半澤 史聡

Physical inactivity as well as breakfast skipping is known as risk factor for various metabolic diseases, such as obesity and type 2 diabetes. We have previously reported that a breakfast skipping model, in which the timing of feeding is delayed, induces abnormal lipid metabolism by altering the circadian rhythm of lipid metabolism-related genes in rats. The purpose of this study was to elucidate the synergistic effect of physical inactivity and breakfast skipping on lipid metabolism. We adopted sciatic neurectomized rats as physically inactive models, because we confirmed that the rats mildly decreased their spontaneous locomotor activity compared to sham-operated rats. And then the physically inactive model rats were fed a mild high-fat diet during zeitgeber time (ZT) 12-0 in the control group and ZT16-0 in the breakfast skipping group for 11 days. Body weight gain and total food intake were similar in both groups. Breakfast skipping induced a significant visceral fat accumulation, which was not observed in our previous breakfast skipping or physically inactive studies. The mRNA levels of clock and lipogenesis-related genes were altered by breakfast skipping in the liver and epididymal adipose tissue, and serum insulin level was altered by breakfast skipping. These results suggest that physical inactivity and breakfast skipping synergistically induces drastic visceral fat accumulation due to the alteration of circadian clock and lipid metabolism in the liver and adipose tissue. Therefore, regular feeding timing plays an important role in the health of a sedentary modern society.

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.

Recent reports have associated the use of social networking sites (SNS) with the drive for thinness in young women; however, its influence on their actual body shape and eating behaviors (EB) remains unclear. We aimed to examine the effect of SNS use on body mass index (BMI), body image (BI), and EB in young women. Participants included 196 healthy women (20–29 years) who answered questions about their SNS use, height, weight, BI and EB via a web-based survey. First, the correlation between time spent on SNS and each variable was determined. Participants were then divided into quartiles according to the duration of daily SNS use as long (≥3 h, n = 52) and short (<1 h, n = 54), and the data were then compared between the groups. Correlation analysis showed that the longer the duration of daily SNS use, the significantly lower the BMI, the use of nutrition labels, and the frequency of consumption of milk and dairy products. The long group had significantly lower BMI and ideal BI than the short group. The results suggest that spending more time on SNS in young women may be associated with thinner actual and ideal body shapes and poorer access to health information and healthy foods.

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.