Fructose is a strong risk factor for non-alcoholic fatty liver disease (NAFLD), resulting from the disruption of redox systems by excessive reactive oxygen species production in the liver cells. Of note, recent epidemiological studies indicated that women are more prone to developing metabolic syndrome in response to fructose-sweetened beverages. Hence, we examined whether disruption of the redox system through a deletion of NADPH supplying mitochondrial enzyme, NADP⁺-dependent isocitrate dehydrogenase (IDH2), exacerbates fructose-induced NAFLD conditions in C57BL/6 female mice. Wild-type (WT) and IDH2 knockout (KO) mice were treated with either water or 34% fructose water over six weeks. NAFLD phenotypes and key proteins and mRNAs involved in the inflammatory pathway (e.g., NF-κB p65 and IL-1β) were assessed. Hepatic lipid accumulation was significantly increased in IDH2 KO mice fed fructose compared to the WT counterpart. Neutrophil infiltration was observed only in IDH2 KO mice fed fructose. Furthermore, phosphorylation of NF-κB p65 and expression of IL-1β was remarkably upregulated in IDH2 KO mice fed fructose, and expression of IκBα was decreased by fructose treatment in both WT and IDH2 KO groups. For the first time, we report our novel findings that IDH2 KO female mice may be more susceptible to fructose-induced NAFLD and the associated inflammatory response, suggesting a mechanistic role of IDH2 in metabolic diseases.

Accumulation of reactive oxygen species (ROS) in response to excess alcohol exposure is a major cause of gut barrier disruption and lipopolysaccharide (LPS)-induced hepatic inflammation, as well as liver steatosis and apoptosis. This study was designed to investigate protective effects of the cricket Gryllus bimaculatus, an edible insect recognized by the Korea Food and Drug Administration, against acute alcoholic liver damage in mice. Administration of G. bimaculatus extracts (GBE) attenuated alcohol-induced steatosis and apoptotic responses in the liver and intestinal permeability to bacterial endotoxin. These protective effects were associated with suppression of ROS-mediated oxidative stress in both the liver and small intestine. Furthermore, in vivo and in vitro studies revealed that GBE inhibits LPS-induced Kupffer cell activation and subsequent inflammatory signaling. Importantly, the protective effects of GBE were more potent than those of silymarin, a known therapeutic agent for alcoholic liver diseases.

This study investigated effects of patchouli essential oil (PEO) inhalation on metabolic parameters. First, to characterize aromatic compounds in PEO, solid-phase microextraction-gas chromatography/mass spectrometric detection was employed in which 19 aromatic compounds were identified. In GC-olfactometry analysis, linalool, α-patchoulene, and β-patchoulene were found to be the constituents exhibiting the highest similarity to the aromatic compounds in patchouli. In an animal experiment using Sprague Darley rats, groups with PEO inhalation had a reduced food intake compared to the control group. Additionally, body weight was lower in the obesity-induced animal model exposed to PEO inhalation than the group without PEO. However, we found no significant difference in organ weights between groups. In our serum analysis, high-density lipoprotein cholesterol was significantly higher in the PEO inhalation groups, while low-density lipoprotein cholesterol content was highest in the positive control group, suggesting that inhalation of the aromatic compounds present in patchouli may improve cholesterol profile. In addition, leptin levels were reduced in the groups treated with PEO inhalation, which explains the differences in food intake and body weight gains. Last, animal groups exposed to PEO inhalation showed a relatively lower systolic blood pressure which suggests that inhalation of PEO (or aromatic compounds therein) may assist in regulating blood pressure. Collectively, our data demonstrate that the inhalation of PEO influenced certain markers related to metabolic diseases, hence provide basic data for future research as to preventive/therapeutic applications of PEO as well as their aromatic constituents.