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Cisplatin exposure dysregulates insulin secretion in male and female mice.
Diabetes
January 2025
Department of Biology & Institute of Biochemistry, Carleton University, Ottawa, ON, Canada.
Cancer survivors have an increased risk of developing Type 2 diabetes compared to the general population. Patients treated with cisplatin, a common chemotherapeutic agent, are more likely to develop metabolic syndrome and Type 2 diabetes than age- and sex-matched controls. Surprisingly, the impact of cisplatin on pancreatic islets has not been reported.
View Article and Find Full Text PDFEvaluation of metabolic syndrome components, serum uric acid levels and epicardial adipose tissue thickness in pubertal children by severity of obesity.
Turk J Pediatr
December 2024
Department of Pediatric Cardiology, Ankara Bilkent City Hospital, Ankara, Türkiye.
Background: We aimed to evaluate how the parameters used in the diagnosis of metabolic syndrome (MetS) and parameters such as epicardial adipose tissue (EAT) thickness, insulin resistance (IR), and serum uric acid (SUA) are affected according to the severity of obesity.
Methods: A total of 120 obese patients aged 10-18 years were classified as class 1-2-3 according to their body mass index (BMI) score. SUA was measured and oral glucose tolerance tests were performed on all patients.
Effects of antidiabetic agents on lipid metabolism of skeletal muscle: A narrative review.
Diabetes Obes Metab
January 2025
Department of Endocrinology, First Hospital of Shanxi Medical University, Taiyuan, China.
Metabolic syndrome-related diseases frequently involve disturbances in skeletal muscle lipid metabolism. The accumulation of lipid metabolites, lipid-induced mitochondrial stress in skeletal muscle cells, as well as the inflammation of adjacent adipose tissue, are associated with the development of insulin resistance and metabolic dysfunction. Consequently, when antidiabetic medications are used to treat various chronic conditions related to hyperglycaemia, the impact on skeletal muscle lipid metabolism should not be overlooked.
View Article and Find Full Text PDFNon-alcoholic fatty liver disease (NAFLD) is a chronic condition characterized by hepatic steatosis in the absence of significant alcohol consumption and is increasingly recognized as the hepatic manifestation of metabolic syndrome (MetS). This review aims to explore the molecular mechanisms underlying the interaction between NAFLD, insulin resistance (IR), and MetS, with a focus on identifying therapeutic targets. A comprehensive review of existing literature on NAFLD, IR, and MetS was conducted.
View Article and Find Full Text PDFIntestinal epithelial cell NCoR deficiency ameliorates obesity and metabolic syndrome.
Acta Pharm Sin B
December 2024
State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
Nuclear receptor corepressor (NCoR1) interacts with various nuclear receptors and regulates the anabolism and catabolism of lipids. An imbalance in lipid/energy homeostasis is also an important factor in obesity and metabolic syndrome development. In this study, we found that the deletion of NCoR1 in intestinal epithelial cells (IECs) mainly activated the nuclear receptor PPAR and attenuated metabolic syndrome by stimulating thermogenesis.
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