Genetic Obesity and Bariatric Surgery Outcome in 1014 Patients with Morbid Obesity.

Autor: Cooiman MI; Department of Bariatric Surgery, Rijnstate Hospital Arnhem/Vitalys, Wagnerlaan 55, 6815 AD, Arnhem, the Netherlands. mcooiman@rijnstate.nl.; Department of Clinical Genetics, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands. mcooiman@rijnstate.nl., Kleinendorst L; Department of Clinical Genetics, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands., Aarts EO; Department of Bariatric Surgery, Rijnstate Hospital Arnhem/Vitalys, Wagnerlaan 55, 6815 AD, Arnhem, the Netherlands., Janssen IMC; Department of Bariatric Surgery, Rijnstate Hospital Arnhem/Vitalys, Wagnerlaan 55, 6815 AD, Arnhem, the Netherlands.; Department of Surgery, Nederlandse Obesitas Kliniek West, The Hague, The Netherlands., van Amstel HKP; Department of Genetics, University Medical Center Utrecht, Utrecht, the Netherlands., Blakemore AI; Department of Life Sciences, Brunel University London, London, UK.; Section of Investigative Medicine, Imperial College London, London, UK., Hazebroek EJ; Department of Bariatric Surgery, Rijnstate Hospital Arnhem/Vitalys, Wagnerlaan 55, 6815 AD, Arnhem, the Netherlands., Meijers-Heijboer HJ; Department of Clinical Genetics, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.; Department of Clinical Genetics, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands., van der Zwaag B; Department of Genetics, University Medical Center Utrecht, Utrecht, the Netherlands., Berends FJ; Department of Bariatric Surgery, Rijnstate Hospital Arnhem/Vitalys, Wagnerlaan 55, 6815 AD, Arnhem, the Netherlands., van Haelst MM; Department of Clinical Genetics, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.; Department of Clinical Genetics, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Jazyk: angličtina
Zdroj: Obesity surgery [Obes Surg] 2020 Feb; Vol. 30 (2), pp. 470-477.
DOI: 10.1007/s11695-019-04184-w
Abstrakt: Background: Mutations in the leptin-melanocortin pathway genes are known to cause monogenic obesity. The prevalence of these gene mutations and their effect on weight loss response after bariatric surgery are still largely unknown.
Objective: To determine the prevalence of genetic obesity in a large bariatric cohort and evaluate their response to bariatric surgery.
Methods: Mutation analysis of 52 obesity-associated genes. Patient inclusion criteria were a BMI > 50 kg/m 2 , an indication for revisional surgery or an early onset of obesity (< 10 years of age).
Results: A total of 1014 patients were included, of whom 30 (3%) were diagnosed with genetic obesity, caused by pathogenic heterozygous mutations in either MC4R, POMC, PCSK1, SIM1, or PTEN. The percentage total body weight loss (%TBWL) after Roux-en-Y gastric bypass (RYGB) surgery was not significantly different for patients with a mutation in MC4R, POMC, and PCSK1 compared with patients lacking a molecular diagnosis. Of the confirmed genetic obesity cases, only patients with MC4R mutations receiving a sleeve gastrectomy (SG) showed significantly lower %TBWL compared with patients lacking a molecular diagnosis, during 2 years of follow-up.
Conclusions: In this cohort of morbid obese bariatric patients, an estimated prevalence of monogenic obesity of 3% is reported. Among these patients, the clinical effects of heterozygous mutations in POMC and PCSK1 do not interfere with the effectiveness of most commonly performed bariatric procedures within the first 2 years of follow-up. Patients with MC4R mutations achieved superior weight loss after primary RYGB compared with SG.
Databáze: MEDLINE
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