Trial reportAmerican journal of physiology. Endocrinology and metabolism2010
A new antidiabetic compound attenuates inflammation and insulin resistance in Zucker diabetic fatty rats.
Trial report in American journal of physiology. Endocrinology and metabolism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- An anti-inflammatory sterol decreases obesity-related inflammation-induced insulin resistance and metabolic dysregulation.Mediators of inflammation · 2013Trial
- Trial
- Article
- An exploratory analysis of bezisterim treatment associated with decreased biological age acceleration, and improved clinical measure and biomarker changes in mild-to-moderate probable Alzheimer's disease.Frontiers in neuroscience · 2025Article
- Clinical Trial Highlights: Anti-Inflammatory and Immunomodulatory Agents.Journal of Parkinson's disease · 2024Review
- Interactions between extracellular vesicles and microbiome in human diseases: New therapeutic opportunities.iMeta · 2023Review
- Oral Delivery of a Synthetic Sterol Reduces Axonopathy and Inflammation in a Rodent Model of Glaucoma.Frontiers in neuroscience · 2017Article
- 4β-Hydroxywithanolide E isolated from Physalis pruinosa calyx decreases inflammatory responses by inhibiting the NF-κB signaling in diabetic mouse adipose tissue.International journal of obesity (2005) · 2014Article
- HE3286 reduces axonal loss and preserves retinal ganglion cell function in experimental optic neuritis.Investigative ophthalmology & visual science · 2014Article
- Artemisia dracunculus L. extract ameliorates insulin sensitivity by attenuating inflammatory signalling in human skeletal muscle culture.Diabetes, obesity & metabolism · 2014Article
- C/EBPα regulates macrophage activation and systemic metabolism.American journal of physiology. Endocrinology and metabolism · 2014Article
- Article
- Neuronal Sirt1 deficiency increases insulin sensitivity in both brain and peripheral tissues.The Journal of biological chemistry · 2013Article
- Challenges of translating basic research into therapeutics: resveratrol as an example.The journals of gerontology. Series A, Biological sciences and medical sciences · 2012Article
- Effects of high fat feeding on liver gene expression in diabetic goto-kakizaki rats.Gene regulation and systems biology · 2012Article
- 17α-Ethynyl-androst-5-ene-3β,7β,17β-triol (HE3286) Is Neuroprotective and Reduces Motor Impairment and Neuroinflammation in a Murine MPTP Model of Parkinson's Disease.Parkinson's disease · 2012Article
- Molecular targets for 17α-ethynyl-5-androstene-3β,7β,17β-triol, an anti-inflammatory agent derived from the human metabolome.PloS one · 2012Article
- Phase I and Phase II clinical trials of androst-5-ene-3β,7β,17β-triol.American journal of translational research · 2011Article
- Brain PPAR-γ promotes obesity and is required for the insulin-sensitizing effect of thiazolidinediones.Nature medicine · 2011Article
- Studies of the pharmacology of 17α-ethynyl-androst-5-ene-3β,7β,17β-triol, a synthetic anti-inflammatory androstene.International journal of clinical and experimental medicine · 2011Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Tissue macrophage inflammatory pathways contribute to obesity-associated insulin resistance. Here, we have examined the efficacy and mechanisms of action of a novel anti-inflammatory compound (HE3286) in vitro and in vivo. In primary murine macrophages, HE3286 attenuates LPS- and TNFalpha-stimulated inflammation. In Zucker diabetic fatty rats, inflammatory cytokine/chemokine expression was downregulated in liver and adipose tissue by HE3286 treatment, as was macrophage infiltration into adipose tissue. In line with reduced inflammation, HE3286 treatment normalized fasting and fed glucose levels, improved glucose tolerance, and enhanced skeletal muscle and liver insulin sensitivity, as assessed by hyperinsulinemic euglycemic clamp studies. In phase 2 clinical trials, HE3286 treatment led to an enhancement in insulin sensitivity in humans. Gluconeogenic capacity was also reduced by HE3286 treatment, as evidenced by a reduced glycemic response during pyruvate tolerance tests and decreased basal hepatic glucose production (HGP) rates. Since serum levels of gluconeogenic substrates were decreased by HE3286, it indicates that the reduction of both intrinsic gluconeogenic capacity and substrate availability contributes to the decrease in HGP. Lipidomic analysis revealed that HE3286 treatment reduced liver cholesterol and triglyceride content, leading to a feedback elevation of LDL receptor and HMG-CoA reductase expression. Accordingly, HE3286 treatment markedly decreased total serum cholesterol. In conclusion, HE3286 is a novel anti-inflammatory compound, which displays both glucose-lowering and cholesterol-lowering effects.
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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.