The primary causes of fatty liver syndrome (hepatic steatosis) induced by excess alcohol consumption are the altered NADH/NAD + levels that in turn inhibits gluconeogenesis, inhibits fatty acid oxidation, and inhibits the activity of the TCA cycle (see below for details)
It is noteworthy that supplementation with iron-modulating agents does not effectively reduce hepatic iron stores and is anticipated to garner significant interest as a novel therapeutic strategy for addressing the pathogenesis of hemochromatosis [108, 109]
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Pharmacological studies For assessment of drug effects under room temperature (22 2 C), male age-matched mice were double housed and fed with a 58% HFD (D12331, Research Diets) for approximately 20 weeks, followed by random assignment into groups of matched genotype, body weight and body composition
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This confirms that the observed metabolic reprogramming was dependent on chronic activation of GLP-1R signalling and independent of its acute stimulation of insulin secretion, which may result in autocrine insulin signalling
