A Population‐Based Twin Study on Sleep Duration and Body Composition

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/93648/1/oby.2011.274.pd

Tracking Blood Glucose and Predicting Prediabetes in Chinese Children and Adolescents: A Prospective Twin Study

We examined the tracking of blood glucose, the development of prediabetes, and estimated their genetic contributions in a prospective, healthy, rural Chinese twin cohort. This report includes 1,766 subjects (998 males, 768 females) aged 6–21 years at baseline who completed a 6-year follow-up study. Oral glucose tolerance test was performed for all subjects at both baseline and follow-up. We found that subjects with low fasting plasma glucose (FPG) or 2 h post-load glucose (PG) levels at baseline tended to remain at the low level at follow-up. Subjects in the top tertile of baseline plasma glucose tended to have a higher risk of developing prediabetes at follow-up compared to the low tertile: in males, 37.6% vs. 27.6% for FPG and 37.2% vs. 25.7% for 2hPG, respectively; in females, 31.0% vs. 15.4% for FPG and 28.9% vs. 15.1% for 2 h PG, respectively. Genetic factors explained 43% and 41% of the variance of FPG, and 72% and 47% for impaired fasting glucose for males and females, respectively; environmental factors substantially contribute to 2hPG status and impaired glucose tolerance. In conclusion, in this cohort of healthy rural Chinese children and adolescents, we demonstrated that both FPG and 2hPG tracked well and was a strong predictor of prediabetes. The high proportion of children with top tertile of blood glucose progressed to prediabetes, and the incidence of prediabetes has a male predominance. Genetic factors play more important role in fasting than postload status, most of which was explained by unique environmental factors

GREB1 Functions as a Growth Promoter and Is Modulated by IL6/STAT3 in Breast Cancer

BACKGROUND: Growth Regulation by Estrogen in Breast cancer (GREB1) was an estrogen receptor (ER) target gene, and GREB1 expression inversely correlated with HER2 status, possibly as a surrogate marker for ER status and a predictor for tamoxifen resistance in breast cancer patients. In the present study, we examine the function and regulation of GREB1 in breast cancer, with the goal to develop GREB1 as a biomarker in breast cancer with de novo and acquired tamoxifen resistance. METHODS: We overexpressed GREB1 using adenovirus containing the full length GREB1 cDNA (Ad-GREB1) in breast cancer cell lines. The soft agar assay was used as a measure of anchorage independent growth. The effects of GREB1 on cell proliferation in MCF-7 cells transduced with Ad-GREB1 were also measured by the me olic activity using AlamarBlue assay. We tested whether there was interaction between STAT3 and ER, which could repress GREB1 expression by immunoprecipitation assay. The effects of IL-6/JAK/STAT3 cascade activation on estrogen-induced GREB1 promoter activity were determined by luciferase assay and those on gene expression were measured by real time reverse transcription polymerase chain reaction (qRT-PCR). RESULTS: We found that the ability of breast cancer cells to grow in soft agar is enhanced following GREB1 transfection. In MCF-7 cells transduced with Ad-GREB1 or transfected with siRNA GREB1, the metabolic activity was increased or completely abolished, suggesting that GREB1 may function as a growth promoter in breast cancer. E2 treatment increased GREB1 promoter luciferase activity. IL-6 inhibited E2-induced GREB1 transcription activity and GREB1 mRNA expression. Constitutively expressing active STAT3 construct (STAT3-C) dramatically decreased GREB1 transcription. CONCLUSIONS: These data indicate that overexpression of GREB1 promotes cell proliferation and increases the clonogenic ability in breast cancer cells. Moreover, Il6/STAT3 modulates estrogen-induced GREB1 transcriptional activity in breast cancer cells