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Metformin Improves Glycemic Control and Postprandial Metabolism and Enhances Postprandial Glucagon-Like Peptide 1 Secretion in Patients With Type 2 Diabetes and Heart Failure: A Randomized, Double-Blind, Placebo-Controlled Trial.
Clin Diabetes
September 2024
Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
This randomized trial tested the effect of metformin on glycemic control and cardiac function in patients with heart failure (HF) and type 2 diabetes while evaluating intestinal effects on selected gut microbiome products reflected by trimethylamine-N-oxide (TMAO) and gut-derived incretins. Metformin treatment improved glycemic control and postprandial metabolism and enhanced postprandial glucagon-like peptide 1 (GLP-1) secretion but did not influence cardiac function or the TMAO levels. Metabolic effects of metformin in HF may be mediated by an improvement in intestinal endocrine function and enhanced secretion of the gut-derived incretin GLP-1.
View Article and Find Full Text PDFImeglimin, unlike metformin, does not perturb differentiation of human induced pluripotent stem cells towards pancreatic β-like cells and rather enhances gain in β cell identity gene sets.
J Diabetes Investig
January 2025
Department of Metabolic Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.
Aims/introduction: Metformin treatment for hyperglycemia in pregnancy (HIP) beneficially improves maternal glucose metabolism and reduces perinatal complications. However, metformin could impede pancreatic β cell development via impaired mitochondrial function. A new anti-diabetes drug imeglimin, developed based on metformin, improves mitochondrial function.
View Article and Find Full Text PDFOvercoming β-Cell Dysfunction in Type 2 Diabetes Mellitus: CD36 Inhibition and Antioxidant System.
Diabetes Metab J
January 2025
Department of Internal Medicine, Yeungnam University College of Medicine, Daegu, Korea.
Type 2 diabetes mellitus (T2DM) is marked by chronic hyperglycemia, gradually worsening β-cell failure, and insulin resistance. Glucotoxicity and oxidative stress cause β-cell failure by increasing reactive oxygen species (ROS) production, impairing insulin secretion, and disrupting transcription factors such as pancreatic and duodenal homeobox 1 (PDX-1) and musculoaponeurotic fibrosarcoma oncogene family A (MafA). Cluster determinant 36 (CD36), an essential glycoprotein responsible for fatty acid uptake, exacerbates oxidative stress and induces the apoptosis of β-cells under hyperglycemic conditions through pathways involving ceramide, thioredoxin-interacting protein (TXNIP), and Rac1-nicotinamide adenine dinucleotide phosphate oxidase (NOX)-mediated redoxosome formation.
View Article and Find Full Text PDFTetrahedral Framework Nucleic Acid (tFNA)-Loaded Metformin (Met) Modulates Cellular Pyroptosis and AMPK to Ameliorate Type II Diabetic Periodontitis.
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January 2025
Sichuan Provincial Engineering Research Center of Oral Biomaterials, Chengdu, Sichuan, 610041, China.
Diabetic periodontitis presents a unique therapeutic challenge, primarily due to its chronic inflammatory profile and the associated bone loss driven by immune dysregulation. Metformin (Met) is recognized for its potent anti-inflammatory properties, yet its limited cellular uptake has hindered its clinical effectiveness in diabetic periodontitis. A tetrahedral framework nucleic acid (tFNA)-based delivery system is developed to enhance Met cellular uptake and investigate its effects on diabetic periodontitis in this study.
View Article and Find Full Text PDFZinc Combined with Metformin Corrects Zinc Homeostasis and Improves Steroid Synthesis and Semen Quality in Male Type 2 Diabetic Mice by Activating PI3K/AKT/mTOR Pathway.
Biol Trace Elem Res
January 2025
Hebei Key Laboratory of Reproductive Medicine, Hebei Reproductive Health Hospital, Shijiazhuang 050071, Hebei, China.
Male infertility is a common complication of diabetes. Diabetes leads to the decrease of zinc (Zn) content, which is a necessary trace element to maintain the normal structure and function of reproductive organs and spermatogenesis. The purpose of this study was to investigate the effect of metformin combined with zinc on testis and sperm in diabetic mice.
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