Kanako Deguchi

Background: Studies outside Japan have linked sugar-sweetened beverage (SSB) intake with weight gain; however, evidence in Japanese adults is scarce, and no study has examined beverage-derived energy in relation to anthropometric indices and handgrip strength. Methods: The participants were employees of Fujita Health University aged 20-39 years (n = 76; male n = 35, average age: 29.97 ± 4.67 years; female n = 41, average age: 27.29 ± 4.53 years). Energy from beverage intake was assessed via the Brief Beverage Intake Questionnaire-15, and energy from alcoholic drinks, milk, SSBs, and total beverages was calculated. The associations of energy from different beverages with nutrient intake, BMI, skeletal muscle mass index (SMI), and handgrip strength were analyzed via ordinary least squares (OLS) regression; quantile regression (QR) and the generalized additive model (GAM) were used for sensitivity analyses. Results: Increased SSB intake was associated with increased BMI (standardized β = 0.35, 95% CI 0.12-0.58, p(OLS) < 0.001; p(QR) = 0.23; p(GAM) < 0.001) and was nonlinearly associated with increased SMI (standardized β = 0.21, 95% CI 0.043-0.37, p(OLS) = 0.02; p(QR) = 0.11; p(GAM) = 0.02), even after adjustment for total energy intake. Modest milk intake was linked to higher protein intake and a higher SMI without a higher BMI (standardized β = 0.18, 95% CI 0.020-0.35, p(OLS) = 0.03; p(QR) = 0.39; p(GAM) = 0.03). Conclusions: A positive association was found between SSB intake and both BMI and SMI and between MILK intake and SMI. Clarification in larger, diverse Japanese populations will be necessary.

Type 1 diabetes mellitus is a major risk factor for both sarcopenia and osteoporosis, primarily due to the body's inability to utilize glucose as a result of insulin deficiency. Impairments in insulin and glucose signaling can accelerate the decline in muscle and bone health. To investigate this interaction, we examined whether insulin deficiency exacerbates muscle and bone deterioration in Chrebp knockout (KO) mice. Male wild-type (WT) and KO mice, aged 18 weeks, were intraperitoneally treated with 200 mg/kg BW streptozotocin (STZ), which selectively destroys pancreatic beta cells, thereby inducing insulin deficiency. Two weeks after STZ administration, compared with STZ-treated WT mice, STZ-treated KO mice presented significantly greater reductions in body weight and gastrocnemius muscle weight (BW: WT-vehicle vs. WT-STZ; 2.58 [-1.23, 6.39] (p = 0.21); KO-vehicle vs. KO-STZ: 8.03 [5.23, 10.82]; GA muscle: WT vehicle vs. WT STZ: 0.084 [0.047, 0.12], p < 0.0001; KO vehicle vs. KO STZ: 0.084, [0.047, 0.12], p < 0.0001). The decrease in grip strength caused by STZ administration was greater in the KO mice than in the WT mice (mean differences [95% CIs]: WT vehicle-WT STZ, 49.6. [0.9, 98.4], p = 0.046; WT STZ-KO STZ: 71.40 [29.1, 113.7], p = 0.0059; KO vehicle-KO STZ: 84.3 [51.9, 116.8], p = 0.0003). Consistent with these findings, STZ administration reduced IGF-1 expression and increased atrogin mRNA levels, with the highest levels in STZ-treated KO mice. In skeletal muscle, the changes in IGF-1 and Atrogen induced by STZ administration were significantly greater in the KO group than in the WT group (IGF-1: WT vehicle-WT STZ: 0.19 [-0.072, 0.46], p = 0.17; KO vehicle-KO STZ: 0.79 [0.53, 1.06], p < 0.0001; Atrogen: WT vehicle-WT STZ: -2.7 [-3.01, -2.29], p < 0.0001; KO vehicle-KO STZ: -3.35 [-3.71, -2.99], p < 0.0001). The BMD in the Chrebp-deficient group was greater than that in the wild-type group (WT vehicle-KO vehicle: -5.2 [-8.4, -1.9], p = 0.0014); however, the administration of STZ significantly decreased the BMD only in the KO group (WT vehicle-WT STZ: p = 0.45, KO vehicle-KO STZ: 7.2 [3.9, 10.4], p < 0.0001). These results suggest that Chrebp deficiency combined with insulin deficiency aggravates sarcopenia and osteoporosis risk. Therefore, insulin and glucose signals are important for maintaining muscle and bone mass and function. However, further studies are needed to elucidate the mechanisms by which ChREBP deletion and insulin deficiency cause osteosarcopenia.

Background and Aim: Underweight young adult women are vulnerable to health risks such as menstrual disorders and vitamin deficiencies. Because few seek medical care for low body weight, the underlying causes remain unclear. This study aimed to examine the associations of body type with dietary patterns and gut microbiota diversity in young women. Methods: We enrolled 40 women aged 20-39 years who visited a nutrition evaluation clinic with a BMI < 17.5 at their first consultation (underweight group) and 40 age-matched women with 18.5 ≤ BMI < 25 (control group). Some women in the underweight group were no longer underweight at the time of analysis but were classified based on their initial BMI. Dietary patterns were assessed based on ten major food categories (meat, fish, eggs, dairy products, soybeans, green and yellow vegetables, seaweed, fruit, tubers, and fats and oil) based on the Food Frequency Questionnaire based on Food Groups. Gut microbiota α-diversity was evaluated using the Shannon, Simpson, and Pielou indices, while β-diversity was analyzed by nonmetric multidimensional scaling (NMDS) and redundancy analysis (RDA). Genera contributing to group differences were identified by RDA and ANOVA-Like Differential Expression tool (ALDEx2). Results: Underweight women had significantly lower gut microbiota α-diversity, while no difference was observed in dietary patterns. NMDS revealed significant β-diversity differences in gut microbiota (PERMANOVA: R2 = 0.064, F = 5.31, p = 0.0001) but not in dietary patterns (p = 0.99). RDA showed that body type explained 4.5% of variance (adjusted R2 = 0.032, F = 3.65, p = 0.0005). Bacteroides, Bifidobacterium, Enterocloster, and Erysipelatoclostridium were enriched in underweight women, whereas Fusicatenibacter, Agathobacter, Dorea, and Prevotella were enriched in controls. AldEx2 confirmed increases in Bacteroides, Enterocloster, and Erysipelatoclostridium and a decrease in Dorea. Conclusions: Underweight women demonstrated reduced gut microbiota diversity and enrichment of taxa associated with inflammatory tendencies. Dietary therapies involving not only prebiotics but also probiotics may beneficially modulate gut microbiota and contribute to the management of low body weight.