ArticleScientific reports2016
Hyperglycemia and hyperlipidemia blunts the Insulin-Inpp5f negative feedback loop in the diabetic heart.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 23 citations in OpenAlex.
- The coordinated actions of metformin in the intestine and liver improves hyperglycemia.Cell reports · 2026Article
- Cardiac sodium-glucose co-transporter 1 (SGLT1) contributes to heart failure in a mouse model of diabetic cardiomyopathy.Basic research in cardiology · 2025Article
- DNA methylation abnormalities of imprinted genes in congenital heart disease: a pilot study.BMC medical genomics · 2021Article
- Imprinting aberrations of SNRPN, ZAC1 and INPP5F genes involved in the pathogenesis of congenital heart disease with extracardiac malformations.Journal of cellular and molecular medicine · 2020Article
- Locating potentially lethal genes using the abnormal distributions of genotypes.Scientific reports · 2019Article
- Pregabalin on Hdac2 and Inpp5f levels in rats with CCI-induced neuropathic pain.Experimental and therapeutic medicine · 2019Article
- LncRNAs and miRs as epigenetic signatures in diabetic cardiac fibrosis: new advances and perspectives.Endocrine · 2018Review
- Losartan Alleviates Renal Fibrosis and Inhibits Endothelial-to-Mesenchymal Transition (EMT) Under High-Fat Diet-Induced Hyperglycemia.Frontiers in pharmacology · 2018Article
- Apigenin alleviates STZ-induced diabetic cardiomyopathy.Molecular and cellular biochemistry · 2017Article
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9 authors at 3 institutions in 1 country.
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Abstract
The leading cause of death in diabetic patients is diabetic cardiomyopathy, in which alteration of Akt signal plays an important role. Inpp5f is recently found to be a negative regulator of Akt signaling, while its expression and function in diabetic heart is largely unknown. In this study, we found that in both the streptozotocin (STZ) and high fat diet (HFD) induced diabetic mouse models, Inpp5f expression was coordinately regulated by insulin, blood glucose and lipid levels. Increased Inpp5f was inversely correlated with the cardiac function. Further studies revealed that Insulin transcriptionally activated Inpp5f in an Sp1 dependent manner, and increased Inpp5f in turn reduced the phosphorylation of Akt, forming a negative feedback loop. The negative feedback plays a protective role under diabetic condition. However, high blood glucose and lipid, which are characteristics of uncontrolled diabetes and type 2 diabetes, increased Inpp5f expression through activation of NF-κB, blunts the protective feedback. Thus, our study has revealed that Inpp5f provides as a negative feedback regulator of insulin signaling and downregulation of Inpp5f in diabetes is cardioprotective. Increased Inpp5f by hyperglycemia and hyperlipidemia is an important mediator of diabetic cardiomyopathy and is a promising therapeutic target for the disease.
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