article · Metabolites
Diabetic cardiomyopathy is a significant cardiovascular complication linked to type 2 diabetes, driven by inflammation, oxidative stress, fibrosis, and suppressed autophagy. In an experimental study using thirty diabetic male rats, researchers examined whether combining the diabetes medication dapagliflozin with swimming exercise provides enhanced protection against heart damage. Diabetic rats received either exercise, dapagliflozin, or both interventions together. The combined regimen produced the greatest cardioprotective benefits across several clinical indicators. It effectively reduced blood glucose, cardiac damage markers, oxidative stress, and inflammatory and fibrotic signalling molecules, while also suppressing apoptosis. Furthermore, the co-treatment increased antioxidant levels, serum insulin, and cardiac autophagy markers, while alleviating tissue alterations and structural fibrosis in the heart. The findings demonstrate that combining physical exercise with an SGLT2 inhibitor improves antioxidant, anti-inflammatory, and antifibrotic defences more effectively than single therapies alone.
Diabetic cardiomyopathy is a major complication for people living with type 2 diabetes that can lead to heart dysfunction. Demonstrating that combining an existing diabetes drug with regular physical exercise significantly reduces cardiac tissue damage, inflammation, and cellular stress provides valuable insight into how lifestyle modifications can work alongside pharmacological treatments to protect heart health.
This research provides preclinical evidence that could inform combined therapeutic strategies and lifestyle guidance for managing diabetic heart disease. The potential users include clinical researchers and healthcare providers designing integrated treatment regimens. Because the findings are derived exclusively from an animal model involving thirty rats, the work is at an early experimental stage and requires validation in human clinical trials before informing clinical practice or commercial health programmes.
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One of the most prevalent cardiovascular problems linked with type 2 diabetes mellitus (T2DM) is diabetic cardiomyopathy (DCM). DCM is associated with myocardial oxidative stress, inflammation, apoptosis, suppressed autophagy, extracellular matrix remodeling, and fibrosis. The current study aims to investigate the protective effect of sodium-glucose transport 2 inhibitor (SGLT2i) dapagliflozin and/or exercise on DCM. Thirty adult male Sprague Dawley rats are used. T2DM is induced by a 6-week high-fat diet (HFD) followed by a single intraperitoneal (IP) injection of 35 mg/kg streptozotocin (STZ). Rats are divided into five groups, control, diabetic (DM), DM + swimming, DM + dapagliflozin, and DM + dapagliflozin and swimming. Serum glucose, insulin, insulin resistance (HOMA-IR), and cardiac enzymes (CK-MB and lactate dehydrogenase (LDH) are measured. Heart specimens are used for evaluation of cellular oxidative stress markers malondialdehyde (MDA), antioxidant enzymes, glutathione (GSH), and catalase (CAT), as well as mRNA expression of TGF-β, MMP9, IL-1β, and TNF-α. Stained sections with haematoxylin and eosin (H & E) and Masson trichrome are used for histopathological evaluation and detection of fibrosis, respectively. Immunohistochemical staining for apoptosis (caspase-3), and autophagy (LC3) are also carried out. The combinations of SGLT2i and exercise exhibited the most significant cardioprotective effect. It improved diabetic-induced histopathological alterations in the myocardium and attenuated the elevation of serum blood glucose, CK-MB, LDH, myocardial MDA, and mRNA expression of TNF-α, IL-1β, TGF-β, MMP9, and the immune expression of caspase-3. Moreover, this combination increased the serum insulin, myocardial antioxidants GSH and CAT, and increase the immune expression of the LC-3. In conclusion, a combination of SGLT2i and exercise exerted a better antioxidant, anti-inflammatory, and antifibrotic effect in DCM. Moreover, the combination enhances the autophagic capacity of the heart.
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DOI: 10.3390/metabo12070635
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