ArticleDiabetes2009
Skeletal muscle-specific deletion of lipoprotein lipase enhances insulin signaling in skeletal muscle but causes insulin resistance in liver and other tissues.
Article in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 64 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
64 citing papers in PubMed, 110 citations in OpenAlex.
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- Insulin Resistance, Obesity, and Lipotoxicity.Advances in experimental medicine and biology · 2024Review
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- HM-Chromanone, a Major Homoisoflavonoid inNutrients · 2022Article
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- Insulin Resistance: From Mechanisms to Therapeutic Strategies.Diabetes & metabolism journal · 2022Review
- An updated ANGPTL3-4-8 model as a mechanism of triglyceride partitioning between fat and oxidative tissues.Progress in lipid research · 2022Review
- Genetic association ofCardiovascular endocrinology & metabolism · 2021Article
- The phospholipase A2 family's role in metabolic diseases: Focus on skeletal muscle.Physiological reports · 2021Review
- Association between ANGPTL3, 4, and 8 and lipid and glucose metabolism markers in patients with diabetes.PloS one · 2021Article
- GIP Receptor Antagonist, SKL-14959 Indicated Alteration of the Lipids Metabolism to Catabolism by the Inhibition of Plasma LPL Activity, Resulting in the Suppression of Weight Gain on Diets-Induced Obesity Mice.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- Carcinoembryonic Cell Adhesion-Related Molecule 2 Regulates Insulin Secretion and Energy Balance.International journal of molecular sciences · 2019Review
- Omega-3 Fatty Acids-Enriched Fish Oil Activates AMPK/PGC-1α Signaling and Prevents Obesity-Related Skeletal Muscle Wasting.Marine drugs · 2019Article
- Adipose Tissue Dysfunction as Determinant of Obesity-Associated Metabolic Complications.International journal of molecular sciences · 2019Review
- Mechanisms of obesity-induced metabolic and vascular dysfunctions.Frontiers in bioscience (Landmark edition) · 2019Review
- Mechanisms of Insulin Action and Insulin Resistance.Physiological reviews · 2018Review
- Article
- Roles of Peroxisome Proliferator-Activated Receptor Gamma on Brain and Peripheral Inflammation.Cellular and molecular neurobiology · 2018Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
17 authors at 5 institutions in 1 country.
Funding
Abstract
objectiveSkeletal 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
methodsTissue-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.
resultsNine-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)-gamma coactivator-1alpha and interleukin-1beta mRNAs were higher, and stearoyl-coenzyme A desaturase-1 and PPARgamma mRNAs were reduced.
conclusionsLPL 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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.