An appetite for research: an interview with Sadaf Farooqi.

IF 4 3区 医学 Q2 CELL BIOLOGY
Disease Models & Mechanisms Pub Date : 2025-04-01 Epub Date: 2025-04-28 DOI:10.1242/dmm.052379
Sadaf Farooqi
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引用次数: 0

Abstract

Professor Sadaf Farooqi is a clinician and researcher investigating the genetics underpinning obesity. Her research uncovered the first known genes that cause severe obesity, highlighting the significant role of appetite in regulating weight gain. Sadaf's work has been instrumental in proving that many observations in mice are also true in humans, paving the way for novel treatments and shifts in policy. After studying medicine at the University of Birmingham, Birmingham, UK, Sadaf completed her PhD on the genetics of severe childhood obesity at the University of Cambridge, Cambridge, UK, marking the beginning of her impressive research career in this field. She is currently Professor of Metabolism and Medicine at the University of Cambridge and Honorary Consultant in Diabetes and Endocrinology at Addenbrooke's Hospital, Cambridge, UK. Sadaf previously served on the Board of Directors for Disease Models & Mechanisms' publisher, The Company of Biologists. Here, we discuss the fascinating insights from her work on obesity and appetite, her approach to exploring new research questions, and how these discoveries can ultimately impact patients and society.

对研究的兴趣:对Sadaf Farooqi的采访。
Sadaf Farooqi教授是一名临床医生和研究人员,研究肥胖的遗传学基础。她的研究首次发现了导致严重肥胖的基因,强调了食欲在调节体重增加方面的重要作用。Sadaf的工作有助于证明在老鼠身上观察到的许多结果在人类身上也是正确的,为新的治疗方法和政策转变铺平了道路。在英国伯明翰大学学习医学后,Sadaf在英国剑桥大学完成了严重儿童肥胖遗传学的博士学位,标志着她在该领域令人印象深刻的研究生涯的开始。她目前是剑桥大学代谢和医学教授,也是英国剑桥阿登布鲁克医院糖尿病和内分泌学荣誉顾问。Sadaf曾担任疾病模型与机制出版商the Company of biology的董事会成员。在这里,我们将讨论她在肥胖和食欲方面的研究成果,她探索新研究问题的方法,以及这些发现最终如何影响患者和社会。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Disease Models & Mechanisms
Disease Models & Mechanisms 医学-病理学
CiteScore
6.60
自引率
7.00%
发文量
203
审稿时长
6-12 weeks
期刊介绍: Disease Models & Mechanisms (DMM) is an online Open Access journal focusing on the use of model systems to better understand, diagnose and treat human disease.
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