Laparoscopic Roux-en-Y gastric bypass (RYGB) induces a more favorable metabolic profile than expected by weight loss alone. In this study, we investigated the effect of RYGB on serum bile acid levels and their relation to clinical outcomes.
We included 30 obese patients who underwent RYGB (BMI?=?46.1?±?5.9 kg/m(2)). Clinical measurements and laboratory determinations were performed before surgery and 1 year after surgery. Fasting serum bile acids were measured by an enzymatic method and individual bile acids were quantified by HLPC-tandem mass spectrometry. Indirect calorimetry was performed to measure the rates of energy expenditure and substrate oxidation.
Fasting total serum bile acid levels increased twofold after RYGB (pre, 3.68?±?2.03 vs. post, 7.06?±?9.65 µmol/l, +92 %, p?=?0.002). This increase in total bile acids was accompanied by a decrease in conjugated bile acids, which correlated with decreased glucose oxidation (r?=?0.571, p?=?0.002) and with increased lipid oxidation (r?=?-0.626, p?=?0.0004). The change in taurine-conjugated bile acids correlated with altered DIO2 mRNA expression in adipose tissue (r?=?-0.498, p?=?0.013) potentially linking bile acid conjugation to substrate oxidation through DIO2.
Fasting serum bile acid levels increase after RYGB. More specifically, changes in bile acid conjugation after RYGB associate with altered energy metabolism.
Postprandial hypoglycaemia is increasingly recognised as a complication of gastric bypass surgery. While post-bypass hypoglycaemia is often responsive to dietary modification, a subset of individuals develop life-threatening neuroglycopenia, with loss of consciousness, seizures and motor vehicle accidents. Such patients require complex nutritional and medical management strategies to reduce postprandial insulin secretion and stabilise glucose excursions, using medications including acarbose, octreotide and diazoxide, and frequent monitoring of glucose values. In an article in this issue of Diabetologia, nationwide registry data from Sweden were used to assess the frequency of severe hypoglycaemia and potentially related diagnoses (e.g. confusion, syncope, seizures, accidental death) following obesity surgery. Relative risk of hypoglycaemia and related diagnoses were two- to sevenfold higher in the post-gastric bypass population, but absolute risk was small. While these data underscore that hypoglycaemia is an important complication of gastric bypass, many questions regarding frequency, pathogenesis and optimal therapy remain unanswered. Given that hypoglycaemia is usually evaluated in the outpatient setting, more precise assessments of hypoglycaemia frequency will require prospective longitudinal studies in post-bypass cohorts. Until such data are available, practitioners should have a higher awareness of symptoms consistent with neuroglycopenia in patients with a history of bariatric surgery. Understanding the beneficial and challenging metabolic consequences of bariatric surgery is a key imperative for the diabetes community, as such data may yield novel insights into mechanisms by which bariatric surgery can lead to diabetes remission.