceral fat mass than their control counterparts and were dyslipidaemic. Significant increases in the ubiquitin ligase and MuRF-1, as well as in caspase-3 and poly-ADP-ribose polymerase cleavage were observed in the muscle of obese animals compared with the control rats. We propose that dyslipidaemia may be a mechanism for the activation of inflammatory/stress-activated signalling pathways in obesity and type II diabetes, which will lead to apoptosis and atrophy in skeletal muscle.
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High-fat diet can lead to animal obesity and muscle atrophy.
“High-fat diet (HFD) has a higher energy density than a regular diet, which can lead to animal obesity and muscle atrophy.”
From GLP-1RA Liraglutide and Semaglutide Improves Obesity-Induced Muscle Atrophy via SIRT1 Pathway (2023) · cites this paper as [24]
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- Authors
- Sishi, B., Loos, B., Ellis, B., Smith, W., du Toit, E. F., & Engelbrecht, A.-M.
- Affiliations
- Stellenbosch University (ZA)
- Venue
- Experimental Physiology
- Publisher
- Wiley
- Published
- 2010-11-10
- Volume
- 96
- Issue
- 2
- Pages
- 179-193
- ISSN
- 0958-0670 (ISSN-L)
- OpenAlex
- W2135467555
- Cited by
- 162
- References
- 49
- Citations by year
- 2026: 9 · 2025: 10 · 2024: 10 · 2023: 9 · 2022: 15 · 2021: 15 · 2020: 10 · 2019: 16 · 2018: 9 · 2017: 9 · 2016: 8 · 2015: 12 · 2014: 7 · 2013: 14 · 2012: 6
- FWCI
- 2.99
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Experimental Physiology (publishedVersion)
- PubMed (publishedVersion)
- Griffith Research Online (submittedVersion)
- SUNScholar (Stellenbosch University) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
- Keywords
- diet-induced obesity, skeletal muscle atrophy, apoptosis, insulin resistance, type 2 diabetes, prediabetes, TNF-α, NF-κB, p38 MAPK, PI3K signaling, ubiquitin ligase, MuRF1, caspase-3, poly(ADP-ribose) polymerase, gastrocnemius, cafeteria diet, dyslipidemia, angiotensin II, inflammation
- MeSH terms
- Adaptation, Physiological, Animals, Atrophy, Dietary Fats, Humans, Insulin Resistance, Male, Muscle Proteins, Obesity, Prediabetic State, Signal Transduction, Rats, Wistar, Muscle, Skeletal, Rats
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