Liver-specific disruption of PPARgamma in leptin-deficient mice improves fatty liver but aggravates diabetic phenotypes.

By K. Matsusue, M. Haluzík, G. Lambert, S. Yim, O. Gavrilova, J. Ward, B. Brewer, M. Reitman, F. Gonzalez. Journal of Clinical Investigation, 2003

620 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/72c59ba3b13750ecc7f1274ea948a3008f6a6ad1

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Citations in the corpus

Enzymes of triacylglycerol synthesis and their regulation. (2004, methodology): “This idea is supported by studies of a liver-specific disruption of PPARg on an ob/ob background [233].”
Triglyceride metabolism in the liver (2017, neutral): “Fsp27 is a target gene of PPAR γ and its transcription is decreased in ob/ob mice with liver-specific knockdown of PPAR γ , accompanied by decreased TG content in the liver (175,176).”
Time-restricted feeding is a preventative and therapeutic intervention against diverse nutritional challenges (2014, background): “’’ Elevated hepatic PPARg is a protective measure to prevent serum hyperlipidemia, triglyceride accumulation in other tissues, and associated insulin resistance (Matsusue et al., 2003).”
Hepatocyte-specific Pten deficiency results in steatohepatitis and hepatocellular carcinomas. (2004, background): “However, PPARγ overexpression in mouse liver enhances SCD1 expression (10), while PPARγ deficiency reduces it (36).”
Lipid metabolism and liver inflammation. II. Fatty liver disease and fatty acid oxidation. (2006, background): “The transcription factor PPAR- is expressed at very low levels in the liver, and overexpression of this transcription factor in the liver leads to hepatic adiposis (adipogenic hepatic steatosis) with the expression of several adipogenic genes in the liver (16, 24).”
Energy Metabolism in the Liver (2014, neutral): “The levels PPARγ in the liver are low in normal mice and increase in mice with obesity (65, 167, 178).”
Molecular mediators of hepatic steatosis and liver injury. (2004, neutral): “The genetic deletion of hepatic PPAR-γ in livers of either ob/ob (44) or AZIP-F-1 (45) mice markedly attenuates the development of hepatic steatosis, independent of the presence of hyperinsulinemia or hyperglycemia.”
The cellular and signaling networks linking the immune system and metabolism in disease (2012, background): “Conversely, local changes in insulin sensitivity in live”