Kanako Deguchi

BACKGROUND: Underweight (BMI < 18.5 kg/m2) remains prevalent among young Japanese women but lacks standardized measurement approaches. We compared four analytical methods and identified discrepancies. METHODS: A retrospective analysis of 883 underweight women aged 20-29 years followed for 6.1 ± 4.2 years was performed. We compared (1) year-to-year transitions, (2) state occupancy, (3) the Aalen-Johansen estimator, and (4) Kaplan-Meier Survival Analysis. We performed bidirectional flow analysis quantifying inflow/outflow rates, BMI distribution analysis, and time-weighted classification. RESULTS: Methods 1 and 4 showed 31-point discrepancies (78.1% vs. 47.1% in women). In bidirectional flow, inflow exceeded outflow at ages 22-27 (35.7%/yr vs. 20.7%/yr, outflow/inflow ratio: 0.58), balanced at ages 27-37 (ratio: 1.02) and showed outflow-dominant pattern at ages 37-47 (ratio: 4.92). BMI clustered at 18.0-19.0 kg/m2 (42.7%); 69.4% crossed the threshold once. Time-weighted classification revealed four phenotypes: persistent (≥75% time underweight; 40.1%, BMI: 17.54 kg/m2), moderate (50-74%; 17.6%, BMI: 18.40 kg/m2), intermittent (25-49%; 17.6%, BMI: 18.97 kg/m2), and transient (<25%; 24.8%, BMI: 19.49 kg/m2). The moderate + intermittent group showed yo-yo phenotypes (35.2%). CONCLUSIONS: Underweight in young Japanese women should be viewed as a heterogeneous dynamic nutritional state. The methodological discrepancy, threshold crossing, and phenotypic classification show that BMI-defined underweight comprises distinct patterns. Cross-sectional data evaluation may lead to incorrect assessments. Future research examining relationships between longitudinal low body weight subgroups and clinical outcomes could identify at-risk populations within the underweight group.

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.