Camelina seeds and their glucosinolate, glucocamelinin, counteract severe fatty liver in rodents with monogenic obesity.

Abstract

Background: Obesity is associated with metabolic dysfunction-associated steatotic liver disease (MASLD), for which drugs and nutraceuticals are being developed. We investigated whether camelina seeds from the Brassicaceae family and their components can attenuate metabolic disorders in animal models of genetic obesity, including fatty liver.

Methods: In two separate 5-week experiments, female obese (fa/fa) Zucker rats and female db/db mice were used. By appropriately incorporating camelina seeds or their oil into the diet, we investigated, in the rat model, the effects of the oil and non-oil fractions on intestinal and liver function, as well as on lipid metabolism. Subsequently, in a mouse model, oral administration of glucocamelinin, the main camelina glucosinolate, was performed to determine whether this group of compounds might be responsible for the observed beneficial effects.

Results: Dietary camelina seeds counteracted liver hypertrophy and steatosis in obese rats, as confirmed by macroscopic and histological images, along with a several-fold lower content of total fat, triglycerides, and cholesterol (p < 0.01 for each). The rat experiment indicated that the non-oil fraction of camelina seeds was responsible for these beneficial effects. Oral glucocamelinin attenuated liver hypertrophy and steatosis in obese mice, as confirmed by macroscopic and histological images, along with considerably lower total fat (p < 0.05) and cholesterol (p < 0.01) contents. In both obese rats and mice, these and other beneficial effects were associated with alterations in the hepatic expression of genes crucial to lipid and glucose metabolism, including a higher expression of those encoding thyroid hormone receptor β (THR-β; p < 0.01 and p < 0.05) and fibroblast growth factor 21 (FGF21; p < 0.01 and p < 0.05).

Conclusion: These findings indicate that camelina seeds may be considered both a dietary component and a source of bioactive glucosinolates relevant to MASLD. The mechanism behind the lipid-lowering effect of glucocamelinin may involve hepatic activation of FGF21 signaling through THR-β.