NDLI: Reconstitution of Insulin Action in Muscle, White Adipose Tissue, and Brain of Insulin Receptor Knock-out Mice Fails to Rescue Diabetes*

Content Provider	PubMed Central
Author	Lin, Hua V. Domenico, Accili
Abstract	Type 2 diabetes results from an impairment of insulin action. The first demonstrable abnormality of insulin signaling is a decrease of insulin-dependent glucose disposal followed by an increase in hepatic glucose production. In an attempt to dissect the relative importance of these two changes in disease progression, we have employed genetic knock-outs/knock-ins of the insulin receptor. Previously, we demonstrated that insulin receptor knock-out mice (Insr −/−) could be rescued from diabetes by reconstitution of insulin signaling in liver, brain, and pancreatic β cells (L1 mice). In this study, we used a similar approach to reconstitute insulin signaling in tissues that display insulin-dependent glucose uptake. Using GLUT4-Cre mice, we restored InsR expression in muscle, fat, and brain of Insr −/− mice (GIRKI (Glut4-insulin receptor knock-in line 1) mice). Unlike L1 mice, GIRKI mice failed to thrive and developed diabetes, although their survival was modestly extended when compared with Insr −/−. The data underscore the role of developmental factors in the presentation of murine diabetes. The broader implication of our findings is that diabetes treatment should not necessarily target the same tissues that are responsible for disease pathogenesis.
Related Links	http://dx.doi.org/10.1074/jbc.M110.210807
Starting Page	9797
File Format	PDF
ISSN	1083351X
e-ISSN	1083351X
Journal	The Journal of Biological Chemistry
Issue Number	11
Volume Number	286
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	2011-03-18
Access Restriction	Open
Rights Holder	American Society for Biochemistry and Molecular Biology
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Reconstitution of Insulin Action in Muscle, White Adipose Tissue, and Brain of Insulin Receptor Knock-out Mice Fails to Rescue Diabetes

Intrinsic Heterogeneity in Adipose Tissue of Fat-specific Insulin Receptor Knock-out Mice Is Associated with Differences in Patterns of Gene Expression

Hyperinsulinaemia increases insulin action in vivo in white adipose tissue but not in muscles.

Major Histocompatibility Class II Transactivator Expression in Smooth Muscle Cells from A2b Adenosine Receptor Knock-out Mice

Chronic treatment with myo-inositol reduces white adipose tissue accretion and improves insulin sensitivity in female mice.

Bex1 knock out mice show altered skeletal muscle regeneration

Insulin Hypersensitivity and Resistance to Streptozotocin-Induced Diabetes in Mice Lacking PTEN in Adipose Tissue

Adipose triglyceride lipase deficiency causes tissue-specific changes in insulin signaling.

Studies on the conversion of pyruvate into fatty acids in white adipose tissue. Effects of insulin, alloxan-diabetes and starvation

Reconstitution of Insulin Action in Muscle, White Adipose Tissue, and Brain of Insulin Receptor Knock-out Mice Fails to Rescue Diabetes*

Similar Documents

Reconstitution of Insulin Action in Muscle, White Adipose Tissue, and Brain of Insulin Receptor Knock-out Mice Fails to Rescue Diabetes

Intrinsic Heterogeneity in Adipose Tissue of Fat-specific Insulin Receptor Knock-out Mice Is Associated with Differences in Patterns of Gene Expression

Hyperinsulinaemia increases insulin action in vivo in white adipose tissue but not in muscles.

Major Histocompatibility Class II Transactivator Expression in Smooth Muscle Cells from A2b Adenosine Receptor Knock-out Mice

Chronic treatment with myo-inositol reduces white adipose tissue accretion and improves insulin sensitivity in female mice.

Bex1 knock out mice show altered skeletal muscle regeneration

Insulin Hypersensitivity and Resistance to Streptozotocin-Induced Diabetes in Mice Lacking PTEN in Adipose Tissue

Adipose triglyceride lipase deficiency causes tissue-specific changes in insulin signaling.

Studies on the conversion of pyruvate into fatty acids in white adipose tissue. Effects of insulin, alloxan-diabetes and starvation

Reconstitution of Insulin Action in Muscle, White Adipose Tissue, and Brain of Insulin Receptor Knock-out Mice Fails to Rescue Diabetes*