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Overcoming 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 PDFCombination of dapagliflozin and pioglitazone lacks superiority against monotherapy in streptozotocin-induced nephropathy.
Sci Rep
January 2025
Faculty of Pharmacy, Department of Pharmacology and Toxicology, Comenius University Bratislava, SK-83232, Bratislava, Slovakia.
Oxidative stress and apoptosis are highly engaged in development of diabetic nephropathy (DN). In monotherapy, dapagliflozin and pioglitazone positively modulate target organ damage even independently of their hypoglycaemic effect. This study evaluated whether a simultaneous PPARγ activation and SGLT cotransporter inhibition offer superior protection against DN-related oxidative and apoptotic processes in a T1DM rat model.
View Article and Find Full Text PDFActivation of PPARγ regulates M1/M2 macrophage polarization and attenuates dextran sulfate sodium salt-induced inflammatory bowel disease via the STAT-1/STAT-6 pathway.
Kaohsiung J Med Sci
December 2024
Department of Gastrointestinal Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
This study aimed to investigate whether activation of PPARγ regulates M1/M2 macrophage polarization to attenuate dextran sulfate sodium salt (DSS)-induced inflammatory bowel disease (IBD) via the STAT-1/STAT-6 pathway in vivo and in vitro. We first examined the effect of PPARγ on macrophage polarization in LPS/IFN-γ-treated M1 RAW264.7 cells and IL-4/IL-13-treated M2 RAW264.
View Article and Find Full Text PDFKetamine impairs the performance of male mice in novel recognition object test and reduces the immunoreactivity of GAD in the hippocampus: Role of pioglitazone.
Pharmacol Biochem Behav
December 2024
Programa de Pós-Graduação em Farmacologia, Universidade Federal de Santa Maria, RS, Brazil. Electronic address:
Schizophrenia is a mental disorder characterized by positive, negative, and cognitive symptoms which is treated with antipsychotics. However, these drugs present several side effects and, some schizophrenia symptoms, like cognitive, are difficult to treat. The peroxisome proliferator-activated receptors-gamma (PPAR-γ) are expressed in dopaminergic neurons of the midbrain participating in the modulation of dopamine-mediated behavior .
View Article and Find Full Text PDFOverview of diabetes agents in cardiovascular disease: it takes an orchestra to play Tchaikovsky in symphony.
Curr Opin Endocrinol Diabetes Obes
February 2025
Department of Endocrinology, Changi General Hospital.
Purpose Of Review: The aim of this review was to discuss the use and concerns of diabetes agents, clinical targets, and key aspects to be considered in the management of patients with type 2 diabetes mellitus (T2DM), and at high risk or established cardiovascular disease (CVD).
Recent Findings: The recent European and American guidelines recommended SGLT2 inhibitors and GLP-1 receptor agonists as the preferred first-line diabetes agents in patients with T2DM and CVD. This is a paradigm shift from using metformin as first-line therapy.
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