ArticleScientific reports2024
Comparison of HIIT and MICT and further detraining on metabolic syndrome and asprosin signaling pathway in metabolic syndrome model of rats.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Adipokines modulation through exercise training: a comparative study of different training models in men with obesity.Journal of endocrinological investigation · 2026Trial
- Effective of high-intensity interval training and moderate-intensity continuous training on body composition, glycolipid metabolism, and cardiopulmonary function in patients with pre-diabetes: a randomized controlled trial.Frontiers in endocrinology · 2025Trial
- Transcriptomic Analysis of High-Intensity Interval Training in High-Fat-Diet-Induced Spontaneous Hypertensive Rats' Brains.International journal of molecular sciences · 2025Article
- Exercise intensity-mediated regulation of gut epithelial cells and immune function in gut microbiota dysbiosis.Journal of translational medicine · 2025Review
- Exercise and Carnosine Modulate Microbiota-Derived Metabolites, Myokines, and Cardiometabolic Profiles in Rats: A Randomized Controlled Trial.Biomedicines · 2025Article
- HIIT versus MICT in MASLD: mechanisms mediated by gut-liver axis crosstalk, mitochondrial dynamics remodeling, and adipokine signaling attenuation.Lipids in health and disease · 2025Article
- Article
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3 authors.
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Abstract
Physical activity promotes various metabolic benefits by balancing pro and anti-inflammatory adipokines. Recent studies suggest that asprosin might be involved in progression of metabolic syndrome (MetS), however, the underlying mechanisms have not been understood yet. This study aimed to evaluate the effects of high-intensity interval training (HIIT), moderate-intensity continuous training (MICT), and further detraining on MetS indices, insulin resistance, serum and the liver levels of asprosin, and AMP-activated protein kinase (AMPK) pathway in menopause-induced MetS model of rats. A total of 64 Wistar rats were used in this study and divided into eight groups: Sham1, OVX1 (ovariectomized), Sham2, OVX2, OVX + HIIT, OVX + MICT, OVX + HIIT + Det (detraining), and OVX + MICT + Det. Animals performed the protocols, and then serum concentrations of asprosin, TNF-α, insulin, fasting blood glucose, and lipid profiles (TC, LDL, TG, and HDL) were assessed. Additionally, the liver expression of asprosin, AMPK, and P-AMPK was measured by western blotting. Both HIIT and MICT caused a significant decrease in weight, waist circumference, BMI (P = 0.001), and serum levels of glucose, insulin, asprosin (P = 0.001), triglyceride, total cholesterol, low-density lipoprotein (LDL), and TNF-α (P = 0.001), but an increase in the liver AMPK, P-AMPK, and P-AMPK/AMPK (P = 0.001), compared with OVX2 noexercised group. MICT was superior to HIIT in reducing serum asprosin, TNF-a, TG, LDL (P = 0.001), insulin, fasting blood glucose, HOMA-IR, and QUEKI index (P = 0.001), but an increase in the liver AMPK, and p-AMPK (P = 0.001). Although after two months of de-training almost all indices returned to the pre exercise values (P < 0.05). The findings suggest that MICT effectively alleviates MetS induced by menopause, at least partly through the activation of liver signaling of P-AMPK and the reduction of asprosin and TNF-α. These results have practical implications for the development of exercise interventions targeting MetS in menopausal individuals, emphasizing the potential benefits of MICT in mitigating MetS-related complications.
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