Experimental gerontology最新文献

Purpose: This study investigated the effects of high-speed (HSRT) and low-speed resistance training (LSRT) on muscle function in individuals with low muscle mass and obesity (LMO).

Methods: Seventy-three participants (65.9 ± 5.8 years; 63 women and 10 men) were randomly assigned to the LSRT, HSRT, and control groups. Participants in the LSRT and HSRT groups received a 16-week resistance training intervention. LSRT and HSRT differed only in concentric speed (4 s vs. 1 s), while the eccentric phase was identical. The control group maintained usual lifestyles. Outcomes were assessed at baseline and after 16 weeks. The primary outcome was quadriceps isokinetic muscle power at 60°/s, 180°/s, and 240°/s. Secondary outcomes were quadriceps isometric and isokinetic muscle torque, rate of force development (RFD) during isometric contraction, muscle electrical activity during both isometric and isokinetic contractions, muscle endurance, and one-repetition maximum (1RM) of all training movements. Analysis of covariance examined between-group effects (α = 0.05).

Results: After the intervention, both LSRT and HSRT groups improved 1RM compared with the control group (p < 0.05), but not peak isometric torque. Only the HSRT group showed greater improvements than the control group in isokinetic muscle power (+19% at 180°/s and + 27% at 240°/s) and RFD (+59%) (all p < 0.05). Neither training group attenuated torque decline during the endurance test (p > 0.05).

Conclusions: Both LSRT and HSRT improved strength, but only HSRT enhanced isokinetic muscle power and RFD in adults with LMO. These findings suggest that incorporating HSRT may provide additional benefits for improving power-related outcomes in this population.

Background: Chronic hyperglycemia, oxidative stress, and mitochondrial dysfunction are central drivers of renal structural and functional alterations associated with metabolic disease and accelerated tissue aging. In type 2 diabetes mellitus (T2DM), these mechanisms contribute to early kidney injury and progressive decline in renal resilience. Dietary interventions, including the Mediterranean diet (MD), have been proposed as complementary strategies to counteract metabolic stress, yet mechanistic evidence at the renal mitochondrial level remains limited.

Methods: Male db/db mice, a model of obesity- and diabetes-associated metabolic stress, were fed for 8 weeks a standard diet (SD), a Western diet (WD), or a lab-designed MD-based food mix. Db/m littermates on SD served as controls. Renal function, morphology, and molecular pathways related to mitochondrial homeostasis, oxidative stress, and tissue remodeling were assessed through metabolic profiling, histological evaluation, and protein expression analyses.

Results: Db/db mice displayed overt metabolic dysfunction with increased glucosuria, polyuria, and water intake. SD- and WD-fed db/db animals showed a significant increase in urinary albumin-to-creatinine ratio (uACR), whereas MD-fed db/db mice maintained uACR at control levels, together with preserved serum creatinine and potassium. Histological analyses revealed attenuation of tubular hydropic changes and prevention of glomerular hypertrophy and hypercellularity under MD. At the molecular level, MD preserved nephrin expression, prevented diabetes-induced increases in NOX2, RAGE, and nitrotyrosine, and maintained mitochondrial dynamics by preserving the fission/fusion balance. Moreover, MD limited alterations in autophagy/mitophagy markers and reduced profibrotic (MT-MMP1, TIMP2) and hypoxia-related (HIF1α, VEGF) signaling.

Conclusions: A balanced MD-based dietary mix preserves renal structure and function in db/db mice by counteracting oxidative stress, mitochondrial dysfunction, and early fibrotic remodeling. These findings support the MD as a potential nutritional strategy to enhance renal resilience and mitigate metabolic stress-induced kidney aging in the context of diabetes and obesity.

Purpose: Aging and sarcopenia are associated with metabolic inflexibility. This study investigated the effects of resistance exercise (RE) and a high protein diet (PRO) on metabolic flexibility (the ability to adjust rates of substrate oxidation to changes in fuel availability) in older men.

Methods: In a pooled groups analysis, 33 healthy older men [(mean ± SE) age: 67 ± 1 years; BMI: 25.4 ± 0.4 kg/m²] were randomized to either RE (2×/week; n = 17) or no exercise (NE; n = 16), and either high protein diet [~1.6 g/kg/day (~25% of energy intake (EI))] via twice daily (25 g) whey protein supplementation (PRO; n = 17) or control (CON, 2 × 23.75 g maltodextrin/day; n = 16). An exploratory sub-analysis was also conducted between RE + CON (n = 8) and RE + PRO (n = 9). At baseline and 12 weeks, participants resided in whole-room indirect calorimeters for 24 h for measurement of metabolic flexibility via changes in relative substrate utilization [non-protein respiratory quotient (npRQ)] under different conditions (fasting sleep to awake, step exercise, and 2 h postprandial meal consumption, and peak step exercise to exercise end).

Results: Compared to NE, RE significantly increased (indicating medium-to-large effects on improved metabolic flexibility) ΔnpRQ (awake-sleep) (+0.02 ± 0.004 vs. 0.00 ± 0.05, p = 0.01, f = 0.48), and ΔnpRQ (steady state exercise-sleep) (p ≤ 0.045) and ΔnpRQ (peak exercise-exercise end) (p ≤ 0.04, f = 0.39-0.64) for two step exercise bouts performed ~2 h postprandially. Compared to CON, PRO increased ΔnpRQ (steady state-sleep) for one step exercise bout (+0.02 ± 0.01 vs. -0.002 ± 0.01, p = 0.047, f = 0.39). No significant differences occurred between the RE + CON and RE + PRO groups (p ≥ 0.06).

Conclusion: In older men, RE improved metabolic flexibility. PRO had a limited benefit. No synergistic effects were observed.

Chronic Liver Disease (CLD) represents a growing epidemic in the Western world, yet treatment options that effectively slow its progression remain limited. Mammalian target of rapamycin (mTOR) inhibitors, such as sirolimus (also known as rapamycin), have been proposed as potential antifibrotic agents over the past decade; however, their role in chronic liver disease remains underexplored. mTOR is a protein kinase integral to a key cellular pathway, which is essential for normal liver physiology but is also implicated in the pathogenesis of CLD and hepatocellular carcinoma (HCC). This narrative review summarises the role of mTOR in the healthy liver, its dysregulation across common aetiologies of CLD, and its role in HCC. An electronic literature search of Ovid MEDLINE was conducted from database inception to 2025 to identify studies evaluating the role of MTOR in CLD. The review underscores a clear unmet need for well-designed human clinical trials to specifically assess mTOR inhibitors as potential anti-fibrotic therapies.

Objectives: Moderately severe or severe acute pancreatitis (MSAP/SAP) is a crucial abdominal disorder. Enteral nutrition (EN) is a central issue after patients pass through the resuscitation stage. The preference for EN formulas and initial timing opportunities are controversial topics. We investigated the linkage between two types of EN formulas, short peptides and intact proteins, and initial time and SAP prognosis.

Methods: 335 enrolled SAP patients were divided into three groups according to the EN formula accepted during two weeks of feeding. The groups were set as SPG (group fed by short peptide, SP), IPG (group fed by intact protein, IP) and CG (group converted from SP to IP at second week). Pearson's chi-square test and the Kruskal-Wallis test were used to compare the descriptive variables. Binary logistic regression was used to analyze the relationship between initial time and mortality. K-M survival curves and log-rank tests were used to evaluate long-term prognosis.

Results: Although the patients were either fed by SP, IP or a mixture of products (from the SP to the IP), the groups showed no difference in the serum albumin/prealbumin recovery, invasive mechanical ventilation or 90-day survival rate. Timely EN formula conversion from the SP to the IP may reduce the insulin dosage for glucose-impaired patients. The results also proved that EN started 3-5 days after the onset of SAP was associated with lower mortality.

Conclusions: Therefore, an optimal EN strategy can be summarized. First, the selection of the EN formula should be based on the patients' basic conditions, especially glucose level, rather than on the pancreatic rest theory. Second, the conversion from SP to IP made it easier for patients to tolerate the EN and decreased insulin use. Finally, the proper opportunity to commence EN was considered to be 3-5 days after SAP onset.