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Skeletal Muscle–Specific Deletion of Lipoprotein Lipase Enhances Insulin Signaling in Skeletal Muscle but Causes Insulin Resistance in Liver and Other Tissues

Wang, Hong, Knaub, Leslie A., Jensen, Dalan R., Young Jung, Dae, Hong, Eun-Gyoung, Ko, Hwi-Jin, Coates, Alison M., Goldberg, Ira J., de la Houssaye, Becky A., Janssen, Rachel C., McCurdy, Carrie E., Rahman, Shaikh M., Soo Choi, Cheol, Shulman, Gerald I., Kim, Jason K., Friedman, Jacob E., Eckel, Robert H.·2009·Diabetes
DOI 10.2337/db07-1839PMC PMC2606858
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Abstract

OBJECTIVE: Skeletal muscle–specific LPL knockout mouse (SMLPL−/−) were created to study the systemic impact of reduced lipoprotein lipid delivery in skeletal muscle on insulin sensitivity, body weight, and composition. RESEARCH DESIGN AND METHODS: Tissue-specific insulin sensitivity was assessed using a hyperinsulinemic-euglycemic clamp and 2-deoxyglucose uptake. Gene expression and insulin-signaling molecules were compared in skeletal muscle and liver of SMLPL−/− and control mice. RESULTS: Nine-week-old SMLPL−/− mice showed no differences in body weight, fat mass, or whole-body insulin sensitivity, but older SMLPL−/− mice had greater weight gain and whole-body insulin resistance. High-fat diet feeding accelerated the development of obesity. In young SMLPL−/− mice, insulin-stimulated glucose uptake was increased 58% in the skeletal muscle, but was reduced in white adipose tissue (WAT) and heart. Insulin action was also diminished in liver: 40% suppression of hepatic glucose production in SMLPL−/− vs. 90% in control mice. Skeletal muscle triglyceride was 38% lower, and insulin-stimulated phosphorylated Akt (Ser473) was twofold greater in SMLPL−/− mice without changes in IRS-1 tyrosine phosphorylation and phosphatidylinositol 3-kinase activity. Hepatic triglyceride and liver X receptor, carbohydrate response element–binding protein, and PEPCK mRNAs were unaffected in SMLPL−/− mice, but peroxisome proliferator–activated receptor (PPAR)-γ coactivator-1α and interleukin-1β mRNAs were higher, and stearoyl–coenzyme A desaturase-1 and PPARγ mRNAs were reduced. CONCLUSIONS: LPL deletion in skeletal muscle reduces lipid storage and increases insulin signaling in skeletal muscle without changes in body composition. Moreover, lack of LPL in skeletal muscle results in insulin resistance in other key metabolic tissues and ultimately leads to obesity and systemic insulin resistance.

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Research works printed but not linked: 31

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Metadata

Authors
Wang, H., Knaub, L. A., Jensen, D. R., Young Jung, D., Hong, E.-G., Ko, H.-J., Coates, A. M., Goldberg, I. J., de la Houssaye, B. A., Janssen, R. C., McCurdy, C. E., Rahman, S. M., Soo Choi, C., Shulman, G. I., Kim, J. K., Friedman, J. E., & Eckel, R. H.
Affiliations
  • Division of Endocrinology, Metabolism and Diabetes, University of Colorado Denver Anschutz Medical Campus, Aurora, Colorado;
  • Department of Cellular & Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania;
  • Department of Medicine, Columbia University, New York City, New York;
  • Department of Pediatrics, University of Colorado Denver Anschutz Medical Campus, Aurora, Colorado;
  • Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut;
  • Department of Internal Medicine, Department of Cellular & Molecular Physiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut.
Venue
Diabetes
Publisher
American Diabetes Association
Published
2008-10-24
Volume
58
Issue
1
Pages
116-124
ISSN
  • 0012-1797
  • 1939-327X
DOI
10.2337/db07-1839
PMC
PMC2606858
Cited by
91
References
5
Language
en
Licence
creativecommons.org/licenses/by-nc-nd/3.0/ (vor, 4690 d)

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