Obesity is a polymorphic chronic disease that has reached epidemic prevalence and is now one of the most important public health issues in the Western world.  Bariatric surgery including sleeve gastrectomy (SG) has an increasingly important role in long-term management of patients and resolution of co-morbid diseases(1,2).  The molecular mechanisms for the enhanced early satiety, weight loss and resolution of comorbid illnesses (including type II diabetes mellitus) following SG are not well understood. The proposed mechanism of action for weight loss and induction of satiety following SG is a combination of volume restriction, induction of favourable hormonal changes including alterations in gut derived hormones such as ghrelin, and impaired gastric motility and or elevated pressure in the sleeve.

We present our data from a cohort of 20 SG patients with matched controls from a single bariatric surgeon affiliated with obesity research in Sydney, with the aim of better understanding the mechanisms by which SG effects weight loss. This was by measuring known key biochemical markers (including GLP-1, insulin, C-peptide) and adipokines (including adiponectin, ghrelin, leptin, visfatin) that contribute to weight gain, in the pre-operative and postoperative (3, 6, 12 months) in conjunction with anthropometric measurements of change in body composition. 

A secondary aim of our study was to assess the improvements in associated obesity related chronic disease associations including; impaired glucose tolerance/ type 2 diabetes mellitus, dyslipidaemia, obstructive sleep apnoea, polycystic ovarian syndrome. 

We demonstrate significant weight loss reduction post GS surgery is correlated with changes in adipokine levels, improvements in glucose homeostasis and body composition.  Our research adds to the literature to identify markers that can be used pre-operatively to predict weight loss and help stratify the suitability of patients for bariatric surgery.