Low phase angle (PhA), as determined via bioelectrical impedance analysis, reflects unhealthy aging and mortality. In this study, we assessed whether nutritional status, including serum nutritional markers and dietary habits, is related to PhA in older individuals. We recruited 212 participants (aged ≥ 65 years) who underwent medical health checkups. PhA was measured using a multi-frequency impedance body composition analyzer. Habitual food and nutrient intake was evaluated using a brief, self-administered diet history questionnaire. Low PhA values were defined as ≤4.95 in males and ≤4.35 in females. Males with low PhA had poor exercise habits (p = 0.0429) and a lower body mass index (p = 0.0024). PhA was significantly correlated with serum cholinesterase levels, a nutritional status marker (r = 0.3313, p = 0.0004 in males; r = 0.3221, p = 0.0070 in females). The low-PhA group had significantly lower total energy and carbohydrate intake per ideal body weight (IBW) than the high-PhA group in males (total energy intake:30.2 ± 9.8 and 34.5 ± 9.3 kcal/kg/day, p = 0.0307; carbohydrate intake:15.2 ± 4.9 and 18.0 ± 5.8 kcal/kg/day, p = 0.0157). Total energy intake per IBW (adjusted odds ratio [95% confidence interval], 0.94 [0.89–1.00] per 1 kcal/kg/day increase) was independently associated with a low PhA in males. Our study revealed that lower total energy intake independently impacted low PhA in older males.

Background: Sarcopenic obesity, the coexistence of sarcopenia and obesity, has been linked to adverse health outcomes due to comorbidity. Evidence on the association between sarcopenic obesity and mortality among individuals with Type 2 diabetes remains limited Methods: Sarcopenic obesity was defined using Japan Working Group on Sarcopenic Obesity criteria. Participants were divided into four groups based on the presence of sarcopenia and obesity. Cox proportional hazards models evaluated the mortality risk. Subgroup analyses were performed by age (40–75 vs. >75 years). Sensitivity analysis was performed by dichotomizing participants into sarcopenic obesity and non‐sarcopenic obesity groups. Results: Of the 799 participants (mean age 68.6 years, 59.3% men), proportions of neither sarcopenia nor obesity, obesity alone, sarcopenia alone and sarcopenic obesity were 56.2%, 34.5%, 6.3% and 3.0%, respectively. During a median follow‐up of 46 months, 41 deaths occurred. Compared with neither of them, the adjusted hazard ratios (aHRs) (95% CI) of mortality in obesity alone, sarcopenia alone and sarcopenic obesity were 0.53 (0.18–1.57) ( p = 0.25), 2.36 (0.99–5.6) ( p = 0.053) and 2.89 (1.01–8.30) ( p = 0.048), respectively. Age‐stratified analyses revealed that sarcopenic obesity markedly increased mortality risk in participants aged 40–75 years (aHR 13.1 [2.93–58.4], p < 0.001), whereas sarcopenia alone (aHR 3.21 [1.07–8.33], p = 0.004), but not sarcopenic obesity (aHR 1.41 [0.34–8.81], p = 0.51), was associated with increased mortality in those aged > 75 years. Compared with non‐sarcopenic obesity, sarcopenic obesity had a significantly higher hazard ratio for mortality (aHR 4.0 [1.44–11.0], p = 0.008). In age‐stratified analysis, this association remained significant in participants aged 40–75 years (aHR 14.1 [3.25–61.5], p < 0.001), but not in those aged > 75 years (aHR 1.55 [0.32–7.46], p = 0.59) (interaction p = 0.03). Conclusions: In Japanese individuals with Type 2 diabetes, sarcopenic obesity was significantly associated with increased mortality risk. This relationship was particularly pronounced in individuals aged 40–75 years, whereas sarcopenia alone was associated with increased mortality risk rather than sarcopenic obesity in individuals aged > 75.

Aim: This study aimed to investigate how sarcopenia and nutritional risk influence all-cause mortality among older individuals with type 2 diabetes mellitus. Methods: In view of the presence of sarcopenia, defined according to the Asian Working Group for Sarcopenia (AWGS) criteria, and nutritional risk, as determined by the Geriatric Nutritional Risk Index (GNRI), a total of 396 participants were divided into four distinct groups (group 1: no nutritional risk and no sarcopenia, n = 306; group 2: nutritional risk and no sarcopenia, n = 32; group 3: no nutritional risk and sarcopenia, n = 36; and group 4: nutritional risk and sarcopenia, n = 22). Mortality risk was assessed through time-to-event analysis using Cox regression. Results: Throughout the 86-month median follow-up, 31 participants died. Compared to group 1, hazard ratios (HRs) for mortality of groups 2, 3, and 4 were 9.08 (95% confidence interval (95% CI), 2.44–33.8), 9.08 (95% CI: 2.44–33.8), and 14.0 (95% CI: 4.62–42.4), respectively. The risk of death was significantly higher in groups 2, 3, and 4 compared to group 1. Additionally, group 4 had a significantly higher risk of death than group 3. However, no significant difference in mortality risk was observed between groups 3 and 4 when compared to group 2. Conclusions: Coexistence of nutritional risk and sarcopenia was linked to an increased risk of mortality across older individuals with type 2 diabetes mellitus. There was no significant difference in mortality between individuals presenting or not presenting with sarcopenia within the nutritional risk group; therefore, greater attention should be directed toward malnutrition.

Bilirubin is associated with vascular complications in diabetes. However, the correlation between bilirubin and sarcopenia or muscle strength has not been investigated. This study aimed to investigate the association between total bilirubin and skeletal muscle mass index (SMI), hand grip strength (HGS), and sarcopenia in patients with type 2 diabetes. This cross-sectional study included 1,108 patients with type 2 diabetes from three hospitals in Japan. Multiple and logistic regression analyses were used to examine the relationships between total bilirubin and SMI, HGS, and sarcopenia. Of the participants, 473 (43%) were women. The median (interquartile range) age, and glycated hemoglobin were 67 (59–73) years, and 7.4 (6.7–8.6) %, respectively. The median SMIs for women and men were 6.32 (5.73–7.04) kg/m2 and 7.53 (7.02–8.19) kg/m2, respectively. The median HGS for women and men were 21.5 (17.5–25.0) kg and 36.0 (30.0–41.5) kg, respectively. Sarcopenia was present in 11% and 12% of women and men, respectively. No correlation was observed between total bilirubin and SMI in both sexes. No significant association was observed between total bilirubin and HGS in men, whereas a positive correlation was observed in women (β = 0.18, p = 0.01). Total bilirubin was negatively associated with sarcopenia in women (odds ratio = 0.80, 95% confidence interval: 0.64–0.98, interaction p = 0.02). The total bilirubin was significantly associated with HGS and sarcopenia in women with type 2 diabetes. Total bilirubin may serve as a useful indicator of sarcopenia in Japanese women.

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) has been linked to dietary fat quality and polyunsaturated fatty-acid metabolism. We evaluated whether dietary n-6 fatty-acid intake, serum dihomo-γ-linolenic acid (DGLA), and desaturase-based indices for Δ5-desaturase (D5D) and Δ6-desaturase (D6D) are associated with MASLD. Methods: We conducted a cross-sectional analysis within the HOZUGAWA health checkup cohort in Japan (n = 289; 100 MASLD, 189 non-MASLD). Participants underwent hepatic ultrasonography, dietary assessment using the Brief Self-Administered Diet History Questionnaire, and fasting serum metabolomics by gas chromatography–mass spectrometry with solid-phase dehydration derivatization. Enzyme indices were defined as the D5D index = arachidonic acid/DGLA and the D6D proxy index = DGLA/linoleic acid (hereafter referred to as the D6D index) because γ-linolenic acid was not measured. Natural-log-transformed D5D index, D6D index, DGLA, and total dietary n-6 fatty-acid intake were entered into multivariable logistic regression models for MASLD adjusted for age, sex, BMI, alcohol intake, and total energy. Results: Compared with non-MASLD, MASLD showed higher serum DGLA, lower D5D index, and higher D6D index (all p ≤ 0.005), with no between-group differences in total energy intake, linoleic acid, total polyunsaturated fatty acids, or total dietary n-6 fatty-acid intake. Higher ln D5D was independently associated with lower odds of MASLD (OR 0.62, 95% CI 0.42–0.86), whereas higher ln D6D index (OR 1.42, 95% CI 1.04–1.95) and ln DGLA (OR 1.62, 95% CI 1.13–2.43) were each positively associated. Total dietary n-6 fatty-acid intake was not independently associated with MASLD. Conclusions: In this Japanese health examination cohort, an imbalance in estimated desaturase activities—lower D5D index and higher D6D index—together with higher serum DGLA was independently associated with MASLD, whereas n-6 intake showed no group difference or independent association. These findings suggest that enzyme-linked endogenous n-6 metabolic status may be more closely related to the MASLD phenotype than intake quantity alone.