8 research outputs found

    The metabolic effects of long term exercise in Type 2 Diabetes patients

    Full text link
    Introduction: The effectiveness of physical exercise in the management of diabetes mellitus type 2 is well established. The purpose of this investigation was to evaluate the effect of long term exercise on glycemic and metabolic control measured after eight months in contrast to patients who had ceased their training after four months. Methods: After an effective 4 months' strength training or endurance training period, ten patients (5 male and 5 female, mean age ± SE:57.1 ± 1.6 yr) were randomised to a further 4 months of combined endurance and strength training, while a control group of 10 patients (5 male and 5 female, mean age ± SE:56. 9± 1.6 yr) ceased training. Results: Long term glycemic control improved and HbA1C values fell from 6.9 ± 0.4 to 6.2 ± 0.2 in active patients and increased from 7.5 ± 0.4 to 8.7 ± 0.6 in control patients (p = 0.002). Baseline levels of total cholesterol significantly decreased in training group (205.5 mg/dl ± 14.1 to 177.5 ± 13.3) and increased in controls (185.9 ± 14.1 to 220.2 ± 15.8) [p = 0.004]. In addition, significant decreases in LDL-cholesterol and triglyceride levels (both p < 0.05) were observed in the training group compared to controls. Conclusion: This study showed that in addition to a 4 month training period, continuation of training proved highly beneficial with further reductions in fasting blood glucose, HbA1C, total cholesterol, LDL-cholesterol, triglyceride, and an elevation in HDL-cholesterol concentrations in diabetes mellitus type 2 patients, thus resulting in a reduced atherogenic lipid profile. In contrast, patients who ceased training after 4 months developed an atherogenic lipid profile and a worsened glycemic control. The results of this study indicate that long term exercise plays an important role in the treatment of diabetes mellitus type 2 and may protect against the development of cardiovascular diseases

    Genotype-phenotype studies in nail-patella syndrome show that LMX1B mutation location is involved in the risk of developing nephropathy.

    Full text link
    Contains fulltext : 47792.pdf (publisher's version ) (Closed access)Nail-patella syndrome (NPS) is characterized by developmental defects of dorsal limb structures, nephropathy, and glaucoma and is caused by heterozygous mutations in the LIM homeodomain transcription factor LMX1B. In order to identify possible genotype-phenotype correlations, we performed LMX1B mutation analysis and comprehensive investigations of limb, renal, ocular, and audiological characteristics in 106 subjects from 32 NPS families. Remarkable phenotypic variability at the individual, intrafamilial, and interfamilial level was observed for different NPS manifestations. Quantitative urinanalysis revealed proteinuria in 21.3% of individuals. Microalbuminuria was detected in 21.7% of subjects without overt proteinuria. Interestingly, nephropathy appeared significantly more frequent in females. A significant association was established between the presence of clinically relevant renal involvement in an NPS patient and a positive family history of nephropathy. We identified normal-tension glaucoma (NTG) and sensorineural hearing impairment as new symptoms associated with NPS. Sequencing of LMX1B revealed 18 different mutations, including six novel variants, in 28 families. Individuals with an LMX1B mutation located in the homeodomain showed significantly more frequent and higher values of proteinuria compared to subjects carrying mutations in the LIM domains. No clear genotype-phenotype association was apparent for extrarenal manifestations. This is the first study indicating that family history of nephropathy and mutation location might be important in precipitating individual risks for developing NPS renal disease. We suggest that the NPS phenotype is broader than previously described and that NTG and hearing impairment are part of NPS. Further studies on modifier factors are needed to understand the mechanisms underlying phenotypic heterogeneity

    Imprinted X chromosome inactivation: evolution of mechanisms in distantly related mammals

    Full text link
    corecore