Loss of insulin signaling in hepatocytes leads to severe insulin resistance and progressive hepatic dysfunction.
By M. Michael, R. Kulkarni, C. Postic, S. Previs, Gerald I. Shulman, M. Magnuson, C. Kahn. Molecules and Cells, 2000
1,311 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology, Surgery
View Paper: https://www.semanticscholar.org/paper/5b08de6b883a53c374b72928131424c751934149
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Citations in the corpus
- Trends in insulin resistance: insights into mechanisms and therapeutic strategy (2022, background): “Specifically, the increased gluconeogenesis and decreased glycogen synthesis in hepatic IR results in fasting hyperglycemia that increases total TG levels and blood pressure (BP), reduces HDL-C levels, and increases the risk of thrombosis formation.(43,356) Moreover, long-term follow up data from pa”
- Mechanisms of insulin resistance in obesity (2013, background): “When these two molecules are deficient from gene inactivation in mice, insulin clearance will be blocked leading to hyperinsulinemia [74–76].”
- The plasticity of aging: insights from long-lived mutants. (2005, background): “First, the specific perturbation is important: whereas loss of the insulin receptor in adipose tissue extends mouse life span, its loss in the liver cause diabetes (Michael et al., 2000).”
- Beta Cell Dysfunction and Insulin Resistance (2013, background): “…systemic factors control beta cell proliferation, including the observation of beta cell hyperplasia in mice lacking insulin receptors in the liver (Michael et al., 2000; Kulkarni et al., 2004; Okada et al., 2007; Imai et al., 2008), and the demonstration that systemic factors in insulin resistant…”
- The forkhead transcription factor Foxo1 (Fkhr) confers insulin sensitivity onto glucose-6-phosphatase expression. (2001, background): “Evidence from clamped dogs (2) and genetically engineered mice indicates that insulin action on glucose production includes indirect and direct effects (3, 4).”
- Fat accumulation in the liver is associated with defects in insulin suppression of glucose production and serum free fatty acids independent of obesity in normal men. (2002, neutral): “insulinemia, glucose intolerance, or diabetes (28), whereas a similar maneuver in the liver leads to marked hyperinsulinemia under fasting conditions and in the fed state and diabetic glucose tolerance (29).”
- Energy Metabolism in the Liver (2014, neutral): “specific deletion of insulin receptors markedly increases hepatic gluconeogenesis in mice, resulting in hyperglycemia and glucose intolerance (173).”
- Selective versus total insulin resistance: a pathogenic paradox. (2008, background): “In this regard, it is of interest that hyperglycemia declines in LIRKO micewithage (Michael et al., 2000), afinding opposite that observed in ob/ob and lipodystrophic mice.”