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Mitochondrial dysfunction is a significant feature of type 2 diabetes. MOTS-C, a peptide derived from mitochondria, has positive effects on metabolism and exercise capacity. This study explored the impact of high and moderate-intensity interval exercises on mitochondrial MOTS-C alterations and their correlation with metabolic markers in male diabetic sand rats. Thirty male sand rats were divided into six groups: control, MIIT, DM + HIIT, DM + MIIT, DM, and HIIT (5 rats each). Diabetes was induced using a high-fat diet (HFD) combined with streptozotocin (STZ). The Wistar sand rats in exercise groups underwent 8 weeks of interval training of varying intensities. Post sample collection, protein expressions of PCG-1a, AMPK, and GLUT4 were assessed through Western blot analysis, while MOTS-C protein expression was determined using ELISA. Both exercise intensity and diabetes significantly affected the levels of PCG-1a, MOTS-C, GLUT4 proteins, and insulin resistance (p < 0.001). The combined effect of diabetes status and exercise intensity on these levels was also significant (p < 0.001). However, the diabetes effect varied when comparing high-intensity to moderate-intensity exercise. The moderate-intensity exercise group with diabetes showed higher levels of PCG-1a, MOTS-C, and GLUT4 proteins and reduced insulin resistance levels (p < 0.001). Exercise intensity (p = 0.022) and diabetes (p = 0.008) significantly influenced AMPK protein levels. The interplay between diabetes status and exercise intensity on AMPK protein levels was noteworthy, with the moderate-intensity diabetes group exhibiting higher AMPK levels than the high-intensity diabetes group (p < 0.001). In conclusion, exercise elevates the levels of PCG-1a, MOTS-C, GLUT4, and AMPK proteins, regulating insulin resistance in diabetic sand rats. Given the AMPK-MOTS-C mitochondrial pathway's mechanisms, interval exercises might enhance the metabolic rates and general health of diabetic rodents., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Diabetes Mellitus (DM) can damage the function of metabolic tissues, including the liver. Liver macrophages are the first responders to tissue damage or exercise. We sought to determine whether eight weeks of interval training (HIIT & MIIT) protect against diabetes-induced modulation of hepatic CD86 and CD206 expression associated with the amelioration of insulin resistance and inflammation in rats. Thirty rats were divided into six groups, including a control group, MIIT, HIIT, DM, DM + MIIT, and DM + HIIT (n = 5 in each group). Diabetes was induced using a combination of a high-fat diet (HFD) and STZ. Wistar rats in the exercise groups were subjected to moderate and high-intensity interval training for eight weeks. After sample collection, liver tissue was removed and weighed. Serum levels of TNFα, IL-6, TGFβ, and IL-10 were measured by ELISA. Protein expression of the immune markers CD86 and CD206 in liver tissue was determined by immunohistochemical staining. Induction of diabetes increased glycemic indices, insulin resistance, and liver injury enzymes, especially in DM and DM + HIIT groups (p < 0.05). Moreover, diabetic groups showed an increase in liver CD86 protein expression, an increase in TNFα, IL-6, and TGFβ serum levels, and a decrease in liver CD206 and serum IL-10 (p < 0.05). Doing exercise while being diabetic, especially MIIT, significantly reversed the aforementioned factors and reduced insulin resistance (p < 0.05), except IL-10). We concluded that performing exercise training specially MIIT by decreasing CD86 and increasing CD206 in the liver, followed by decreasing pro-inflammatory factors (TNFα, IL-6) caused the regulation of liver enzymes and insulin resistance in diabetic rats. Therefore, it seems that exercise training by regulating macrophage markers CD86 and CD206 can reduce damage to the insulin-signaling pathway by reducing pro-inflammatory cytokines., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier GmbH.)