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Biomedical subjects

N Kibiryeva

Publications and source records attributed to N Kibiryeva.

5 recordsLinked to original sources
PubMed2006

Abnormal EKG stress test in rats with type 1 diabetes is deterred with low-intensity exercise programme.

The focus of this study was to determine whether minimal levels of exercise could halt the formation of diabetes-induced heart pathology. Seven-week-old male rats were divided into four groups: sedentary nondiabetic, exercise-trained non-diabetic, sedentary diabetic and exercise-trained diabetic. Individualised exercise programmes were based on the animal's tolerance, and continued for 7 weeks after the induction of diabetes. At the completion of the study, no differences were found in skeletal muscle citrate synthase activity between diabetic sedentary and exercise-trained rats, indicating that the exercise was low intensity. Diabetes-induced heart hypertrophy was not reversed with exercise as measured by heart-to-body weight ratios and EKG (R wave height). There was no statistical difference between groups in the response to an exercise stress test prior to the induction of diabetes. However, 4 weeks of diabetes resulted in a significant decrease in resting and post-stress test heart rates (9% and 20%, respectively), which remained depressed at week 7. The sedentary diabetic animals demonstrated an abnormal response during the recovery period of the EKG exercise test, which was not present in non-diabetic or exercise-trained diabetic animals. In conclusion, lowintensity exercise training improved the cardiac response to an exercise stress test in diabetic animals.

Animals↗
PubMed2006

Circulating adiponectin levels, body composition and obesity-related variables in Prader-Willi syndrome: comparison with obese subjects.

BACKGROUND: People with obesity and/or the metabolic syndrome have an increased risk for developing diabetes and cardiovascular disease and may have low adiponectin levels. The obesity associated with Prader-Willi syndrome (PWS) would be expected to have similar complications. However, it was recently reported that, despite their adiposity, people with PWS have reduced visceral fat and are less likely to develop diabetes mellitus or the metabolic syndrome compared with people with simple obesity. OBJECTIVE: To determine if plasma adiponectin levels and other variables relevant to diabetes and cardiovascular risk are different in a cohort of PWS subjects with known genetic subtypes compared with age-, sex- and weight-matched control subjects. RESULTS: Fasting plasma glucose, C-peptide, triglycerides, leptin and cholesterol levels were similar in PWS and obese subjects. Our 20 PWS subjects (mean age = 27.7 years) had higher percent body fat (54.1 vs 48.5%) determined by DEXA measurements and lower percent lean mass (45.9 vs 51.5%) compared with 14 obese controls (mean age = 26.9 year). Plasma adiponectin levels were significantly higher in PWS (15.5 +/- 8.2 microg/ml) than in obese controls (7.5 +/- 2.7 microg/ml). A significant positive correlation was found with insulin sensitivity in PWS subjects (r = 0.75, P = 0.0003) but not in obese controls (r = 0.36, P = 0.20). DISCUSSION: Our study confirmed an earlier observation of higher adiponectin levels in PWS subjects and less insulin resistance proportionate to their obesity status than found in subjects with simple obesity. Furthermore, no differences were seen in PWS subjects with the chromosome 15 deletion or maternal disomy 15. The reported excessive visceral adiposity in subjects with simple obesity compared with PWS may be associated with decreased production and lower circulating levels of adiponectin.

Adiponectin↗
PubMed2005

Brief report: non-random X chromosome inactivation in females with autism.

Autism is a heterogeneous neurodevelopmental disorder with a 3-4 times higher sex ratio in males than females. X chromosome genes may contribute to this higher sex ratio through unusual skewing of X chromosome inactivation. We studied X chromosome skewness in 30 females with classical autism and 35 similarly aged unaffected female siblings as controls using the polymorphic androgen receptor (AR) gene. Significantly, increased X chromosome skewness (e.g., >80:20%) was detected in our autism group (33%) compared to unaffected females (11%). X chromosome skewness was also seen in 50% of the mothers with autistic daughters. No mutation was seen in the promoter region of the XIST gene reported to be involved in X chromosome inactivation in our subjects. X chromosome skewness has been reported in female carriers of other neurological disorders such as X-linked mental retardation, adrenoleukodystrophy and Rett syndrome.

Autistic Disorder↗
PubMed2003

Microarray analysis of gene/transcript expression in Prader-Willi syndrome: deletion versus UPD.

BACKGROUND: Prader-Willi syndrome (PWS), the most common genetic cause of marked obesity, is caused by genomic imprinting and loss of expression of paternal genes in the 15q11-q13 region. There is a paucity of data examining simultaneous gene expression in this syndrome. METHODS: We generated cDNA microarrays representing 73 non-redundant genes/transcripts from the 15q11-q13 region, the majority within the PWS critical region and others distally on chromosome 15. We used our custom microarrays to compare gene expression from actively growing lymphoblastoid cell lines established from nine young adult males (six with PWS (three with deletion and three with UPD) and three controls). RESULTS: There was no evidence of expression of genes previously identified as paternally expressed in the PWS cell lines with either deletion or UPD. We detected no difference in expression of genes with known biallelic expression located outside the 15q11-q13 region in all cell lines studied. There was no difference in expression levels of biallelically expressed genes (for example, OCA2) from within 15q11-q13 when comparing UPD cell lines with controls. However, two genes previously identified as maternally expressed (UBE3A and ATP10C) showed a significant increase in expression in UPD cell lines compared with control and PWS deletion subjects. Several genes/transcripts (for example, GABRA5, GABRB3) had increased expression in UPD cell lines compared with deletion, but less than controls indicating paternal bias. CONCLUSIONS: Our results suggest that differences in expression of candidate genes may contribute to phenotypic differences between PWS subjects with deletion or UPD and warrant further investigations.

Adult↗