ArticleDiabetologia2011
New emerging role of protein-tyrosine phosphatase 1B in the regulation of glycogen metabolism in basal and TNF-α-induced insulin-resistant conditions in an immortalised muscle cell line isolated from mice.
Article in Diabetologia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 7 citations in OpenAlex.
- Discovery of Novel PTP1B Inhibitors by High-throughput Virtual Screening.Current computer-aided drug design · 2026Article
- Article
- Prevalent role of the insulin receptor isoform A in the regulation of hepatic glycogen metabolism in hepatocytes and in mice.Diabetologia · 2016Article
- Inducible liver-specific knockdown of protein tyrosine phosphatase 1B improves glucose and lipid homeostasis in adult mice.Diabetologia · 2013Article
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Authors and funding
6 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisProtein-tyrosine phosphatase 1B (PTP1B) negatively regulates insulin action, promoting attenuation of the insulin signalling pathway. The production of this phosphatase is enhanced in insulin-resistant states, such as obesity and type 2 diabetes, where high levels of proinflammatory cytokines (TNF-α, IL-6) are found. In these metabolic conditions, insulin action on glycogen metabolism in skeletal muscle is greatly impaired. We addressed the role of PTP1B on glycogen metabolism in basal and insulin-resistant conditions promoted by TNF-α.
methodsWe studied the effect of TNF-α in the presence and absence of insulin on glycogen content and synthesis, glycogen synthase (GS) and glycogen phosphorylase (GP) activities and on glycogen synthesis and degradation signalling pathways. For this purpose we used immortalised cell lines isolated from skeletal muscle from mice lacking PTP1B.
resultsAbsence of PTP1B caused activation of GS and GP with a net glycogenolytic effect, reflected in lower amounts of glycogen and activation of the glycogenolytic signalling pathway, with higher rates of phosphorylation of cyclic adenosine monophosphate-dependent kinase (PKA), phosphorylase kinase (PhK) and GP phosphorylation. Nevertheless, insulin action was strongly enhanced in Ptp1b (also known as Ptpn1)(-/-) cells in terms of glycogen content, synthesis, GS activation rates and GS Ser641 dephosphorylation. Treatment with TNF-α augmented the activity ratios of both GS and GP, and impaired insulin stimulation of glycogen synthesis in wild-type myocytes, whereas Ptp1b (-/-) myocytes restored this inhibitory effect. We report a glycogenolytic effect of TNF-α, as demonstrated by greater activation of the degradation signalling cascade PKA/PhK/GP. In our model, this effect is mediated by the activation of PKA. CONCLUSIONS/
interpretationWe provide new data about the role of PTP1B in glycogen metabolism and confirm the beneficial effect that absence of the phosphatase confers against an insulin-resistant condition.
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