The global epidemic of obesity is a challenge to healthcare systems due to the increase in the incidence of type 2 diabetes (T2D) and its associated morbidities. Although the small intestine is the first absorptive organ to encounter the ingested and digesting nutrients, it has gained little attention in the research of T2D and obesity. 

In the present study, multimodality imaging by Positron emission tomography (PET) combined with magnetic resonance imaging (MRI) or computed tomography (CT) modalities were utilized to study intestinal blood flow and metabolic substrate uptake in healthy normal-weight controls and obese patients with T2D before and after surgical or medical treatments. In the PET imaging, we focused on intestinal blood flow and volume, fatty acid, glucose uptake using 15O-water, 15O-labeled carbon monoxide, palmitate analogue 14(RS)-[18F]fluoro-6-thia-heptadecanoic acid, ([18F]FTHA) and 2-[18F]fluoro- 2-deoxy-D-glucose ([18F]FDG), respectively. 

Morbidly obese subjects (mean BMI 41±4.5kg/m2) with T2D had similar blood flow in the intestine even after bariatric surgery when compared to healthy controls. The bariatric surgery was either Roux-en Y gastric bypass (n=13) or Sleeve gastrectomy (n=20). Postprandially, nutrient contact with the small intestine and infusion of glucose dependent insulinotrophic polypeptide (GIP) stimulated blood flow in the small intestine of all groups. These findings suggest that despite the adaptation changes after bariatric surgery of the intestine, postprandial blood flow regulation in the small intestine remains intact in T2D and obese individuals. Intestinal fatty acid (FA) uptake was higher in obese subjects compared to healthy counterparts and unexpectedly this increased after bariatric surgery. The FA extraction rate in the small intestine also increased after bariatric surgery and this phenomenon suggests that intestinal energy expenditure relies on high FFA-to-glucose ratio in obese patients, which persists even after weight loss. Glucose uptake in the small intestines of metformin treated study subjects with T2D was increased compared to baseline and reached the level observed in healthy study subjects in previous studies. 

Taken together, the data of the present study provide novel insight on the role of the small intestine in the multiorgan metabolic derangements associated with T2D. It is not known whether these changes are part of the adaptation mechanism, due to improved glycaemic control and insulin resistance breakdown or due to the fundamental pathophysiology behind T2D. The actual mechanism behind these changes should be addressed in future research.