Adipose-selective targeting of the GLUT4 gene impairs insulin action in muscle and liver

By E. Dale Abel, O. Peroni, Jason K. Kim, Young-Bum Kim, O. Boss, Ed Hadro, T. Minnemann, Gerald I. Shulman, B. Kahn. Nature, 2001

1,260 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology, Surgery

View Paper: https://www.semanticscholar.org/paper/b841c06db015fdc9dc2d635578ce78893f18611c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. Gerald I. Shulman
2. Max C. Petersen
3. V. Samuel
4. B. Thorens
5. Christopher B. Newgard
6. M. Mueckler
7. A. Hevener
8. R. Barnard

In Physiology

1. J. Kirkland
2. T. Tchkonia
3. V. Samuel
4. Max C. Petersen
5. Gerald I. Shulman
6. Christopher B. Newgard
7. I. Wood
8. A. Hevener

In Surgery

1. Gerald I. Shulman
2. V. Samuel
3. Max C. Petersen
4. B. Thorens
5. M. Mueckler
6. C. R. Kahn
7. R. Barnard
8. B. Kahn

Citations in the corpus

• Mechanisms of Insulin Action and Insulin Resistance. (2018, background): “Despite this, adipose-specific deletion of GLUT4 in mice results in liver and skeletal muscle insulin resistance without altering adiposity or body weight (1), pointing to indirect, physiologically significant consequences of insulin resistance to glucose uptake in adipocytes (725).”
• Beneficial effects of subcutaneous fat transplantation on metabolism. (2008, background): “Conversely, specific impairment of glucose transporter 4 (GLUT4) in adipose tissue results in decreased glucose uptake into muscle, possibly as a result of altered release of specific molecules from fat (Abel et al., 2001).”
• MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity. (2006, background): “Mice that lack the glucose transporter GLUT4 specifically in adipocytes manifest insulin resistance in remote organs such as the liver and skeletal muscle (17), suggesting that adipocytes deficient in GLUT4-mediated glucose uptake might secrete a factor (or factors) that induces insulin resistance i”
• Discovery of a class of endogenous mammalian lipids with anti-diabetic and anti-inflammatory effects (2014, background): “Glut4 knockdown selectively in adipocytes in mice results in insulin resistance and increased T2D risk (Abel et al., 2001), whereas adipose-selective overexpression of Glut4 (AG4OX) lowers fasting glycemia and enhances glucose tolerance (Carvalho et al., 2005; Shepherd et al., 1993).”
• Transcriptional control of adipose lipid handling by IRF4 (2011, neutral): “Cre-lox recombination offers such an opportunity; however, the traditional adipose-selective Cre-driver mouse uses the Fabp4 (also called aP2) promoter (Abel et al., 2001; Barlow et al., 1997).”
• The pathogenesis of insulin resistance: integrating signaling pathways and substrate flux. (2016, background): “For example, loss of adipose GLUT4 in mice does not alter adiposity or weight gain but leads to insulin resistance in skeletal muscle and liver (84).”
• TNF-α and adipocyte biology (2007, neutral): “systemic glucose intolerance and hyperinsulinaemia [59].”
• Increased Insulin Sensitivity and Reduced Adiposity in Phosphatidylinositol 5-Phosphate 4-Kinase β−/− Mice (2004, background): “However, the physiology of glucose homeostasis is controlled by complex communication between multiple tissues, including the brain (1, 4, 5, 18, 19, 24).”
• Glucose transporters (GLUT and SGLT): expanded families of sugar transport proteins (2003, background): “Global or tissue-specific GLUT4 knockout mouse models (Katz et al. 1995; Stenbit et al. 1997; Zisman et al. 2000; Abel et al. 2001) exhibit a varying degree of pathophysiology relating to type II diabetes.”