Sadia Saeed1,2, Muhammad Arslan3,4, Philippe Froguel1,2. 1. Department of Genomics of Common Disease, Imperial College London, London, UK. 2. CNRS, Pasteur Institute of Lille, University of Lille, Lille, France. 3. Centre for Research in Molecular Medicine, The University of Lahore, Lahore, Pakistan. 4. Department of Biological Sciences, Forman Christian College, Lahore, Pakistan.
Abstract
OBJECTIVE: Consanguinity has been instrumental in the elucidation of many Mendelian genetic diseases. Here, the unique advantage of consanguineous populations was considered in the quest for genes causing obesity. METHODS: PubMed was searched for articles relevant to consanguinity and obesity published between 1995 and 2016. Some earlier articles of interest were also consulted. RESULTS: Although obesity is the most heritable disorder, even in outbred populations, only 2% to 5% of severe obesity cases have so far been proven to be caused by single gene mutations. In some highly consanguineous populations, a remarkably higher proportion of obesity cases because of known and novel monogenic variants has been identified (up to 30%). CONCLUSIONS: Combining the power conferred by consanguinity with current large-capacity sequencing techniques should bring new genetic factors and molecular mechanisms to the fore, unveiling a large part of the yet-elusive neurohumoral circuitry involved in the regulation of energy homeostasis and appetite. Importantly, the undertaking of such initiatives is destined to unfold novel targets for the development of precision medicine relevant to different forms of obesity.
OBJECTIVE: Consanguinity has been instrumental in the elucidation of many Mendelian genetic diseases. Here, the unique advantage of consanguineous populations was considered in the quest for genes causing obesity. METHODS: PubMed was searched for articles relevant to consanguinity and obesity published between 1995 and 2016. Some earlier articles of interest were also consulted. RESULTS: Although obesity is the most heritable disorder, even in outbred populations, only 2% to 5% of severe obesity cases have so far been proven to be caused by single gene mutations. In some highly consanguineous populations, a remarkably higher proportion of obesity cases because of known and novel monogenic variants has been identified (up to 30%). CONCLUSIONS: Combining the power conferred by consanguinity with current large-capacity sequencing techniques should bring new genetic factors and molecular mechanisms to the fore, unveiling a large part of the yet-elusive neurohumoral circuitry involved in the regulation of energy homeostasis and appetite. Importantly, the undertaking of such initiatives is destined to unfold novel targets for the development of precision medicine relevant to different forms of obesity.
Authors: Claudia Terezia Socol; Alexandra Chira; Maria Antonia Martinez-Sanchez; Maria Angeles Nuñez-Sanchez; Cristina Maria Maerescu; Daniel Mierlita; Alexandru Vasile Rusu; Antonio Jose Ruiz-Alcaraz; Monica Trif; Bruno Ramos-Molina Journal: Int J Mol Sci Date: 2022-04-24 Impact factor: 6.208
Authors: Hernan Yupanqui-Lozno; Raul A Bastarrachea; Maria E Yupanqui-Velazco; Monica Alvarez-Jaramillo; Esteban Medina-Méndez; Aida P Giraldo-Peña; Alexandra Arias-Serrano; Carolina Torres-Forero; Angelica M Garcia-Ordoñez; Claudio A Mastronardi; Carlos M Restrepo; Ernesto Rodriguez-Ayala; Edna J Nava-Gonzalez; Mauricio Arcos-Burgos; Jack W Kent; Shelley A Cole; Julio Licinio; Luis G Celis-Regalado Journal: Genes (Basel) Date: 2019-05-07 Impact factor: 4.096
Authors: Eric M Bomberg; Justin R Ryder; Richard C Brundage; Robert J Straka; Claudia K Fox; Amy C Gross; Megan M Oberle; Carolyn T Bramante; Shalamar D Sibley; Aaron S Kelly Journal: Ther Adv Endocrinol Metab Date: 2019-07-27 Impact factor: 3.565
Authors: Khalid Khalaf Alharbi; Yazeed A Al-Sheikh; Muslim M Alsaadi; Balavenkatesh Mani; G K Udayaraja; Muhammad Kohailan; Imran Ali Khan Journal: Saudi J Biol Sci Date: 2019-09-09 Impact factor: 4.219