Adipose tissue selective insulin receptor knockout protects against obesity and obesity-related glucose intolerance.

By M. Blüher, M. Michael, O. Peroni, K. Ueki, N. Carter, B. Kahn, C. R. Kahn. Developmental Cell, 2002

825 citations recorded by the source corpus.

Subfields: Endocrine and Autonomic Systems, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/6d5efdb71636f17fc93f124d13a931a8f0e16afe

How researchers see this paper

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

In Endocrine and Autonomic Systems

1. P. Scherer
2. B. Kahn
3. D. Hardie
4. Haiming Cao

In Epidemiology

1. H. Lodish
2. H. Ruan
3. P. Scherer
4. C. R. Kahn
5. Haiming Cao
6. M. Blüher
7. Byung-Cheol Lee
8. Jongsoon Lee

In Physiology

1. H. Lodish
2. K. Copps
3. H. Ruan
4. J. Silva
5. P. Scherer
6. J. Rutkowski
7. Lewis C. Cantley
8. B. Kahn

Citations in the corpus

• Role of caveolae and caveolins in health and disease. (2004, background): “Furthermore, the now dubious role of adipose tissue in whole body insulin resistance is supported by findings in Cav-1 null mice showing a 90% reduction in insulin receptor levels in adipocytes, without severe whole body insulin resistance, similar to findings reported in an adipose-tissue specific ”
• Regulation of insulin sensitivity by serine/threonine phosphorylation of insulin receptor substrate proteins IRS1 and IRS2 (2012, background): “in all tissues, exhibit abnormal or severely compromised adipocyte differentiation [16, 17].”
• A crucial role for adipose tissue p53 in the regulation of insulin resistance (2009, background): “In contrast, low circulating insulin concentrations are generally associated with longevity, and the activation of longevity signals in adipose tissue has been reported to lower the circulating insulin level and extend the lifespa”
• Insulin signaling in osteoblasts integrates bone remodeling and energy metabolism (2010, neutral): “Surprisingly, these studies failed to demonstrate a major influence of insulin signaling in the control of whole-body glucose homeostasis in two classical insulin target tissues, muscle, and white fat (Bluher et al., 2002; Bruning et al., 1998).”
• Transcriptional control of adipose lipid handling by IRF4 (2011, neutral): “Similarly, Irf4 mRNA levels were elevated in mice lacking insulin receptors exclusively in adipose tissue (so-called fat-specific insulin receptor knockout [FIRKO] mice [Bluher et al., 2002]) (Figure 1F).”
• 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).”
• Insulin resistance in adipose tissue: direct and indirect effects of tumor necrosis factor-alpha. (2003, background): “[15] Bluher M, Michael MD, Peroni OD, Ueki K, Carter N, Kahn BB, et al.”
• Inflammation, stress, and diabetes. (2005, neutral): “…that experimentally induced local inflammation or insulin resistance in adipose tissue, such as that in adipose-specific insulin receptor knockout mice and adipose-specific TNF transgenic mice, is metabolically favorable, resulting in a lean phenotype and systemic insulin sensitivity (103, 104).”
• Thermogenic mechanisms and their hormonal regulation. (2006, background): “Furthermore, normal muscle has the capacity to increase glucose consumption if more is available, as it occurs in the selective deletion IR in adipose tissue, which is associated with resistance to obesity and more glycolysis and glucose oxidation (27).”
• Adiponectin, Leptin, and Fatty Acids in the Maintenance of Metabolic Homeostasis Through Adipose Tissue Crosstalk (2016, result): “The results of this study initially appear to contradict the observation that mice with adipose-tissue-specific deletion of the insulin receptor (FIRKO) are leaner and are protected against age-related and diet-induced glucose intolerance (Blüher et al., 2002).”
• Developmental origin of fat: tracking obesity to its source. (2007, neutral): “…populations of adipocytes—one with a small diameter (<50 µm) and the other having a large diameter (>150 µm)—rather than a normal distribution of size (Bluher et al., 2002; Evidence for two distinct subtypes of preadipocytes in human subcutaneous fat can be found in differences in replication…”
• From mice to men: insights into the insulin resistance syndromes. (2006, background): “These differences become even more profound when control and FIRKO mice are put on a high-fat diet or are treated with gold thioglucose, a hypothalamic toxin that causes severe hyperphagia (11, 14).”