The study involved four groups of seven-week old male mice: one was a control group fed normal chow, one group was fed normal chow with glucoraphanin, another was put on a high-fat diet, and the last on a high-fat diet with glucoraphanin.
The mice on a high-fat diet with glucoraphanin had considerably lower fasted blood glucose than the vehicle-treated controls. Glucoraphanin also reduced plasma insulin concentrations significantly and improved glucose tolerance.
The study stated that in response to a high-fat diet, liver-resident macrophages heightened the production of pro-inflammatory cytokines that caused the mice to develop non-alcoholic fatty liver disease and insulin resistance. Glucoraphanin was found to suppress inflammatory pathways, as well as the “pro-inflammatory activation of macrophages in liver and adipose tissue”.
Additionally, chronic inflammation caused by gut microbiota-derived lipopolysaccharide (LPS) eventually leads to insulin resistance in obesity (metabolic endotoxemia), and glucoraphanin was shown to decrease circulating LPS.
The study said that "glucoraphanin restores energy expenditure and limits gut-derived metabolic endotoxemia" in obese mice, hence preventing chronic inflammation, hepatic steatosis and insulin resistance.
It added that glucoraphanin may effectively prevent obesity and related metabolic disorders like type 2 diabetes and non-alcoholic fatty liver disease.
It also referred to another clinical study that had demonstrated that daily supplementation (69 µmol/day) with a dietary dose of glucoraphanin for two months “significantly decreased plasma liver enzymes…although body mass did not change”.
The study concluded that long-term treatment with a “higher dose of glucoraphanin (800 µmol/day), which can be safely administered without harmful adverse effects, may be required to achieve an anti-obesity effect in humans”.
“Glucoraphanin Ameliorates Obesity and Insulin Resistance Through Adipose Tissue Browning and Reduction of Metabolic Endotoxemia in Mice”
Authors: Naoto Nagata, et al.