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[This corrects the article DOI: 10.1007/s40200-022-01074-4.].
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Objectives: Glucose intolerance and insulin resistance are hallmarks of metabolic syndrome and lead to Alzheimer's disease (AD). The purpose of this study is to elucidate the neuroprotective effect of metformin through insulin regulation with cardiometabolic and neurotransmitter metabolic enzyme regulation in high-fat, high-sucrose diet and streptozotocin (HFHS-STZ)-induced rats. Methods: Male Wistar rats were treated with metformin (180 mg/kg and 360 mg/kg). STZ (35 mg/kg i.p.) injection was performed on the 14th day of 42 days of HFHS diet treatment. Brain neurotransmitter metabolic enzymes (acetylcholinesterase and monoamine oxidase) were determined along with sodium-potassium ATPase (Na+K+-ATPase). Plasma lipids and homeostasis model assessment of insulin resistance (HOMA-IR) was performed. Mean arterial blood pressure, heart rate and electrocardiogram (QT, QTc and RR intervals) were analysed with PowerLab. Results: Metformin treatment significantly (p < 0.001) reduced the HOMA-IR index and decreased neurotransmitter metabolic enzymes such as AChE and MAO (p < 0.01 and p < 0.05). The lipid profile was significantly (p < 0.001) controlled with cardiometabolic functions. Conclusions: Our investigation revealed that metformin has a remarkable role in regulating brain insulin, vascular system with monoaminergic metabolic enzymes and enhancing synaptic plasticity. Metformin may be a selective early therapeutic agent in metabolic syndrome associated with cognitive decline.
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Diabetes is one of the most common disorders that substantially contributes to an increase in global health burden. As a metabolic disorder, diabetes is associated with various medical conditions and diseases such as obesity, hypertension, cardiovascular diseases, and atherosclerosis. In this review, we cover the scientific studies on sodium/glucose cotransporter (SGLT) inhibitors published during the last decade. Our focus on providing an exhaustive overview of SGLT inhibitors enabled us to present their chemical classification for the first time.
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OBJECTIVES: The present study was designed to evaluate the ameliorative effect of Elaeocarpus ganitrus on gentamicin (GM)-induced nephrotoxicity in rats. MATERIALS AND METHODS: E. ganitrus (100, 200, and 400 mg/kg body weight) was administered orally to male Wistar rats. GM (100 mg/kg) was used to induce nephrotoxicity. Study parameters include serum albumin, creatinine, blood urea nitrogen (BUN), uric acid, creatinine, and albuminuria. Total protein in serum, antioxidant enzymes activities, phagocytic index, and neutrophil adhesion assays were performed to determine oxidative stress and immunomodulatory action of E. ganitrus. RESULTS: The results revealed that coadministration of E. ganitrus significantly reduced the elevated level of serum creatinine, BUN, uric acid, and albuminuria with considerable increase in the serum albumin and urine creatinine. Furthermore, E. ganitrus noticeably increased serum total protein and antioxidant enzyme levels with significant alteration in phagocytic index and neutrophil adhesion assay when compared with GM-treated group in a dose-dependent manner. CONCLUSION: The present study revealed that ethanolic extract of E. ganitrus seeds has immunomodulatory and nephroprotective activity.
