Reduced mitochondrial density and increased IRS-1 serine phosphorylation in muscle of insulin-resistant offspring of type 2 diabetic parents.

By K. Morino, K. Petersen, S. Dufour, D. Befroy, J. Frattini, Nadine Shatzkes, S. Neschen, M. White, S. Bilz, Sakiko Sono and 2 more. Journal of Clinical Investigation, 2005

841 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/e8ba7a44e9dc622cba4d34f025608b768b7cf333

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Citations in the corpus

Mechanisms of insulin resistance in obesity (2013, background): “Although the hypothesis explains the association of improved mitochondrial function and insulin sensitivity in the models of physical exercise in humans and rodents [55], most exiting evidence suggests that mitochondrial dysfunction is a result of insulin resistance [56–58], instead of a cause of in”
The pathogenesis of insulin resistance: integrating signaling pathways and substrate flux. (2016, background): “In contrast to aging, these reductions in mitochondrial activity appear to be secondary to reduction in mitochondrial density (54) and may be due in part to diminished expression of LpL in skeletal muscle, which could limit PPARδ-mediated mitochondrial biogenesis (55).”
Regulation of insulin sensitivity by serine/threonine phosphorylation of insulin receptor substrate proteins IRS1 and IRS2 (2012, background): “Given their co-incidence and propensity to aggravate one another, it cannot be stated whether hyperinsulinaemia or dyslipidaemia (or still other factors) underlie increased IRS S/T phosphorylation in the pre-diabetic period [85].”
Disordered lipid metabolism and the pathogenesis of insulin resistance. (2007, neutral): “Increases in intracellular DAG, due to increased lipogenesis and/or decreased mitochondrial fatty acid oxidation activate PKC- , which binds to and inactivates the insulin receptor kinase resulting in reduced insulin-stimulated IRS-1 and IRS-2 tyrosine phosphorylation.”
PGC-1 coactivators: inducible regulators of energy metabolism in health and disease. (2006, background): “separate recent study did not find a correlation between muscle mitochondrial derangements and PGC-1α levels in insulin-resistant humans (89).”
Peroxisome proliferator-activated receptor gamma coactivator 1 coactivators, energy homeostasis, and metabolism. (2006, result): “Moreover, at least one other study failed to replicate the PGC-1 dysregulation in skeletal muscle of type 2 diabetic patients (73).”
Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010, neutral): “Moreover, mitochondria of offspring of diabetic subjects are lower in density compared with those of controls (225).”