Coordinated reduction of genes of oxidative metabolism in humans with insulin resistance and diabetes: Potential role of PGC1 and NRF1

By M. Patti, Atul J. Butte, Sarah Crunkhorn, K. Cusi, R. Berria, S. Kashyap, Y. Miyazaki, Isaac S. Kohane, M. Costello, Robert A. Saccone and 7 more. Proceedings of the National Academy of Sciences of the United States of America, 2003

2,100 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/f12533a17bac59646b2dbd3ba620a48e5784cdf5

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Alternative M2 activation of Kupffer cells by PPARdelta ameliorates obesity-induced insulin resistance. (2008, background): “Since reduction in oxidative phosphorylation (OXPHOS) is causally linked to development of insulin resistance in mice and humans (Mootha et al., 2003; Patti et al., 2003; Petersen et al., 2003; Vianna et al., 2006), we looked for evidence ofmitochondrialdysfunction inall three tissues.”
Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010, neutral): “Family members of persons with insulin-resistant type 2 diabetes (247) demonstrate reduced expression of the PGC-1 a and PGC-1 b , coactivators of NRF-1 and PPAR g -dependent transcription involved in the expression of multiple genes associated with oxidative phosphorylation.”
Metabolic control through the PGC-1 family of transcription coactivators. (2005, background): “Transcription factor targets of the PGC-1 coactivators Transcription factor PGC-1α PGC-1β Function References NRF-1 + + mitochondrial genes Wu et al., 1999 NRF-2 + ND mitochondrial genes Mootha et al., 2003 PPARα + + fatty-acid oxidation Vega et al., 2000 PPARβ/δ + ND fatty-acid oxidation Wang et al”
Deficiency of subsarcolemmal mitochondria in obesity and type 2 diabetes. (2005, background): “Two recently published studies using gene array expression analyses have reported a significant decrease in the nuclear expression of genes encoding proteins of oxidative phosphorylation and other mitochondrial proteins in type 2 diabetes (42,43).”
Mitochondrial remodeling in adipose tissue associated with obesity and treatment with rosiglitazone. (2004, background): “A link between insulin resistance and the mitochondrial oxidative phosphorylation pathway has recently emerged in the analysis of genes expressed in human populations of insulin-resistant individuals (25, 26).”
Insulin resistance, lipotoxicity, type 2 diabetes and atherosclerosis: the missing links. The Claude Bernard Lecture 2009 (2010, background): “A twofold increase of plasma NEFA in participants with normal glucose tolerance reduced muscle expression of PGC-1 and multiple mitochondrial genes to levels observed in diabetic individuals [134], providing evidence of ‘mitochondrial lipotoxicity’.”
Fiber types in mammalian skeletal muscles. (2011, background): “ity, may contribute to insulin resistance and type 2 diabetes (492, 590).”
Pathogenesis of Insulin Resistance in Skeletal Muscle (2010, background): “The decrease in mitochondrial density in skeletal muscle in insulin-resistant individuals is consistent with decreased expression of PGC-1 gene [113], the master regulator for mitochondrial biogenesis.”
Skeletal Muscle Insulin Resistance Is the Primary Defect in Type 2 Diabetes (2009, background): “Recently, two groups independently showed that NGT offspring of two type 2 diabetic parents had a reduced expression of key mitochondrial genes involved in the regulation of oxidative metabolism in skeletal muscle (63,64).”