Lipid-induced insulin resistance in human muscle is associated with changes in diacylglycerol, protein kinase C, and IkappaB-alpha.

By Samar I. Itani, N. Ruderman, Frank A. Schmieder, G. Boden. Diabetes, 2002

658 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/7e185ede5e9ba50f0fd2a3123f32bc12de8ade64

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Citations in the corpus

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. (2009, background): “Diacylglycerol is a known activator of novel PKC (51), and increases of both diacylglycerol and novel PKC activity are associated with lipid-induced insulin resistance (52, 53).”
Metabolic flexibility in health and disease (2017, unknown): “Similarly, lipid overload, often used as a model for insulin resistance (Brehm et al., 2006; Itani et al., 2002; Yu et al., 2002a), may represent a model of metabolic flexibility rather than revealing a pathological mechanism of insulin resistance.”
Insulin resistance, lipotoxicity, type 2 diabetes and atherosclerosis: the missing links. The Claude Bernard Lecture 2009 (2010, background): “In animals [147] and humans [148], plasma NEFA elevation by lipid infusion also increased intramyocellular diacylglycerol, a potent activator of protein kinase C (PKC) isoforms, which inhibit insulin signalling through serine phosphorylation of IRS-1 [149].”
Molecular Mechanisms of Insulin Resistance in Humans and Their Potential Links With Mitochondrial Dysfunction (2006, background): “In this regard, PKC- and PKC- and - have been shown to be activated during a lipid infusion in rodents (15,31) and humans (42), respectively.”
Inhibition of ceramide synthesis ameliorates glucocorticoid-, saturated-fat-, and obesity-induced insulin resistance. (2007, background): “Thus, some scientists have argued that it either is unimportant in lipid-induced insulin resistance or, alternatively, plays only a minor role in the regulation of glucose homeostasis following nutrient oversupply (Itani et al., 2002; Yu et al., 2002).”
Integrating Mechanisms for Insulin Resistance: Common Threads and Missing Links (2012, unknown): “Lipids infused together with insulin over 6 hr result in activation of PKC d (Itani et al., 2002).”
A ceramide-centric view of insulin resistance. (2012, background): “In an isolated muscle system, resistin was shown to blunt insulin action, but only in the presence of palmitate (Junkin et al., 2009).”
Disordered lipid metabolism and the pathogenesis of insulin resistance. (2007, unknown): “Candidates include members of the nPKC family, which may be activated by accumulation of lipid intermediates (particularly DAGs), as well as inflammatory intermediates such as IKK , JNK1, and tumor necrosis factor- .”
Non-Alcoholic Fatty Liver Disease as a Nexus of Metabolic and Hepatic Diseases (2017, unknown): “Lipid infusions in healthy human volunteers similarly increased skeletal muscle DAG, nPKC activation (both PKCd [Itani et al., 2002] and PKCq [Szendroedi et al., 2014]), and caused muscle insulin resistance.”