Endocrine Abstracts

Introduction: Improvement in glycaemia is observed early after Roux-en-Y Gastric Bypass surgery (RYGB) in patients with diabetes. Commonly cited mechanisms to account for these changes include the elevation of gut hormones, increase in bile acids levels, changes in the gut microbiota and calorie restriction. Calorie restriction is believed to play a role in improving hepatic insulin sensitivity and reduce hepatic glucose output early after RYGB, in the context of non-significant weight loss.

Aim: To compare the effect of RYGB on glycaemia at two weeks post-operatively versus a Very-Low-Calorie diet (VLCD) of 800 kcal/day at matched weight loss.

Methods: Eleven obese volunteers with diabetes treated with either diet or single oral hypoglycaemic agent, and due for RYGB were recruited from the Imperial Weight Centre. A separate matched cohort of seventeen volunteers was recruited and given a VLCD of 800 kcal/day (Cambridge diet). Both groups were studied before and at 2 weeks after the intervention. Weight and body composition were measured using a Bio-impedance scale (Tanita BC-418MA). Fasting glucose and insulin blood levels were measured and an index of insulin resistance calculated using the HOMA-IR model. Data is presented as Means±S.E.M.. A Student unpaired t-test was used for group comparison.

Results: The RYGB and VLCD cohort were well matched for age, BMI and glycaemia (Fasting glucose; RYGB: 9.3±0.6 mmol/l, VLCD: 8.2±0.7 mmol/l, P=0.3). Weight loss was comparable across the two groups at two weeks (RYGB: 5.5±0.4%, versus VLCD: 4.9±0.4%, P=0.3) as were changes in body composition (fat mass RYGB −2.8±0.5 kg versus VLCD −2.5±0.6 kg, P=0.7 and free fat mass RYGB −4.7±1.2 kg versus VLCD −3.0±0.5 kg, P=0.1). Similar changes in fasting glucose (−2.3±0.5 mmol/l versus −2.1±0.4 mmol/l, P=0.8), fasting insulin (−5.4±1.2 mU/l versus −6.9±1.5 mU/l, P=0.5) and HOMA-IR (−0.87±0.2 versus −1.1±0.2, P=0.5) were also observed following RYGB and VLCD respectively.

Discussion: Our data is consistent with the argument that calorie restriction is a key mediator of the early ‘anti-diabetes’ effects of RYGB. However, as the very low calorie restriction after RYGB is a temporary phenomenon, other mechanisms (for example elevations in gut hormone secretion or changes in gut microbiota) must supervene at later stages.