Biochemical Basis and Clinical Consequences of Glucolipotoxicity: A Primer
Abbreviated Journal Title
Heart Fail. Clin.
Glucolipotoxicity; Pancreatic beta-cell dysfunction; Insulin resistance; RAT PANCREATIC-ISLETS; DEPENDENT DIABETES-MELLITUS; INSULIN; GENE-TRANSCRIPTION; BETA-CELL DYSFUNCTION; FREE FATTY-ACIDS; ACTIVATED; SIGNALING PATHWAYS; AORTIC ENDOTHELIAL-CELLS; LOW-DENSITY LIPOPROTEINS; CORONARY-ARTERY-DISEASE; LONG-TERM EXPOSURE; Cardiac & Cardiovascular Systems
Both glucose and fatty acids may have good/adaptive or toxic/maladaptive actions on the pancreatic beta cell, depending on their concentrations. Hyperglycemia, via metabolic intermediates, may result in multiple cellular effects that are toxic to the pancreatic beta cell and indeed other tissues. While free fatty acids may affect cellular processes beyond lipid metabolism by interacting with transcription factors, triglyceride rich lipoproteins are endothelial cell-toxic and facilitate atherogenesis. The paradigm of "glucolipotoxicity" espouses that increased glucose and fatty acid levels act synergistically in causing toxicity to pancreatic islets and other organs, a process that eventually leads to the multiple defects seen in the metabolic syndrome and diabetes mellitus.
Heart Failure Clinics
"Biochemical Basis and Clinical Consequences of Glucolipotoxicity: A Primer" (2012). Faculty Bibliography 2010s. 3343.