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Chunk #0 — INTRODUCTION

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Replication and extension of genome-wide association study results for obesity in 4923 adults from northern Sweden.
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Obesity is a major global health burden with a multitude of co-morbidities including type 2 diabetes, cardiovascular disease, certain cancers, sleep apnea, and osteoarthritis (1). Although the current obesity epidemic is likely related to decreased habitual physical activity levels and changes in dietary nutrient intake, heritability studies indicate that genetic factors also affect the predisposition to obesity (2). While several monogenic causes of obesity have been well-described during the past decade, the progress in defining the genetic basis of common obesity had been frustratingly slow prior to 2007; since then, obesity-predisposing variants in the FTO (3), MC4R (4,5), TMEM18, GNPDA2, SH2B1, KCTD15, MTCH2, NEGR1 (6) and PCSK1 (7) genes have emerged. All of these studies focused primarily on anthropometric measures of obesity, such as body mass index (BMI) or bioimpedance, with none having described associations with objectively assessed adipose distribution.