Short summary

We intent to test the hypotheses 1) that T2D is associated with exaggerated AT dysfunction compared with obesity alone, 2) that increased insulin sensitivity and remission of T2D after bariatric surgery is in part explained by improved AT function. This will be done to recruit 30 participants who will undergo bariatric surgery, which of 15 will have T2D and 15 without, and test them extensively prior to surgery and agian 9-12 month after surgery.

Rationale

Insulin resistance (IR) plays a major role in the pathogenesis of type 2 diabetes (T2D). Adipose tissue (AT) dysfunction leading to systemic low-grade inflammation and ectopic lipid deposition plays an important role in obesity-induced IR, but its role in T2D pathogenesis and to what extent insulin-sensitizing interventions can reverse AT dysfunction remain to be clarified.

Description of the cohort

30 patients eligible for bariatric surgery: 15 obese with type 2 diabetes, 15 obese without type 2 diabetes. Will be testet two times: before operation and one year after. 15 lean healthy controls whioch will be testet one time.

Data and biological material

Blood samples, urine, DEXA scan,anthropometric measurements, indirect calirometry, VO2max, muscle and fat biopsies, insulin sensitivity test and beta cell function test.

Collaborating researchers and departments

Department of Biochemistry and Molecular Biology, University of Southern Denmark

• Professor Nils Færgeman

Department of Clinical Genetics, Odense University Hospital

• Associate Professor, PhD Klaus Brusgaard

Department of Endocrinology, Hospital of Southwest Jutland

• Consultant, Professor Claus Bogh Juhl