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Transgenic rescue of insulin receptor–deficient mice
Haruka Okamoto, … , Ioannis Dragatsis, Domenico Accili
Haruka Okamoto, … , Ioannis Dragatsis, Domenico Accili
Published July 15, 2004
Citation Information: J Clin Invest. 2004;114(2):214-223. https://doi.org/10.1172/JCI21645.
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Article Metabolism Article has an altmetric score of 11

Transgenic rescue of insulin receptor–deficient mice

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Abstract

The role of different tissues in insulin action and their contribution to the pathogenesis of diabetes remain unclear. To examine this question, we have used genetic reconstitution experiments in mice. Genetic ablation of insulin receptors causes early postnatal death from diabetic ketoacidosis. We show that combined restoration of insulin receptor function in brain, liver, and pancreatic β cells rescues insulin receptor knockout mice from neonatal death, prevents diabetes in a majority of animals, and normalizes adipose tissue content, lifespan, and reproductive function. In contrast, mice with insulin receptor expression limited to brain or liver and pancreatic β cells are rescued from neonatal death, but develop lipoatrophic diabetes and die prematurely. These data indicate, surprisingly, that insulin receptor signaling in noncanonical insulin target tissues is sufficient to maintain fuel homeostasis and prevent diabetes.

Authors

Haruka Okamoto, Jun Nakae, Tadahiro Kitamura, Byung-Chul Park, Ioannis Dragatsis, Domenico Accili

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Figure 3

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Immunoblot analysis of Insr expression in different tissues of the trans...
Immunoblot analysis of Insr expression in different tissues of the transgenic knockouts. (A) Liver. The upper panel represents an autoradiogram showing immunoreactivity with anti-Insr antiserum; the lower panel shows an immunoblot with anti-tubulin antiserum to confirm equal loading of all lanes. We used 3- to 4-month-old animals for these determinations. (B) Islets. For these experiments, we partially purified islets by Ficoll density gradient centrifugation. Please note the prominent band corresponding to the receptor precursor (Insr precursor). To normalize for β-cell content, we used the β cell–specific marker Glut2 (middle panel). We used tubulin to normalize for total protein content (bottom panel). We used 2-month-old animals for these experiments. (C) Widespread transgene expression in brains of L1 Ttr-Insr mice. We obtained specimens from different brain sections and analyzed them by immunoblot. On the left, we present a control obtained with anti–glutamate receptor antiserum (GluR) to normalize for gel loading. On the right, we show immunoblots with anti-Insr antiserum. Arrows indicate the position of the Insr β-subunit. We used 3- to 4-month-old animals for these determinations. (D) Lack of Insr expression in muscle, heart, spleen, and adipose tissue. We show representative blots of 3- to 4-month-old mice. We obtained similar results with specimens from mice of different ages. We could not obtain adipose tissue from L2 and L3 mice because they are lipoatrophic.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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