We reported that the compositions of arachidonic acid (ARA) in erythrocytes and plasma phospholipids (PL) in the elderly were lower than those in the young, though the ARA intake was nearly identical. We further analyzed data in four study groups with different ages and sexes, and determined that the blood ARA levels were affected by the kinds of dietary fatty acids ingested. One hundred and four healthy young and elderly volunteers were recruited. Dietary records together with photographic records from 28 consecutive days were reviewed and the fatty acid composition in plasma lipid fractions and erythrocyte PL was analyzed. No correlations for ARA between dietary fatty acids and blood lipid fractions were observed. A significant negative correlation between eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA) intake and ARA composition in erythrocyte PL was observed. ARA composition in erythrocyte PL was significantly lower in elderly subjects than in young subjects, because EPA and DHA intake in elderly subjects was higher than in young subjects. However, after removing the effect of dietary EPA+DHA intake, the ARA composition in erythrocyte PL in elderly subjects was significantly lower than that in young subjects. Changes in physical conditions with aging influenced the low ARA composition of erythrocyte in elderly subjects in addition to the effects of dietary EPA and DHA.

It was reported that egg white protein (EWP) reduced body fat in rats. We developed a lactic-fermented egg white (LE) that facilitates the consumption of egg whites by fermenting them with lactobacillus, and were able to study their intake in humans. In this double-blind, placebo-controlled design, we evaluated the effect of LE on visceral fat area (VFA). Participants included 37 adult males and females aged ≥40 years (VFA at navel ≥100 cm2). They were divided into two groups: the control group and the LE group. The control and LE groups consumed drinks containing whey and LE, respectively, for 12 weeks (providing 8 g protein/day). VFA was measured at baseline and at week 12 of intake. Abdominal girth was measured at baseline and at weeks 6 and 12. LE intake decreased VFA significantly compared with baseline (−8.89 cm2, p < 0.05), and VFA was significantly lower than that in the control group (+1.71 cm2, p < 0.05). The LE group showed significant improvement in the ratio of visceral to subcutaneous fat area compared with baseline and the control group (p < 0.05). The results demonstrated that LE reduces VFA and improves the ratio of visceral to subcutaneous fat area. As other measurement items were not influenced, we concluded that LE improves visceral fat obesity. This clinical trial was retrospectively registered with the University hospital Medical Information Network (UMIN) Center, ( UMIN000026949 ; registered on 11/04/2017; http://www.umin.ac.jp /).

To assess the effect of rice bran oil emulsified formulation (EMF) on cooked rice, a single-arm open clinical trial and in vitro testing for digestion and glycemic response were performed. Fifteen Japanese men consumed 200 g of packed rice, cooked with or without EMF. Blood samples were collected 0, 30, 60, and 120 min post-consumption and analyzed for glucose, insulin, and triglyceride levels. Continuous glucose monitoring (CGM) and sensory evaluation were also performed. A two-step in vitro digestion test, simulating gastric and small intestinal digestion was conducted. EMF-added rice group showed higher insulin response levels at 60 min than the placebo group. Stratification of participants with HbA1c ≥ 5.6 or an insulinogenic index ≤ 0.4 revealed a significant reduction in C_max glucose levels. A significant correlation was observed between venous and CGM blood glucose levels and no significant sensory differences were observed. The in vitro test revealed significantly lower C_∞, equilibrium starch concentrations, with EMF. Clinical trial suggests that EMF may stimulate insulin secretion and reduce blood glucose levels in participants with lower insulin responses. In vitro tests suggest that EMF inhibits glycemic digestion. This trial was registered at the UMIN Center (UMIN000053495; registered 31 January 2024).

Background/Objectives: Adherence to treatment instructions is essential in managing chronic diseases related to obesity. One gene associated with adherence is the serotonin transporter (5-HTTLPR) gene, which has long (L) and short (S) alleles, resulting in LL, SL, and SS genotypes. Risk alleles for obesity include the R variant of the β3-adrenergic receptor (β3AR) and the G variant of uncoupling protein 1 (UCP1). This study aimed to evaluate whether the S/L variant of 5-HTTLPR, the R variant of β3AR, and the G variant of UCP1 are associated with adherence to a weight loss program. To assess the factors influencing adherence, eating behavior was evaluated using the Eating Behavior Questionnaire (EBQ). Methods: The study included 56 women with a mean age of 57.3±10 years and a mean BMI of 27.2±5.6 kg/m2. Long-read sequencing was used to analyze S/L mutations. Participants followed a six-month diet and exercise regimen for obesity management. Outcomes were assessed using clinical data and EBQ scores. Results: Participants were classified as SS (69.6%), SL (17.9%), or LL (12.5%). The R variant of β3AR was present in 34% of participants, with the G variant of UCP1 in 75%. After the intervention, SS participants showed significantly greater reductions in weight, body fat percentage, and waist circumference than LL participants (p < 0.05). Among EBQ items, significant improvements (p<0.05) were observed in SS participants for eating as a diversion, feeling of fullness, bad eating habits, unsteady eating patterns, and total EBQ score. In SL participants, only bad eating habits improved, whereas no significant changes were observed in LL participants. Obesity risk alleles did not significantly affect clinical outcomes. Conclusions: SS genotype participants demonstrated higher adherence to the weight loss program, leading to improved clinical outcomes and EBQ scores, independent of obesity risk genes.

Background/Objectives: Adherence to treatment instructions is essential in managing chronic diseases related to obesity. One gene associated with adherence is the serotonin transporter (5-HTTLPR) gene, which has long (L) and short (S) alleles, resulting in LL, SL, and SS genotypes. Risk alleles for obesity include the R variant of the β3-adrenergic receptor (β3AR) and the G variant of uncoupling protein 1 (UCP1). This study aimed to evaluate whether the S/L variant of 5-HTTLPR, the R variant of β3AR, and the G variant of UCP1 are associated with adherence to a weight loss program. To assess the factors influencing adherence, eating behavior was evaluated using the Eating Behavior Questionnaire (EBQ). Methods: This study included 56 well-educated and middle-class women with a mean age of 57.3 ± 10 years and a mean BMI of 27.2 ± 5.6 kg/m². Long-read sequencing was used to analyze S/L mutations. Participants followed a six-month diet and exercise regimen for obesity management. Outcomes were assessed using clinical data and EBQ scores. Adherence was objectively measured by the reduction in body fat percentage. Results: Participants were classified as SS (69.6%), SL (17.9%), or LL (12.5%). The R variant of β3AR was present in 34% of participants, with the G variant of UCP1 in 75%. After the intervention, SS participants showed significantly greater reductions in weight and body fat percentage than LL participants (p < 0.05). Among EBQ items, significant improvements (p < 0.05) were observed in SS participants for eating as a diversion, feeling of fullness, bad eating habits, unsteady eating patterns, and total EBQ score. In SL participants, only bad eating habits improved, whereas no significant changes were observed in LL participants. Obesity risk alleles did not significantly affect clinical outcomes, though there may be small number bias. Conclusions: SS genotype participants demonstrated higher adherence to the weight loss program, leading to improved clinical outcomes and EBQ scores, independent of obesity risk genes.