半澤 史聡

Development of an accurate and efficient dietary method is required for national nutrition surveys. Some countries conduct dietary surveys and combine 24-h dietary records or 24-h dietary recalls with dietary questionnaires. This scoping review aimed to summarize studies that used results from national surveys that combined detailed dietary surveys (dietary records or 24-h dietary recall) and dietary questionnaires and identify the purpose of combining the two methods. The PubMed database and manual searches were used for the literature review. We extracted 58 articles from 16 national nutrition surveys from 14 countries. Most studies used 24-h dietary recall for detailed dietary surveys and the food frequency questionnaire (FFQ) or food propensity questionnaire (FPQ) for questionnaire surveys. Among 37 studies from eight countries, the purpose of combining the two dietary survey methods was to estimate energy and nutrient intakes from detailed dietary surveys and habitual food intake from questionnaires. These findings are useful as a reference when introducing new dietary survey methods in future national nutrition surveys.

Skipping breakfast is an irregular feeding behavior, typically in young people. In our previous study, we established a 4 h-delayed feeding protocol for rats as a breakfast-skipping model and showed that the 4 h-delayed feeding of a high-fat diet led to body weight gain in rats. Excess sucrose induces metabolic syndrome and fatty liver. Recently, excess sucrose intake has received increased attention. Young people generally consume more sugar than adults do. In the present study, we investigated whether a 4 h-delayed feeding promoted high-sucrose diet-induced abnormalities in lipid metabolism, such as fatty liver and obesity in rats. The 4 h-delayed feeding rats showed increased body weight gain, although it did not induce fatty liver and hyperlipidemia compared to normal feeding rats. Serum insulin concentration during the feeding period was higher than in the control rats, suggesting that slight insulin resistance was induced by the 4 h-delayed feeding. The surge in body temperature was also delayed by 4 h in response to the 4 h-delayed feeding. This delay would result in less energy expenditure to increase body weight. The oscillations of hepatic lipid and glucose metabolism-related gene expression were delayed by almost 2-4 h, and the clock genes were delayed by approximately 2 h. The 4 h-delayed feeding induced weight gain by affecting body temperature, insulin resistance, and circadian oscillation of lipid metabolism-related genes in rats fed a high-sucrose diet, suggesting that a high sucrose intake with breakfast skipping leads to obesity.

For athletes, it is important to acquire lean body mass (LBM) involving the skeletal muscle mass during their growth periods; however, the influence of chronotype on LBM gain remains unclear. We therefore aimed to investigate whether chronotype, sleep-wake cycle on weekdays (SWC-W), and their interaction contribute to LBM gain among adolescent male athletes in a 4-month intervention study. The participants were 45 male high-school baseball players. The intervention, including exercise menu (running and muscle strength training) and nutritional education, was conducted during a 4-month period of season-off training. The chronotype, body composition, lifestyle, and dietary intake were investigated before intervention (baseline) and after 4 months. Among the participants [Morningness (n = 14), Eveningness (n = 15), Intermediate (n = 16); ME score based on the Morningness/Eveningness Scale for Children (MES-C)], the midpoint of sleep on weekdays (MSW) was calculated in the "Morningness" and "Eveningness" participants, respectively. They were divided into 4 groups based on a match/mismatch with the chronotype: Type M-match (n = 8), Type M-mismatch (n = 6), Type E-match (n = 7), and Type E-mismatch (n = 8) groups. The data were compared among the 4 groups. Moreover, multiple regression analysis was conducted using an increase (kg) LBM gain as a response variable. When comparing the data between the "Morningness" and "Eveningness" participants, there were no differences in nutrient intake, the duration of training, or each parameter of body composition (per body weight) at baseline or after 4 months. There were also no differences in the rates of change in the body weight or each parameter of body composition. In groups in which the chronotype was consistent with the SWC-W (the Type M-match and Type E-match groups), the LBM gain were slightly greater than in the Type M-mismatch and Type E-mismatch groups (Type M-match: 3.5 ± 2.0 kg, Type M-mismatch: 1.6 ± 1.7 kg, Type E-match: 3.4 ± 2.2 kg, and Type E-mismatch: 1.2 ± 1.8 kg, p = .057). Multiple regression analysis revealed that an extent of the LBM gain was associated with a match between the chronotype and SWC-W (ß = 0.37, p = .030), independent of a long duration of training (ß = 0.52, p = .004). The results suggested that training-related LBM gain is associated with interactions between the chronotype and SWC-W in adolescent male athletes.Abbreviations: LBM: Lean body mass; SWC-W: Sleep-wake cycle on weekdays; ME score: Morningness-eveningness score; MES-C: Morningness/Eveningness Scale for Children; MSW: Midpoint of sleep on weekdays; MSF: Midpoint of sleep on free days; MSFsc: Midpoint of sleep on free days corrected for sleep debt accumulated through weekdays.

<bold>Background:</bold> To investigate whether shifted timing of eating, breakfast skipping, induces alterations in the circadian clock and abnormal lipid metabolism, we have established a delayed meal timing (DMT) protocol for rats, which started eating food 4 h delay. In the present study, control and DMT rats were fed a high-cholesterol diet during zeitgeber time (ZT) 12-24 and ZT 16-4, respectively. The DMT protocol increased the hepatic lipids and epididymal adipose tissue weight without changes in food intake and body weight. The surge in body temperature was delayed by 4 h in the DMT group, suggesting that energy expenditure was decreased in response to DMT. The peaks of the diurnal rhythm of serum non-esterified fatty acids and insulin were delayed by 2 and 4 h due to DMT, respectively. The oscillation peaks of hepatic <italic>de novo</italic> fatty acid synthesis gene expression was delayed by 4 h in response to DMT, whereas the peak of hepatic clock genes were 2 h delayed or not by DMT. Although metabolic oscillation is considered to be controlled by clock genes, the disintegration rhythms between the clock genes and lipid metabolism-related genes were not observed in rats fed a high-fat diet in our previous study. These data suggest that the circadian rhythm of <italic>de novo</italic> fatty acid metabolism is regulated by timing of eating, but is not directly controlled by clock genes. The present study suggests that breakfast skipping would complicate fatty liver and body fat accumulation.

Excess sucrose intake has been found to be a major factor in the development of metabolic syndrome, especially in promoting nonalcoholic fatty liver disease. The excess fructose is believed to targets the liver to promote de novo lipogenesis, as described in major biochemistry textbooks. On the contrary, in this study, we explored the possible involvement of gut microbiota in excess sucrose-induced lipid metabolic disorders, to validate a novel mechanism by which excess sucrose causes hepatic lipid metabolic disorders via alterations to the gut microbial community structure. Wistar male rats were fed either a control starch diet or a high-sucrose diet for 4 weeks. Half of the rats in each group were treated with an antibiotic cocktail delivered via drinking water for the entire experimental period. After 4 weeks, rats fed with the high-sucrose diet showed symptoms of fatty liver and hyperlipidemia. The architecture of cecal microbiota was altered in rats fed with high-sucrose diet as compared to the control group, with traits including increased ratios of the phyla Bacteroidetes/Firmicutes, reduced α-diversity, and diurnal oscillations changes. Antibiotic administration rescued high-sucrose diet-induced lipid accumulation in the both blood and liver. Levels of two microbial metabolites, formate and butyrate, were reduced in rats fed with the high-sucrose diet. These volatile short-chain fatty acids might be responsible for the sucrose-induced fatty liver and hyperlipidemia. Our results indicate that changes in the gut microbiota induced by a high-sucrose diet would promote the development of nonalcoholic fatty liver disease via its metabolites, such as short-chain fatty acids.

Using rats, we previously found that vitamin C deficiency increases serum levels of interleukin-6 (IL-6) and glucocorticoid, and changes the gene expression of acute phase proteins (APP) in the liver. However, it remains unclear how vitamin C deficiency causes these inflammation-like responses. In this study, we investigated the possibility that changes in gut microbiota are involved in the induction of APP gene expression by vitamin C deficiency. ODS rats that cannot genetically synthesize vitamin C were divided into 4 groups based on the presence or absence of vitamin C or antibiotics and were raised for 15 d. Neomycin, vancomycin, and ampicillin were used as antibiotics, and 300 mg L-ascorbic acid/kg was added to the AIN93G diet. Vitamin C deficiency affected neither the wet tissue weights nor relative abundance of bacteria in the cecal contents. Antibiotic administration increased wet weights of the cecum, cecal contents, and colon, changed the relative abundance of some bacteria in the cecal contents, and decreased serum IL-6 level. However, antibiotic administration had no effect on serum concentrations of corticosterone and α1-acid glycoprotein (AGP), vitamin C concentration in the liver, and mRNA levels of haptoglobin and AGP in the liver. Therefore, disturbance of gut microbiota did not attenuate the increase in glucocorticoid level and induction of APP gene expression due to vitamin C deficiency. This suggests that gut microbiota is not involved in the inflammation-like responses caused by vitamin C deficiency.

Metabolic syndrome has become a global health challenge and was recently reported to be positively correlated with increased sucrose consumption. Mechanistic analyses of excess sucrose-induced progression of metabolic syndrome have been focused mainly on abnormal hepatic lipogenesis, and the exact contribution of excess sucrose to metabolic disorders remains controversial. Considering that carbohydrate and lipid metabolisms exhibit clear circadian rhythms, here we investigated the possible contribution of diurnal oscillations to responses of hepatic lipid metabolism to excess sucrose. We found that excess sucrose dose-dependently promotes fatty liver and hyperlipidemia in in rats fed a high-sucrose diet (HSD). We observed that excess sucrose enhances the oscillation amplitudes of the expression of clock genes along with the levels of hepatic lipid and carbohydrate metabolism-related mRNAs that increase lipogenesis. We did not observe similar changes in the levels of the transcription factors regulating the expression of these genes. This suggested that the excess sucrose-induced, circadian rhythm-dependent amplification of lipogenesis is post-transcriptionally regulated via the stability of metabolic gene transcripts. Of note, our findings also provide evidence that fructose causes some of the HSD-induced, circadian rhythm-dependent alterations in lipogenic gene expression. Our discovery of HSD-induced circadian rhythm-dependent alterations in lipogenesis at the post-transcriptional level may inform future studies investigating the complex relationships among sucrose uptake, circadian rhythm, and metabolic enzyme expression. Our findings could contribute to the design of chrono-nutritional interventions to prevent or manage the development of fatty liver and hyperlipidemia in sucrose-induced metabolic syndrome.

Excessive sucrose intake, known as fructose toxicity, leads to fatty liver, hyperlipidemia, and metabolic syndrome. Circadian disorders also contribute to metabolic syndrome. Here, we investigated the effect of excessive sucrose intake on circadian rhythms of the small intestine, the main location of sucrose absorption, to elucidate a mechanism of sucrose-induced abnormal lipid metabolism. Male Wistar rats were fed control starch or high-sucrose diets for 4 weeks. High-sucrose diet-induced fatty liver and hypertriglyceridemia in rats. Amplitudes of PER1/2 expression oscillations in the small intestine were reduced by excessive sucrose, while gene expression of GLUT5 and gluconeogenic enzymes was enhanced. These changes would contribute to interfering in lipid homeostasis as well as adaptive responses to control fructose toxicity in rats.