Study 16 of 16BAM-15 literatureScience (New York, N.Y.) · PreclinicalTop journal2015

Controlled-release mitochondrial protonophore reverses diabetes and steatohepatitis in rats.

Not reported in abstract.

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Preclinical · this one

Observational

Open-label

Randomised

Reviews

Summary and findings

Not reported in abstract.

How much of this paper we could read: title only (0.10). The feed gave us little more than the title, so our summary is thin. This says nothing about the study's quality — read the source. What this means →

Preclinical2015

Abstract

The authors’ words, as Science (New York, N.Y.) supplied them

Nonalcoholic fatty liver disease (NAFLD) is a major factor in the pathogenesis of type 2 diabetes (T2D) and nonalcoholic steatohepatitis (NASH). The mitochondrial protonophore 2,4 dinitrophenol (DNP) has beneficial effects on NAFLD, insulin resistance, and obesity in preclinical models but is too toxic for clinical use. We developed a controlled-release oral formulation of DNP, called CRMP (controlled-release mitochondrial protonophore), that produces mild hepatic mitochondrial uncoupling. In rat models, CRMP reduced hypertriglyceridemia, insulin resistance, hepatic steatosis, and diabetes. It also normalized plasma transaminase concentrations, ameliorated liver fibrosis, and improved hepatic protein synthetic function in a methionine/choline-deficient rat model of NASH. Chronic treatment with CRMP was not associated with any systemic toxicity. These data offer proof of concept that mild hepatic mitochondrial uncoupling may be a safe and effective therapy for the related epidemics of metabolic syndrome, T2D, and NASH.

Background

Not reported in abstract.

Methods

Not reported in abstract.

Results

Not reported in abstract.

Interpretation

Not reported in abstract.

Limitations

Not reported in abstract.

Elsewhere in the BAM-15 corpus

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