ArticleDiabetes2010
Deficiency of phosphoinositide 3-kinase enhancer protects mice from diet-induced obesity and insulin resistance.
Article in Diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Muscle-generated BDNF is a sexually dimorphic myokine that controls metabolic flexibility.Science signaling · 2019Article
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- Alteration of FXR phosphorylation and sumoylation in liver in the development of adult catch-up growth.Experimental biology and medicine (Maywood, N.J.) · 2017Article
- α-Synuclein binds and sequesters PIKE-L into Lewy bodies, triggering dopaminergic cell death via AMPK hyperactivation.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
- Fyn is a redox sensor involved in solar ultraviolet light-induced signal transduction in skin carcinogenesis.Oncogene · 2016Article
- Fyn-phosphorylated PIKE-A binds and inhibits AMPK signaling, blocking its tumor suppressive activity.Cell death and differentiation · 2016Article
- Activation of muscular TrkB by its small molecular agonist 7,8-dihydroxyflavone sex-dependently regulates energy metabolism in diet-induced obese mice.Chemistry & biology · 2015Article
- Voluntary physical activity prevents insulin resistance in a tissue specific manner.Physiological reports · 2015Article
- PIKE is essential for oligodendroglia development and CNS myelination.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Article
- The roles of PIKE in tumorigenesis.Acta pharmacologica Sinica · 2013Review
- Fyn regulates adipogenesis by promoting PIKE-A/STAT5a interaction.Molecular and cellular biology · 2013Article
- Loss of TDAG51 results in mature-onset obesity, hepatic steatosis, and insulin resistance by regulating lipogenesis.Diabetes · 2013Article
- Phosphoinositide 3-kinase enhancer (PIKE) in the brain: is it simply a phosphoinositide 3-kinase/Akt enhancer?Reviews in the neurosciences · 2012Review
- Essential role of PIKE GTPases in neuronal protection against excitotoxic insults.Advances in biological regulation · 2012Article
- The association of phosphoinositide 3-kinase enhancer A with hepatic insulin receptor enhances its kinase activity.EMBO reports · 2011Article
- Phosphoinositide 3-kinase enhancer regulates neuronal dendritogenesis and survival in neocortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Frontier of epilepsy research - mTOR signaling pathway.Experimental & molecular medicine · 2011Review
- What we have learnt about PIKE from the knockout mice.International journal of biochemistry and molecular biology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
objectivePhosphoinositide 3-kinase enhancer A (PIKE-A) is a proto-oncogene that promotes tumor growth and transformation by enhancing Akt activity. However, the physiological functions of PIKE-A in peripheral tissues are unknown. Here, we describe the effect of PIKE deletion in mice and explore the role of PIKE-A in obesity development. RESEARCH DESIGN AND
methodsWhole-body PIKE knockout mice were generated and subjected to high-fat-diet feeding for 20 weeks. The glucose tolerance, tissue-specific insulin sensitivity, adipocyte differentiation, and lipid oxidation status were determined. The molecular mechanism of PIKE in the insulin signaling pathway was also studied.
resultsWe show that PIKE-A regulates obesity development by modulating AMP-activated protein kinase (AMPK) phosphorylation. PIKE-A is important for insulin to suppress AMPK phosphorylation. The expression of PIKE-A is markedly increased in adipose tissue of obese mice, whereas depletion of PIKE-A inhibits adipocyte differentiation. PIKE knockout mice exhibit a prominent phenotype of lipoatrophy and are resistant to high-fat diet-induced obesity, liver steatosis, and diabetes. PIKE knockout mice also have augmented lipid oxidation, which is accompanied by enhanced AMPK phosphorylation in both muscle and adipose tissue. Moreover, insulin sensitivity is improved in PIKE-A-deficient muscle and fat, thus protecting the animals from diet-induced diabetes.
conclusionsOur results suggest that PIKE-A is implicated in obesity and associated diabetes development by negatively regulating AMPK activity.
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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.