Targeted disruption of AdipoR1 and AdipoR2 causes abrogation of adiponectin binding and metabolic actions

By Toshimasa Yamauchi, Yasunori Nio, Toshiyuki Maki, Masaki Kobayashi, Takeshi Takazawa, Masato Iwabu, Miki Okada-Iwabu, Sachiko Kawamoto, N. Kubota, Tetsuya Kubota and 19 more. Nature Medicine, 2007

1,388 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/99672ea100ae8a1d290db809c8a5a6143202eff5

How researchers see this paper

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

In Cardiology and Cardiovascular Medicine

1. H. Fang
2. R. L. Judd
3. Herbert Tilg
4. A. Moschen
5. K. Walsh
6. J. Forbes
7. P. Scherer
8. N. Ouchi

In Epidemiology

1. H. Fang
2. R. L. Judd
3. P. Scherer
4. Herbert Tilg
5. A. Moschen
6. Takashi Kadowaki
7. K. Walsh
8. Toshimasa Yamauchi

In Physiology

1. H. Fang
2. R. L. Judd
3. P. Scherer
4. Sushil Kumar Jain
5. Herbert Tilg
6. Toshimasa Yamauchi
7. A. Moschen
8. Takashi Kadowaki

Citations in the corpus

• Metabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training (2013, neutral): “Experimental disruption of AdipoR1 or R2 causes blunted adiponectin-induced AMPK and PPARα responses, respectively, both leading to increased hepatic glucose production and hepatic insulin resistance (708).”
• Mechanisms of diabetic complications. (2013, background): “Adiponectin circulates in multimeric forms and binds to two adiponectin receptors (AdipoR1 and AdipoR2) inducing signaling via stimulation of 5’-adenosine monophosphate activated protein (AMPK) and likely other intracellular pathways (658).”
• GENeration (2015, neutral): “Once the "front-end" concept was working, the remaining conversion effort, to get all of NASTRAN on a "4G" computer, while involving significant volumes of code, would not require the further system type extensions.”
• Trends in insulin resistance: insights into mechanisms and therapeutic strategy (2022, background): “Thus, chemerin may increase insulin sensitivity in adipose tissue.(141,142) Adipocytes also produce apelin that is increased in insulin resistant individuals(143) and morbidly obese subjects with T2DM.”
• Regulation of energy metabolism by long-chain fatty acids. (2014, background): “In contrast, ADIPOR1 and 2 double knockout mice developed severe insulin resistance including elevated plasma insulin by glucose tolerance test [220].”
• Inflammatory Mechanisms in the Regulation of Insulin Resistance (2008, background): “The importance of targeted disruption of adipoR1 and R2 has recently been demonstrated (43).”
• Adiponectin, a Therapeutic Target for Obesity, Diabetes, and Endothelial Dysfunction (2017, background): “Although AdipoR1 and AdipoR2 are mainly involved in the metabolic action of adiponectin, some studies have investigated other receptors for adiponectin in heart [31,82].”
• Adiponectin stimulates AMP-activated protein kinase in the hypothalamus and increases food intake. (2007, background): “The blood-CSF barrier in the choroid plexus and the BBB in the cerebral endothelium are the two major sites controlling the entry of proteins into the brain (Zlokovic et al., 2000; Schwartz and Porte, 2005).”
• Adipokines in inflammation and metabolic disease (2011, background): “Accordingly, adiponectin receptor 1 deficiency results in reduced adiponectin-induced AMPK activation, increased glucose production and impaired insulin resistance, whereas adiponectin receptor 2 deficiency causes decreased activity of PPARα signalling pathways and enhanced insulin resistanc”