lipotoxicity

lipotoxicity

The pathologic changes in organs resultant from elevated fat levels in blood or tissues, as in the diabetic liver.
Farlex Partner Medical Dictionary © Farlex 2012

lipotoxicity

(lip″ŏ-tok-sis′ĭt-ē) [ lipo- + toxicity]
The adverse effects on glucose metabolism of excessive concentrations of free fatty acids in the blood. These effects include an increase in the resistance of the liver and muscle to the effects of insulin, an increase in glucose production, and reductions in insulin secretion by the pancreas.
Medical Dictionary, © 2009 Farlex and Partners
References in periodicals archive ?
And it was suggested that excess lipid accumulation may lead to lipotoxicity and may be the major driver of organ dysfunction (Decleves & Sharma, 2015).
Fenofibrate improves renal lipotoxicity through activation of AMPK-PGC-1[alpha] in db/db mice.
The damage mechanism of lipotoxicity on microvascular endothelial cells is the increasing production of reactive oxygen species (ROS) caused by the up regulation of the expression level of the NADPH oxidase complex active functional subunit 16.
Beta cell glucose toxicity, lipotoxicity and chronic oxidative stress in type 2 diabetes.
Insulin resistance, lipotoxicity, type 2 diabetes and atherosclerosis: the missing links.
High-fat diet-induced juvenile obesity leads to cardiomyocyte dysfunction and upregulation of Foxo3a transcription factor independent of lipotoxicity and apoptosis.
This is called the "thrifty phenotype hypothesis." [10] And the third is, unfavourable metabolic environment, especially increased glucose levels which may induce glucotoxicity and a persistent increase in NEFA levels that may induce lipotoxicity. [11] Gluco-lipotoxicity and the resultant increase in inflammatory mediators are also important.
Heparin has a transient effect in lowering triglyceride levels, it may have potential risk of lipotoxicity from free fatty acids and increased incidence of bleeding.
Beta-cell glucose toxicity, lipotoxicity, and chronic oxidative street in type 2 diabetes.
The excess fatty acids interfere with insulin receptor signaling and lead to decreased glucose transport, often referred to as lipotoxicity. They also activate protein kinase C.
Gilead is advancing multiple novel investigational compounds for the treatment of advanced fibrosis due to NASH, evaluating single-agent and combination therapy approaches against the core pathways associated with NASH hepatocyte lipotoxicity, inflammation and fibrosis.
The adaptive endoplasmic reticulum stress response to lipotoxicity in progressive human nonalcoholic fatty liver disease.