Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Surg Obes Relat Dis. 2017 Aug;13(8):1321-1325. doi: 10.1016/j.soard.2017.04.024. Epub 2017 Apr 26.
Chromosome 16 p11.2 microdeletion is associated with early-onset obesity. Information is limited about the effect of bariatric surgery in patients with genetic obesity.
To examine the effects of bariatric surgery in obese patients with chromosome 16 p11.2 microdeletion.
Academic research institution.
The Swedish Obese Subjects study is a prospective study with 2010 participants receiving bariatric surgery. DNA was available for 1843 participants. Multiplex ligation-dependent probe amplification was used to identify 16 p11.2 microdeletion carriers. Follow-up time was 10 years. In carriers and noncarriers, follow-up rate was 86% and 82%, respectively, at 10 years.
Nine carriers of the chromosome 16 p11.2 microdeletion (9/1843, .49%) were found. At baseline, most risk factors were similar; however, carriers had higher body mass index (BMI), insulin levels, and systolic blood pressure compared to noncarriers. At the 1-year examination, the percent excess BMI lost (%EBMIL) in carriers and noncarriers was 71.9 and 62.2, respectively; P = .031 (37.9 and 30.6 kg). This was followed by partial weight regain in both groups, and after 10 years %EBMIL was 25.5 and 41.5 (15.7 and 21.3 kg), respectively (P = .377). Changes in risk factors were similar in the carriers and noncarriers. Two carriers who had type 2 diabetes at baseline were both in remission at 2-year follow-up but relapsed at 10-year follow-up. Perceived health status was similar in carriers and noncarriers during follow-up (overall P = .198).
Despite a small sample size, our results indicate that bariatric surgery is a treatment option for obese patients with chromosome 16 p11.2 microdeletion.
16 号染色体 p11.2 微缺失与早发性肥胖有关。关于肥胖患者接受减肥手术的效果信息有限。
检查肥胖患者染色体 16 p11.2 微缺失减肥手术的效果。
学术研究机构。
瑞典肥胖患者研究是一项前瞻性研究,共有 2010 名参与者接受了减肥手术。1843 名参与者有 DNA。使用多重连接依赖性探针扩增来鉴定 16 号染色体 p11.2 微缺失携带者。随访时间为 10 年。在携带者和非携带者中,10 年后的随访率分别为 86%和 82%。
在 1843 名参与者中发现了 9 名染色体 16 p11.2 微缺失的携带者(9/1843,0.49%)。在基线时,大多数危险因素相似;然而,与非携带者相比,携带者的体重指数(BMI)、胰岛素水平和收缩压更高。在 1 年检查时,携带者和非携带者的超重指数(%EBMIL)分别为 71.9%和 62.2%;P =.031(37.9 和 30.6kg)。随后两组均出现部分体重反弹,10 年后 %EBMIL 分别为 25.5%和 41.5%(15.7 和 21.3kg);P =.377。在携带者和非携带者中,危险因素的变化相似。两名基线时患有 2 型糖尿病的携带者在 2 年随访时均处于缓解状态,但在 10 年随访时复发。在随访期间,携带者和非携带者的健康感知状况相似(整体 P =.198)。
尽管样本量较小,但我们的结果表明,减肥手术是肥胖患者染色体 16 p11.2 微缺失的一种治疗选择。