Singh S, Sharma R, Kumari M, Tiwari S. Insulin receptors in the kidneys in health and disease. World J Nephrol 2019; 8(1): 11-22 [PMID: 30705868 DOI: 10.5527/wjn.v8.i1.11]
本文章的通讯作者
Swasti Tiwari, PhD, Professor, Department of Molecular Medicine and Biotechnology, Sanjay Gandhi Postgraduate Institute and Chair of Medical Sciences, Lucknow 226014, India. tiwaris@sgpgi.ac.in
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Biochemistry & Molecular Biology
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
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Insulin receptors in the kidneys in health and disease
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Jan 21, 2019 (publication date) through Mar 28, 2024
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World Journal of Nephrology
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2220-6124
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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
World J Nephrol. Jan 21, 2019; 8(1): 11-22 Published online Jan 21, 2019. doi: 10.5527/wjn.v8.i1.11
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Figure 1 Architecture of insulin and insulin-like growth factor-1 receptors.
Insulin and IGF-1 receptors consist of two extracellular α-chains and two transmembrane β-chains. The α-subunits have binding sites for insulin and IGF-1, whereas the cytoplasmic kinase domain comprises major sites for tyrosine autophosphorylation that are crucial for receptor activation. The α- and β-subunits are connected together via disulfide linkages (Figure is adapted from reference[ 9]). IGF: Insulin-like growth factor.
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Figure 2 Schematics of the insulin receptor signaling.
Binding of insulin to its receptor causes autophosphorylation of specific tyrosine residues. Upon activation IR recruits different adaptor proteins and initiates a cascade of phosphorylation events. These signaling events ultimately lead to activation or repression of an array of proteins, which regulate various biological functions (Figure is adapted from reference[ 8]).
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Figure 3 Altered natriuresis and impaired nitric oxide metabolism in insulin receptor-knockout mice.
A: Urinary sodium excretion after oral administration of saline with and without dextrose in 4 h; B: Mean arterial blood pressure (ΔMAP) after NaCl and dextrose administration in mice; C: Urinary nitrate and nitrite excretion in wild-type and insulin receptor-knockout mice after 24 h. (Figure is a modification of figures published in reference[ 19] and taken with permission).
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Figure 4 Expression patterns of insulin receptor and gluconeogenic enzymes in normal and diabetic human kidney.
A: Expression of FBPase, PEPCK, IR, and tubulin in renal cortex biopsies of control and Type 2 diabetic individuals analyzed by western blotting; B: Immunohistochemical analysis of FBPase, PEPCK, and IR in renal cortex biopsies of control and Type 2 diabetic individuals (Figure is taken from reference number[ 6] with permission). PEPCK: Phosphoenolpyruvate carboxykinase; IR: Insulin receptor.
Citation: Singh S, Sharma R, Kumari M, Tiwari S. Insulin receptors in the kidneys in health and disease. World J Nephrol 2019; 8(1): 11-22