Tissue-specific overexpression of lipoprotein lipase causes tissue-specific insulin resistance
By Jason K. Kim, Jonathan J. Fillmore, Yan Chen, Chun-lian Yu, Irene K. Moore, M. Pypaert, E. P. Lutz, Yuko Kako, W. Vélez-Carrasco, I. Goldberg and 2 more. Proceedings of the National Academy of Sciences of the United States of America, 2001
741 citations recorded by the source corpus.
Subfields: Biochemistry, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/a84a9ecb23ebeffcf843a7203ba0dfc130b09f2e
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Biochemistry
- Gerald I. Shulman
- V. Samuel
- Ralph DeFronzo
- Muhammad Abdul-Ghani
- P. Scherer
- Xianlin Han
- Liangyou Rui
- R. Medzhitov
In Molecular Biology
- Gerald I. Shulman
- Ralph DeFronzo
- K. Petersen
- V. Samuel
- Muhammad Abdul-Ghani
- Liangyou Rui
- Xianlin Han
- M. Trujillo
In Physiology
- Gerald I. Shulman
- V. Samuel
- Ralph DeFronzo
- K. Petersen
- K. Morino
- Muhammad Abdul-Ghani
- Liangyou Rui
- M. Trujillo
Citations in the corpus
- Lipoprotein lipase: from gene to obesity. (2009, background): “When LPL is overexpressed in the liver in mice, a twofold increase in liver TG content and insulin resistance is observed (119).”
- The pathogenesis of insulin resistance: integrating signaling pathways and substrate flux. (2016, background): “Similarly, mice overexpressing LpL in the liver develop hepatic steatosis and liver-specific insulin resistance (65).”
- Leptin reverses insulin resistance and hepatic steatosis in patients with severe lipodystrophy. (2002, positive): “In the livers of both lipodystrophic mice (19) and transgenic mice with steatosis due to over-expression of lipoprotein lipase (20), decreased insulin activation of IRS-2–associated phosphatidylinositol 3-kinase activity was observed.”
- The effects of rosiglitazone on insulin sensitivity, lipolysis, and hepatic and skeletal muscle triglyceride content in patients with type 2 diabetes. (2002, positive): “In support of fatty acids being an important factor in this regard, recent studies have demonstrated a strong relationship between tissue lipid content and insulin resistance in both skeletal muscle (14–20) and liver (15,16,21).”
- The cardiac phenotype induced by PPARalpha overexpression mimics that caused by diabetes mellitus. (2002, background): “(39) recently demonstrated that transgenic overexpression of lipoprotein lipase in skeletal muscle caused insulin resistance in nondiabetic mice.”
- Non-Alcoholic Fatty Liver Disease as a Nexus of Metabolic and Hepatic Diseases (2017, positive): “Similarly, mice overexpressing LpL in the liver develop hepatic steatosis and liver-specific insulin resistance (Kim et al., 2001).”
- Energy Metabolism in the Liver (2014, positive): “Transgenic mice with liver-specific overexpression of LPL develop hepatic steatosis and insulin resistance (114).”
- Insulin Resistance: From Mechanisms to Therapeutic Strategies (2021, background): “In addition, overexpression of lipoprotein lipase (LPL) in liver or muscle induced peripheral insulin resistance and the accumulation of lipid in respective tissues [87,88], and skeletal muscle-specific LPL deletion enhanced”