ArticleThe Journal of clinical investigation1996
Glycogen synthase activity is reduced in cultured skeletal muscle cells of non-insulin-dependent diabetes mellitus subjects. Biochemical and molecular mechanisms.
Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03665051 (Electrical Stimulation of Human Myocytes in Microgravity), which is not on this map. Cited by 27 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.
The trial behind it
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.
Electrical Stimulation of Human Myocytes in Microgravity: An In Vitro Model to Evaluate Therapeutics to Counteract Muscle Wasting (microG)
Who cites it
27 citing papers in PubMed, 130 citations in OpenAlex.
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- Insulin Resistance in Skeletal Muscle of Chronic Stroke.Brain sciences · 2020Article
- Gut microbiota and metabolic health among overweight and obese individuals.Scientific reports · 2020Article
- Engineered skeletal muscles for disease modeling and drug discovery.Biomaterials · 2019Review
- AJS1669, a novel small-molecule muscle glycogen synthase activator, improves glucose metabolism and reduces body fat mass in mice.International journal of molecular medicine · 2017Article
- Deficiency of a glycogen synthase-associated protein, Epm2aip1, causes decreased glycogen synthesis and hepatic insulin resistance.The Journal of biological chemistry · 2013Article
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- Is there a metabolic program in the skeletal muscle of obese individuals?Journal of obesity · 2011Article
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- GSK-3beta and control of glucose metabolism and insulin action in human skeletal muscle.Molecular and cellular endocrinology · 2010Article
- Myotoxic reactions to lipid-lowering therapy are associated with altered oxidation of fatty acids.Endocrine · 2009Article
- Polycystic ovary syndrome is associated with tissue-specific differences in insulin resistance.The Journal of clinical endocrinology and metabolism · 2009Article
- Transcriptional profiling of myotubes from patients with type 2 diabetes: no evidence for a primary defect in oxidative phosphorylation genes.Diabetologia · 2008Article
- Isoform-specific defects of insulin stimulation of Akt/protein kinase B (PKB) in skeletal muscle cells from type 2 diabetic patients.Diabetologia · 2008Article
- Palmitate action to inhibit glycogen synthase and stimulate protein phosphatase 2A increases with risk factors for type 2 diabetes.American journal of physiology. Endocrinology and metabolism · 2008Article
- Activation of liver X receptors promotes lipid accumulation but does not alter insulin action in human skeletal muscle cells.Diabetologia · 2006Article
- Different metabolic responses to central and peripheral injection of enterostatin.American journal of physiology. Regulatory, integrative and comparative physiology · 2006Article
- Elevated stearoyl-CoA desaturase-1 expression in skeletal muscle contributes to abnormal fatty acid partitioning in obese humans.Cell metabolism · 2005Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
To determine whether glycogen synthase (GS) activity remains impaired in skeletal muscle of non-insulin-dependent diabetes mellitus (NIDDM) patients or can be normalized after prolonged culture, needle biopsies of vastus lateralis were obtained from 8 healthy nondiabetic control (ND) and 11 NIDDM subjects. After 4-6 wk growth and 4 d fusion in media containing normal physiologic concentrations of insulin (22 pM) and glucose (5.5 mM), both basal (5.21 +/- 0.79 vs 9.01 +/- 1.25%, P < 0.05) and acute insulin-stimulated (9.35 +/- 1.81 vs 16.31 +/- 2.39, P < 0.05) GS fractional velocity were reduced in NIDDM compared to ND cells. Determination of GS kinetic constants from muscle cells of NIDDM revealed an increased basal and insulin-stimulated Km(0.1) for UDP-glucose, a decreased insulin-stimulated Vmax(0.1) and an increased insulin-stimulated activation constant (A(0.5)) for glucose-6-phosphate. GS protein expression, determined by Western blotting, was decreased in NIDDM compared to ND cells (1.57 +/- 0.29 vs 3.30 +/- 0.41 arbitrary U/mg protein, P < 0.05). GS mRNA abundance also tended to be lower, but not significantly so (0.168 +/- 0.017 vs 0.243 +/- 0.035 arbitrary U, P = 0.08), in myotubes of NIDDM subjects. These results indicate that skeletal muscle cells of NIDDM subjects grown and fused in normal culture conditions retain defects of basal and insulin-stimulated GS activity that involve altered kinetic behavior and possibly reduced GS protein expression. We conclude that impaired regulation of skeletal muscle GS in NIDDM patients is not completely reversible in normal culture conditions and involves mechanisms that may be genetic in origin.
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