ArticleDiabetologia2007
Pten (phosphatase and tensin homologue gene) haploinsufficiency promotes insulin hypersensitivity.
Article in Diabetologia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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42 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- Four pleiotropic loci associated with fat mass and lean mass.International journal of obesity (2005) · 2020Pooled it
- Article
- Epigenetic crossroads in metabolic and cardiovascular health: the role of DNA methylation in type 2 diabetes and cardiovascular diseases.Cardiovascular diabetology · 2025Review
- Hepatic IR and IGF1R signaling govern distinct metabolic and carcinogenic processes upon PTEN deficiency in the liver.JHEP reports : innovation in hepatology · 2025Article
- The Proteome of Exosomes at Birth Predicts Insulin Resistance, Adrenarche and Liver Fat in Childhood.International journal of molecular sciences · 2025Article
- Epigenetic regulation in lung cancer.MedComm · 2023Review
- Synthetic lethal approaches to target cancers with loss of PTEN function.Genes & diseases · 2023Article
- Nuclear PTEN Regulates Thymidylate Biosynthesis in Human Prostate Cancer Cell Lines.Metabolites · 2023Article
- Targeting protein modifications in metabolic diseases: molecular mechanisms and targeted therapies.Signal transduction and targeted therapy · 2023Review
- Long-term treatment of cancer-prone germline PTEN mutant mice with low-dose rapamycin extends lifespan and delays tumour development.The Journal of pathology · 2022Article
- PTEN Deletion in Adult Mice Induces Hypoinsulinemia With Concomitant Low Glucose Levels.Frontiers in endocrinology · 2022Article
- Hepatic HuR protects against the pathogenesis of non-alcoholic fatty liver disease by targeting PTEN.Cell death & disease · 2021Article
- Class IA PI3K regulatory subunits: p110-independent roles and structures.Biochemical Society transactions · 2020Review
- Loss of Ceacam1 promotes prostate cancer progression in Pten haploinsufficient male mice.Metabolism: clinical and experimental · 2020Article
- Genome sequencing analysis of a family with a child displaying severe abdominal distention and recurrent hypoglycemia.Molecular genetics & genomic medicine · 2020Article
- Review
- Analysis of PTEN expression and promoter methylation in Uyghur patients with mild type 2 diabetes mellitus.Medicine · 2018Article
- The functions and regulation of the PTEN tumour suppressor: new modes and prospects.Nature reviews. Molecular cell biology · 2018Review
- Biochemical and cellular properties of insulin receptor signalling.Nature reviews. Molecular cell biology · 2018Review
- CK2 modulates adipocyte insulin-signaling and is up-regulated in human obesity.Scientific reports · 2017Article
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisInsulin controls glucose metabolism via multiple signalling pathways, including the phosphatidylinositol 3-kinase (PI3K) pathway in muscle and adipose tissue. The protein/lipid phosphatase Pten (phosphatase and tensin homologue deleted on chromosome 10) attenuates PI3K signalling by dephosphorylating the phosphatidylinositol 3,4,5-trisphosphate generated by PI3K. The current study was aimed at investigating the effect of haploinsufficiency for Pten on insulin-stimulated glucose uptake. MATERIALS AND
methodsInsulin sensitivity in Pten heterozygous (Pten(+/-)) mice was investigated in i.p. insulin challenge and glucose tolerance tests. Glucose uptake was monitored in vitro in primary cultures of myocytes from Pten(+/-) mice, and in vivo by positron emission tomography. The phosphorylation status of protein kinase B (PKB/Akt), a downstream signalling protein in the PI3K pathway, and glycogen synthase kinase 3beta (GSK3beta), a substrate of PKB/Akt, was determined by western immunoblotting.
resultsFollowing i.p. insulin challenge, blood glucose levels in Pten(+/-) mice remained depressed for up to 120 min, whereas glucose levels in wild-type mice began to recover after approximately 30 min. After glucose challenge, blood glucose returned to normal about twice as rapidly in Pten(+/-) mice. Enhanced glucose uptake was observed both in Pten(+/-) myocytes and in skeletal muscle of Pten(+/-) mice by PET. PKB and GSK3beta phosphorylation was enhanced and prolonged in Pten(+/-) myocytes. CONCLUSIONS/
interpretationPten is a key negative regulator of insulin-stimulated glucose uptake in vitro and in vivo. The partial reduction of Pten due to Pten haploinsufficiency is enough to elicit enhanced insulin sensitivity and glucose tolerance in Pten(+/-) mice.
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