Abstract
This study aims to explore the immediate effects of bariatric surgery on serum tryptophan–kynurenine pathway metabolites in individuals with type 2 diabetes and BMI > 30. With the goal of providing insight into the link between tryptophan pathway metabolites, type 2 diabetes, and chronic obesity-induced inflammation. This longitudinal study included 20 participants. Half were diagnosed with type 2 diabetes. 11 and 9 underwent RYGB and SG respectively. Blood samples were obtained at pre-operative and 3 months post-operative timepoints. Tryptophan and downstream metabolites of the kynurenine pathway were quantified with an ultrahigh-performance liquid chromatography tandem mass spectrometry with electrospray ionisation method. At 3 months post-operation, RYGB led to significant reductions in tryptophan, kynurenic acid and xanthurenic acid levels when compared to baseline. Significant reductions of the same metabolites after surgery were also observed in individuals with T2D irrespective of surgical procedure. These metabolites were significantly correlated with serum HbA1c levels and BMI. Bariatric surgery, in particular RYGB reduces serum levels of tryptophan and its downstream kynurenine metabolites. These metabolites are associated with T2D and thought to be potentially mechanistic in the systemic processes of obesity induced inflammation leading to insulin resistance. Its reduction after surgery is associated with an improvement in glycaemic control (HbA1c).
Highlights
This study aims to explore the immediate effects of bariatric surgery on serum tryptophan–kynurenine pathway metabolites in individuals with type 2 diabetes and BMI > 30
It has been reported that this systemic inflammation is reflected in an individual’s metabolic p henotype[14,15] with metabolites from the tryptophan (TRP)–kynurenine (KYN) pathway thought to be potentially mechanistic in the systemic processes that lead to clinical insulin r esistance[15]
This study aims to utilise these powerful metabolic effects to provide an insight into the link between tryptophan–kynurenine pathway metabolites, type 2 diabetes (T2D), and obesity induced systemic inflammation
Summary
This study aims to explore the immediate effects of bariatric surgery on serum tryptophan–kynurenine pathway metabolites in individuals with type 2 diabetes and BMI > 30. With the goal of providing insight into the link between tryptophan pathway metabolites, type 2 diabetes, and chronic obesityinduced inflammation. In particular RYGB reduces serum levels of tryptophan and its downstream kynurenine metabolites. These metabolites are associated with T2D and thought to be potentially mechanistic in the systemic processes of obesity induced inflammation leading to insulin resistance. There are many postulated mechanisms of action, which contribute to such improvements, including calorie restriction, weight loss, modifications in bile acid metabolism, alteration in gut hormones and in the gut microbiome[6] Some of these changes seem to occur in the early post-operative period and may be independent to weight loss[7]. Further minor routes of catabolism include hydroxylation (serotonin), decarboxylation (tryptamine), and transamination (indolepyruvic acid)[18]
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