Investigation on the Effects of GLP1 analog and SGLT2 inhibitor against Diabetic Cardiomyopathy in Type 2 Diabetic Rats: Possible Underlying Mechanisms

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Investigation on the Effects of GLP1 analog and SGLT2 inhibitor against Diabetic Cardiomyopathy in Type 2 Diabetic Rats: Possible Underlying Mechanisms

June 1, 2021 Medicine and Medical 0

Background information: The current study looked at the potential cardioprotective benefits of GLP1 and SGLT2i against diabetic cardiomyopathy (DCM) in type 2 diabetic rats, as well as the mechanisms behind them. The existence of heart failure in the absence of coronary artery disease is referred to as DCM.

Methods: Forty-two male Sprague Dawley rats were randomized into four equal groups at random; a) DM+ GLP1, as DM group with GLP1 analogue (liraglutide) at a dose of 75 g/kg for 4 weeks, and DM+ SGLT2i: as DM group with SGLT2 inhibitor (dapagliflozin) at a dose of 1 mg/kg for 4 weeks. Serum blood glucose, HOMA-IR, insulin, and cardiac enzymes (LDH, CK-MB) were all tested at the end of the four-week treatment.

Myocardial oxidative stress markers (MDA, GSH, and CAT) as well as norepinephrine (NE), myocardial fibrosis, and the expression of caspase-3, TGF-, TNF-, and tyrosine hydroxylase (TH) in myocardial tissues were all assessed. As a result, T2DM resulted in a considerable increase in blood sugar levels. (p 0.05) serum glucose, HOMA-IR, serum CK-MB, and LDH In addition, DM resulted in severe myocardial damage and fibrosis, as well as an increase in myocardial MDA, NE, and upregulation of myocardial caspase-3, TNF, TGF, and TH, as well as a substantial drop in serum insulin, myocardial GSH, and CAT (p0.05). All examined indicators improved significantly (p 0.05) after administration of either GLP1 analog or SGLT2i. Conclusion: We found that both GLP1 and SGLT2i had cardioprotective effects against DCM in T2DM, with SGLT2i having the upper hand. This could be related to fibrosis, oxidative stress, apoptosis (caspase-3), sympathetic nerve activity, and other factors.

Author (s) Details

Prof. Dr. Abdelaziz M. Hussein
Department of Medical Physiology, Mansoura Faculty of Medicine, Mansoura, Egypt

Elsayed A. Eid
Department of Internal Medicine and Endocrinology, Delta University for Science and Technology, Gamasa, Egypt

Medhat Taha
Department of Anatomy, Mansoura Faculty of Medicine, Mansoura, Egypt.

Rami M. Elshazli
Department of Biochemistry, Faculty of Physical Therapy, Horus University-Egypt, New Damietta, Egypt.

Raouf Fekry Bedir
Department of Anatomy, Mansoura Faculty of Medicine, Mansoura, Egypt.

Lashin Saad Lashin
Department of Medical Physiology, Mansoura Faculty of Medicine, Mansoura, Egypt and Department of Medical Physiology, Horus University, Damietta, Egypt.

View Book :- https://stm.bookpi.org/HMMR-V9/article/view/1021

 

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