Search

The relationship between serum uric acid (sUA) and cognitive function is contradictory. This study assessed the association between sUA and cognitive impairment in 10,039 community–dwelling subjects aged ≥55 years living in Beijing, China. Participants underwent determination of sUA and an evaluation of cognitive function using the scholarship-adjusted Mini-Mental State Examination (MMSE): MMSE ≤17 for illiterates; MMSE ≤ 20 for primary school graduates (≥6 years of education); and MMSE ≤ 24 for junior school graduates or above (≥9 years of education). Among the 10016 persons with valid MMSE scores, the prevalence of cognitive impairment was 9.14%. A multivariate logistic regression model including demographic, clinical and genetic parameters was performed to assess the relationship between sUA and cognitive impairment. Persons with cognitive impairment had lower sUA levels than those with normal cognitive function: (302.30 ± 82.80 vs. 312.20 ± 84.01 μmol/L, p = 0.001). After adjusting for age, sex, lifestyle, relevant diseases and the apolipoprotein E (APOE) ε4 allele, stepwise logistic regression showed that participants with higher levels of sUA had a lower risk of cognitive impairment (hazard ratio (HR): 0.78; 95% confidence interval (CI): 0.62–0.96; p = 0.022). In this baseline cross-sectional population-based sample, high levels of sUA were associated with a decreased risk of cognitive impairment. [ABSTRACT FROM AUTHOR]

With aging populations around the world, frailty is becoming more prevalent increasing the need to early identify those at risk of frailty. The association between thyroid hormone levels and frailty in subjects with type 2 diabetes mellitus (T2DM) remains unclear. The objective of the study was to evaluate the relationship between thyroid hormone concentrations and frailty in older adults with T2DM. A total of 240 older adults with T2DM were divided into three groups according to the frailty phenotype criteria: robust group (n = 94), pre-frail (n = 110) and frail group (n = 36). Concentrations of free triiodothyronine (FT3), free thyroxine (FT4) and thyroid-stimulating hormone (TSH), 25-hydroxyvitamin D 3 [25(OH) D 3 , highly sensitive C-reactive protein (hs-CRP) and interleukin-6 (IL-6) were determined. Handgrip strength was measured using a Jamar hand dynamometer. Physical function was assessed by gait speed and the timed go and up (TUG) test. Logistic regression analysis was performed to evaluate the association between FT3 and frailty. The FT3 level was the lowest among frail people (2.56 ± 0.42 pg/mL), followed by pre-frail participants (2.73 ± 0.38 pg/mL), with the highest among the robust subjects (2.83 ± 0.43 pg/mL). FT3 level was positively correlated with handgrip strength and gait speed (R = 0.313, P < 0.001; R = 0.250, P < 0.001, respectively), while negatively correlated with TUG time (R = −0.276, P < 0.001). After adjusting for age, sex, TSH, 25(OH) D 3 and estimate glomerular filtration rate (eGFR), logistic regression showed that low FT3 was significantly associated with an increased risk of frailty (odds ratio (OR): 4.53; 95% confidence interval (CI): 1.89–10.83; P = 0.001). Low levels of FT3 were associated with an increased risk of frailty in older adults with T2DM. Measuring FT3 might be useful for identifying those at high risk of frailty. • The association between thyroid hormone concentrations and frailty in older adults with T2DM was investigated. • The free triiodothyronine (FT3) FT3 level was the lowest among frail people • Low levels of FT3 were associated with an increased risk of frailty [ABSTRACT FROM AUTHOR]

• Ketone diet reduced blood glucose and prevented body weight increase in db/db mice. • Ketone diet regulated expressions of genes involved in neurodegenerative disease in db/db mouse brains. • Ketone diet improved proteasomal activities in db/db mouse brains. Type 2 diabetes mellitus (T2DM) is a major risk factor of a number of neurodegenerative diseases (NDDs). Ketogenic diet (KD) has significant beneficial effects on glycemic control and may act effectively against NDDs, but the mechanism remains unclear. In this study, we aimed to investigate the potential effects of KD on gene expressions in the brains of T2DM model mice. Male db/db mice at the age of 9 weeks were fed with KD or normal diet to the age of 6 months, and the whole brains were subjected to mRNA-seq analysis for differentially expressed genes. KD significantly lowered fasting glucose and body weights in db/db mice (P < 0.05), and the expression of 189 genes in the brain were significantly changed (P < 0.05, |log2| > 1). Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses revealed that the differentially expressed genes upon KD are involved in inflammatory responses and the functions of biosynthesis. In inflammatory responses, NF-κB signaling pathway, viral protein interaction with cytokine and cytokine receptor, and cytokine-cytokine receptor interaction pathways were enriched, and in biosynthesis pathways, genes functioning in lipid and amino acid metabolism, protein synthesis, and energy metabolism were enriched. Moreover, consistent with the gene set enrichment analysis results, proteasomal activity measured biochemically were enhanced in KD-fed T2DM mice. These data may facilitate the understanding of how KD can be protective to the brain in T2DM background. KD could be a new strategy for the prevention of NDDs in T2DM patients. [ABSTRACT FROM AUTHOR]