No abstract

No abstract

Few studies on humans have comprehensively evaluated the intake composition of methyl-donor nutrients (MDNs: choline, betaine, and folate) in relation to visceral obesity (VOB)-related hepatic steatosis (HS), the hallmark of non-alcoholic fatty liver diseases. In this case–control study, we recruited 105 patients with HS and 104 without HS (controls). HS was diagnosed through ultrasound examination. VOB was measured using a whole-body analyzer. MDN intake was assessed using a validated quantitative food frequency questionnaire. After adjustment for multiple HS risk factors, total choline intake was the most significant dietary determinant of HS in patients with VOB (Beta: −0.41, p = 0.01). Low intake of choline (<6.9 mg/kg body weight), betaine (<3.1 mg/kg body weight), and folate (<8.8 μg/kg body weight) predicted increased odds ratios (ORs) of VOB-related HS (choline: OR: 22, 95% confidence interval [CI]: 6.5–80; betaine: OR: 14, 95% CI: 4.4–50; and folate: OR: 19, 95% CI: 5.2–74). Combined high intake of choline and betaine, but not folate, was associated with an 81% reduction in VOB-related HS (OR: 0.19, 95% CI: 0.05–0.69). Our data suggest that the optimal intake of choline and betaine can minimize the risk of VOB-related HS in a threshold-dependent manner.

Inhibition of acetyl-CoA carboxylase (ACC) is one approach used for treating metabolic syndrome. Using partially purified ACC to screen herbs commonly used in Taiwanese folk medicine, we previously showed that an ethanol extract of Polygonum hypoleucum Ohwi (EP) had potent ACC inhibitory activity and partially alleviated metabolic disorders induced by a high fat diet. Since ACC plays a crucial role in de novo lipogenesis, the favorable effects of EP on metabolism were tested under lipogenic conditions in the present study. On incubating high glucose (30 mM)-stimulated HepG2 cells with EP (72.5 or 145 microg/mL), ACC and fatty acid synthase activity, triacylglycerol content, and microsomal triacylglycerol transfer protein mRNA levels were all significantly reduced (P < 0.05, vs vehicle). When EP was given at low, medium, and high dosages (94, 188, and 470 mg/kg) to sucrose water-treated Wistar rats for four weeks, alleviation of symptoms associated with metabolic syndrome, including obesity, insulin resistance, hypertriglyceridemia, and hypertension, accompanied by hepatic ACC inactivation, was seen in the low dosage group. Four compounds (emodin, emodin-8-O-beta-D-glucopyranoside, (+)-catechin, and (-)-epicatechin) isolated from EP were identified as ACC inhibitors. These results confirm that P. hypoleucum Ohwi, acting partly through ACC inhibition, has favorable effects in alleviating metabolic disturbances occurring under lipogenic conditions.

The aim of this study was to investigate whether maternal ingestion of oxidized frying oil (OFO) during pregnancy influences the susceptibility to diet-induced obesity (DIO) of the adult offspring. Pregnant C57BL/6J mice were fed either a control diet [10% fresh soybean oil (SO)] or an OFO-containing diet (10% OFO) throughout the entire gestational period. After parturition, all pups were nursed by SO-fed dams for 3 wk, weaned onto a nonpurified standard diet for 4 wk, and shifted to a high-fat diet (29% butter + 1% SO) for 5 wk. Consequently, 4 groups of offspring were obtained, consisting of the male (m) or female (f) offspring of dams fed the OFO diet (OFO-m and OFO-f) or the SO diet (SO-m and SO-f). At pregnancy d 18, higher amounts (P < 0.05) of mRNA for PPARα target genes were found in the liver of the OFO-fed dams and their fetuses than in their SO controls. Although all pups were raised under the same conditions in postnatal life, a comparison based on the gender of pups from dams fed the different diets showed that adult OFO-f mice were prone to DIO, whereas adult OFO-m mice were resistant. The adult OFO-m mice also had higher expression of PPARα target genes in the liver and white adipose tissue (WAT) and of thermogenic genes in the WAT than adult SO-m mice, whereas adult OFO-f and SO-f mice did not differ. We conclude that uterine PPARα activation caused by maternal OFO ingestion affects hepatic PPARα activity and adipose thermogenic capacity and contributes to the differential susceptibility to DIO in the male and female offspring in adulthood.