The up-regulation of hepatic acyl-coA oxidase and cytochrome P<Subscript>450</Subscript> 4A1 mRNA expression by dietary oxidized frying oil is comparable between male and female rats

We previously demonstrated that oxidized frying oil (OFO) activates peroxisome proliferator-activated receptor α (PPARα) and up-regulates hepatic acyl-CoA oxidase (ACO) and cytochrome P₄₅₀ 4A1 (CYP4A1) genes in male rats. As female rats were shown to be less responsive to some peroxisome proliferators (PP), this study compared the expression of a few PPARα target genes in male and female rats fed diets containing OFO. Male and female rats were fed a diet containing 20 g/100 g OFO (O diet) or fresh soybean oil (F diet) for 6 wk. Both male and female rats fed the O diet showed significantly higher liver weight, hepatic ACO and catalase activities, CYP4A protein, and expression of ACO and CYP4A1 mRNA (P<0.05) compared with their control groups. The mRNA expression of two other PPARα target genes, FA-binding protein and HMG-CoA synthase, were marginally increased by dietary OFO (P=0.0669 and 0,0521, respectively). Female rats fed the O diet had significantly lower CYP4A protein than male rats fed the same diet. The remaining OFO-induced effects were not significantly different between male and female rats fed the O diet. These results indicate that dietary OFO, unlike clofibrate or other PP, had minimal sexual dimorphic effect on the induction of hepatic PPARα target gene expression.     

Wild bitter gourd increased metabolic rate and up-regulated genes related to mitochondria biogenesis and UCP-1 in mice

The effects of bitter gourd (Momordica charantia, BG) on metabolic rate, mRNA expressions of UCP-1, genes related to mitochondria biogenesis and glucose homeostasis were investigated. C57BL/6J male mice were fed modified AIN-93G diets supplemented without (the Basal group) or with 5% (w/w) lyophilized BG powder (the BGP group) for 22 weeks. The BGP group had higher O₂ consumption, CO₂ production and respiratory quotient in the dark phase (p < 0.05) measured at 5th week. Compared to the Basal group, the BGP group had lower body weight and adipose mass, higher mRNA of UCP1, PGC-1α and NrF1 in white adipose tissue (p < 0.05), PGC-1α and NrF1 or tfam in skeletal muscle and brown adipose tissue (p < 0.05) and better glucose homeostasis. These results imply that BGP might increase mitochondria biogenesis and metabolic rate, which may lead to less fat accumulation and contribute, at least in part, to the improved control of glucose homeostasis.     

Triglycerides constituted of short and medium chain fatty acids and dicarboxylic acids in Momordica charantia, as well as capric acid,inhibit PGE2 production in RAW264.7 macrophages

This study was aimed to identify compounds in bitter gourd (Momordica charantia) ethyl acetate extract (EAE), which inhibit lipopolysaccharide-induced prostaglandin E₂ (PGE₂) production in RAW264.7 cells. Bitter gourd EAE was partitioned between n-hexane and methanol/H₂O (90/10). The hexane fraction was further separated by repeated silica gel chromatographies, and a reverse phase (RP) C18 chromatography. Fraction RP-10 showed the highest inhibition effect on PGE₂ production (Max inhibition = 96%, IC₅₀ = 2.3 μg/ml) and was identified to be triglycerides constituted of short and medium chain fatty acids by ¹H NMR, IR and H–HCOSY, and dicarboxylic acids by GC/MS. Fatty acids with 3–20 carbons were tested for the inhibitory activity, and capric acid exhibited the highest effect (Max inhibition = 99%, IC₅₀ = 6.5 μM). In conclusion, triglycerides composed of short and medium chain fatty acids and dicarboxylic acids in bitter gourd inhibit PGE₂ production, and capric acid is the most potent inhibitor among the fatty acids.     

Fucoxanthin Enhances Chain Elongation and Desaturation of Alpha-Linolenic Acid in HepG2 Cells

Dietary fucoxanthin (FX), a carotenoid compound from brown algae, was found to increase docosahexaenoic acid (DHA, 22:6n‐3) and arachidonic acid (ARA, 20:4n‐6) in the liver of mice. DHA and ARA are known to be biosynthesized from the respective precursor α‐linolenic acid (ALA, 18:3n‐3) and linoleic acid (LNA, 18:2n‐6), through desaturation and chain elongation. We examined the effect of FX on the fatty acid metabolism in HepG2 cells (Hepatocellular carcinoma, human). In the first experiment, cells were co‐treated with ALA (100 μM) and FX (0–100 μM) or vehicle for 48 h. FX increased eicosapentaenoic acid (EPA, 20:5n‐3), docosapentaenoic acid (DPA, 22:5n‐3), DHA at concentrations of ≥50 μM. To clarify the change in the metabolism of polyunsaturated fatty acid (PUFA), in the second experiment, cells were co‐treated with universally‐[¹³C]‐labeled (U‐[¹³C]‐) ALA (100 μM) and FX (100 μM) for 0.5, 3, 6, 24 and 48 h. [¹³C] labeled‐EPA, DPA and DHA content in HepG2 cells were all increased by FX after 48 h treatment. Furthermore, estimated delta‐5 desaturase (D5D) but not delta‐6 desaturase (D6D) activity index was increased at 48 h. These results suggested that FX may enhance the conversion of ALA to longer chain n‐3 PUFA through increasing D5D activity in the liver.