UCL Institute of Cardiovascular Science

Bariatric (weight-loss) surgery is the most effective method for long-term weight reduction in patients with morbid obesity, reducing co-morbid conditions and mortality. There is increasing evidence that the reduced appetite and improved glucose homeostasis observed in the early post-operative period after certain types of bariatric surgery is due to alterations in circulating gut hormones. In order to gain further understanding of these processes we undertake studies on patients undergoing bariatric surgery at UCLH. In addition, we have established a mouse model of bariatric surgery to enable us to gain further mechanistic insights. 

We are undertaking brain functional magnetic resonance imaging (fMRI) studies coupled with detailed physiological studies in human subjects to investigate how peripheral signals act upon the brain to regulate appetite. Recently, using this approach we have shown that the gut hormone, peptide, acts upon homeostatic and hedonic brain circuits to regulate feeding behaviour.

GWAS studies have identified several obesity SNPs however, the mechanisms by which these SNPs mediate their effects on bodyweight is unclear. In order to gain insights into the mechanisms by which GWAS identified obesity SNPs mediate their effects on body weight we have generated a database of normal weight volunteers and patients with raised body mass index in whom we are undertaking detailed phenotyping studies based on genotype.