ArticleDiabetes2017
Hepatic Expression of Adenovirus 36 E4ORF1 Improves Glycemic Control and Promotes Glucose Metabolism Through AKT Activation.
Article in Diabetes, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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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.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Pre-clinical studies show anti-diabetic effect of INSPARIN, a protein derived from the E4orf1 gene of a human adenovirus.Nutrition & diabetes · 2025Article
- Dose-finding andMolecular therapy. Methods & clinical development · 2025Article
- Subcutaneous administration of adipose-tropic gene therapy for congenital leptin deficiency.Research square · 2025Article
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- The human adenovirus PI3K-Akt activator E4orf1 is targeted by the tumor suppressor p53.Journal of virology · 2024Article
- E4orf1 improves adipose tissue-specific metabolic risk factors and indicators of cognition function in a mouse model of Alzheimer's disease.Nutrition & diabetes · 2023Article
- E4orf1 Prevents Progression of Fatty Liver Disease in Mice on High Fat Diet.International journal of molecular sciences · 2022Article
- E4orf1-induced reduction in endogenous insulin level is independent of pancreas endocrine function.International journal of obesity (2005) · 2022Article
- Findings from Studies Are Congruent with Obesity Having a Viral Origin, but What about Obesity-Related NAFLD?Viruses · 2021Review
- Antidiabetic E4orf1 protein prevents hepatic steatosis and reduces markers of aging-related cellular damage in high fat fed older mice.BMJ open diabetes research & care · 2021Article
- Adipose Tissue: An Emerging Target for Adeno-associated Viral Vectors.Molecular therapy. Methods & clinical development · 2020Review
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- Characterization of the adipogenic protein E4orf1 from adenovirus 36 through an in silico approach.Journal of molecular modeling · 2020Article
- Nanoparticle-mediated in vitro delivery of E4orf1 to preadipocytes is a clinically relevant delivery system to improve glucose uptake.International journal of obesity (2005) · 2020Article
- What we know and what we need to know about adenovirus 36-induced obesity.International journal of obesity (2005) · 2020Review
- Adenovirus 36 seropositivity is related to obesity risk, glycemic control, and leptin levels in Chilean subjects.International journal of obesity (2005) · 2020Article
- E4orf1 protein reduces the need for endogenous insulin.Nutrition & diabetes · 2019Article
- Review
- E4orf1: A protein for enhancing glucose uptake despite impaired proximal insulin signaling.PloS one · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Considering that impaired proximal insulin signaling is linked with diabetes, approaches that enhance glucose disposal independent of insulin signaling are attractive. In vitro data indicate that the E4ORF1 peptide derived from human adenovirus 36 (Ad36) interacts with cells from adipose tissue, skeletal muscle, and liver to enhance glucose disposal, independent of proximal insulin signaling. Adipocyte-specific expression of Ad36E4ORF1 improves hyperglycemia in mice. To determine the hepatic interaction of Ad36E4ORF1 in enhancing glycemic control, we expressed E4ORF1 of Ad36 or Ad5 or fluorescent tag alone by using recombinant adeno-associated viral vector in the liver of three mouse models. In db/db or diet-induced obesity (DIO) mice, hepatic expression of Ad36E4ORF1 but not Ad5E4ORF1 robustly improved glycemic control. In normoglycemic wild-type mice, hepatic expression of Ad36E4ORF1 lowered nonfasting blood glucose at a high dose of expression. Of note, Ad36E4ORF1 significantly reduced insulin levels in db/db and DIO mice. The improvement in glycemic control was observed without stimulation of the proximal insulin signaling pathway. Collectively, these data indicate that Ad36E4ORF1 is not a typical sensitizer, mimetic, or secretagogue of insulin. Instead, it may have insulin-sparing action, which seems to reduce the need for insulin and, hence, to reduce insulin levels.
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What OpenQuestion holds
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.