ArticlePloS one2015
Voluntary Exercise Can Ameliorate Insulin Resistance by Reducing iNOS-Mediated S-Nitrosylation of Akt in the Liver in Obese Rats.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Physical exercise in liver diseases.Hepatology (Baltimore, Md.) · 2026Review
- Akt3 links mitochondrial function to the regulation of Aurora B and mitotic fidelity.PloS one · 2025Article
- Comparing prophylactic effect of exercise and metformin on cognitive brain functions in rats with type 3 diabetes mellitus.Archives of medical science : AMS · 2024Article
- iNOS contributes to heart failure with preserved ejection fraction through mitochondrial dysfunction and Akt S-nitrosylation.Journal of advanced research · 2023Article
- The manifold roles of protein S-nitrosylation in the life of insulin.Nature reviews. Endocrinology · 2022Review
- Mitigation of MAFLD in High Fat-High Sucrose-Fructose Fed Mice by a Combination of Genistein Consumption and Exercise Training.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
- Short-Term Strength Exercise Reduces Hepatic Insulin Resistance in Obese Mice by Reducing PTP1B Content, Regardless of Changes in Body Weight.International journal of molecular sciences · 2021Article
- ER-Mitochondria Contacts and Insulin Resistance Modulation through Exercise Intervention.International journal of molecular sciences · 2020Review
- Impacts of exercise intervention on various diseases in rats.Journal of sport and health science · 2020Review
- Exercise alters the molecular pathways of insulin signaling and lipid handling in maternal tissues of obese pregnant mice.Physiological reports · 2019Article
- Flavonoids fromSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2019Article
- Running wheel access fails to resolve impaired sustainable health in mice feeding a high fat sucrose diet.Aging · 2019Article
- Physical exercise reduces pyruvate carboxylase (PCB) and contributes to hyperglycemia reduction in obese mice.The journal of physiological sciences : JPS · 2018Article
- The Effects of Physical Exercise on Fatty Liver Disease.Gene expression · 2018Review
- Article
- Previous physical exercise alters the hepatic profile of oxidative-inflammatory status and limits the secondary brain damage induced by severe traumatic brain injury in rats.The Journal of physiology · 2017Article
- iNOS promotes hypothalamic insulin resistance associated with deregulation of energy balance and obesity in rodents.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voluntary exercise can ameliorate insulin resistance. The underlying mechanism, however, remains to be elucidated. We previously demonstrated that inducible nitric oxide synthase (iNOS) in the liver plays an important role in hepatic insulin resistance in the setting of obesity. In this study, we tried to verify our hypothesis that voluntary exercise improves insulin resistance by reducing the expression of iNOS and subsequent S-nitrosylation of key molecules of glucose metabolism in the liver. Twenty-one Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model of type 2 diabetes mellitus, and 18 non-diabetic control Long-Evans Tokushima Otsuka (LETO) rats were randomly assigned to a sedentary group or exercise group subjected to voluntary wheel running for 20 weeks. The voluntary exercise significantly reduced the fasting blood glucose and HOMA-IR in the OLETF rats. In addition, the exercise decreased the amount of iNOS mRNA in the liver in the OLETF rats. Moreover, exercise reduced the levels of S-nitrosylated Akt in the liver, which were increased in the OLETF rats, to those observed in the LETO rats. These findings support our hypothesis that voluntary exercise improves insulin resistance, at least partly, by suppressing the iNOS expression and subsequent S-nitrosylation of Akt, a key molecule of the signal transduction pathways in glucose metabolism in the liver.
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