期刊
CURRENT OPINION IN CLINICAL NUTRITION AND METABOLIC CARE
卷 11, 期 4, 页码 366-370出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MCO.0b013e3283034990
关键词
epigenetic; genome-wide association scan; homologous recombination; obesity; stem cell
资金
- [1 R01 DK077120-01A2]
Purpose of review Many genes affect pathways that predispose to and protect against obesity. We ask how many different variants affect human obesity and how common are they? Recent findings The current generation of genome-wide association scans is moderately powered to detect and replicate associations between single nucleotide polymorphisms, or common copy number variations and common diseases. They are not designed either to find rare germline variants or those somatic changes, unique to an individual, that arise with high frequency in adult stem cells. They do not directly assay the epigenetic reprogramming of outcomes related to maternal or environmental exposures. Summary There are more gene variants, more gene-gene and gene-environmental interactions leading to obesity than current genome-wide association scan studies can verify. Those genetic associations that can be validated provide valuable insight into the pathways contributing to human obesity.
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