Publications by authors named "K Maedler"
Intermittent fasting (IF) improves metabolic health in some individuals but increases health risks in others. Matta et al. now show that IF oppositely affects β cells depending on age: beneficial at old but deleterious at young age.
View Article and Find Full Text PDFWhile pancreatic beta-cell proliferation has been extensively studied, the role of cell death during islet development remains incompletely understood. Using a genetic model of caspase inhibition in beta cells coupled with mathematical modeling, we here discover an onset of beta-cell death in juvenile zebrafish, which regulates beta-cell mass. Histologically, this beta-cell death is underestimated due to phagocytosis by resident macrophages.
View Article and Find Full Text PDFCD36 inhibition corrects lipid-FetuinA mediated insulin secretory defects by preventing intracellular lipid accumulation and inflammation in the pancreatic beta cells.
Biochim Biophys Acta Mol Basis Dis
February 2025
Article Synopsis
- CD36 is a protein that helps with fat uptake and immune response, and it's found to be more active in the pancreatic islets of obese diabetic people, which can lead to issues with insulin secretion.
- The study found that when beta cells were exposed to a combination of palmitate (a fatty acid) and fetuinA (a protein linked to inflammation), it triggered an inflammatory response that worsened lipid buildup and insulin secretion problems.
- Inhibiting CD36 or the inflammatory receptor TLR4 helped reduce this lipid accumulation and restored insulin secretion in beta cells, indicating that targeting CD36 could be a potential treatment for obesity-related beta cell dysfunction.
Article Synopsis
- * Researchers developed a small molecule inhibitor called mCLC846 that targets serine/threonine kinase MST1/2 to enhance liver regeneration, particularly in models that replicate diseased patient conditions.
- * In preclinical studies, mCLC846 not only accelerated liver regeneration and improved survival rates in mice with metabolic liver disease but also activated key regenerative pathways in the liver after surgical resection.
Progression of β-cell loss in diabetes mellitus is significantly influenced by persistent hyperglycemia. At the cellular level, a number of signaling cascades affect the expression of apoptotic genes, ultimately resulting in β-cell failure; these cascades have not been elucidated. Mitochondrial aldehyde dehydrogenase-2 (ALDH2) plays a central role in the detoxification of reactive aldehydes generated from endogenous and exogenous sources and protects against mitochondrial deterioration in cells.
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