Prince Dadson1, Linda Landini2, Mika Helmiö3, Jarna C Hannukainen1, Heidi Immonen4, Miikka-Juhani Honka1, Marco Bucci1, Nina Savisto1, Minna Soinio5, Paulina Salminen3, Riitta Parkkola6, Jussi Pihlajamäki7, Patricia Iozzo8, Ele Ferrannini8, Pirjo Nuutila9. 1. Turku PET Centre, University of Turku, Turku, Finland. 2. Turku PET Centre, University of Turku, Turku, Finland Institute of Clinical Physiology, National Research Council, Pisa, Italy. 3. Division of Digestive Surgery and Urology, Department of Acute and Digestive Surgery, Turku University Hospital, Turku, Finland. 4. Turku PET Centre, University of Turku, Turku, Finland Department of Endocrinology, Turku University Hospital, Turku, Finland. 5. Department of Endocrinology, Turku University Hospital, Turku, Finland. 6. Medical Imaging Center, Turku University Hospital, Turku, Finland Department of Radiology, University of Turku and Turku University Hospital, Turku, Finland. 7. Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland Department of Clinical Nutrition and Obesity Center, University of Eastern Finland, Kuopio, Finland. 8. Institute of Clinical Physiology, National Research Council, Pisa, Italy. 9. Turku PET Centre, University of Turku, Turku, Finland Department of Endocrinology, Turku University Hospital, Turku, Finland pirjo.nuutila@utu.fi.
Abstract
OBJECTIVE: We investigated fat distribution and tissue-specific insulin-stimulated glucose uptake (GU) in seven fat compartments (visceral and subcutaneous) and skeletal muscle in morbidly obese patients with (T2D) and without (ND) type 2 diabetes before and 6 months after bariatric surgery. RESEARCH DESIGN AND METHODS: A total of 23 obese patients (BMI 43.0 ± 3.6 kg/m(2); 9 T2D and 14 ND) were recruited from a larger, randomized multicenter SLEEVEPASS study. MRI (for fat distribution) and [(18)F]-fluorodeoxyglucose PET (for GU) studies were performed for the obese patients before and 6 months postsurgery; 10 lean subjects served as control subjects and were studied once. RESULTS: At baseline, visceral fat GU was 30 ± 7% of muscle GU in control subjects and 57 ± 5% in obese patients. Visceral and deep subcutaneous fat were more abundant (despite same total fat mass) and less insulin sensitive in T2D than ND; in both, GU was impaired compared with control subjects. Postsurgery, visceral fat mass decreased (∼40%) more than subcutaneous fat (7%). Tissue-specific GU was improved, but not normalized, at all sites in T2D and ND alike. The contribution of visceral fat to whole-body GU was greater in T2D than ND but decreased similarly with surgery. Subcutaneous fat made a fourfold greater contribution to whole-body GU in obese versus lean subjects (15% vs. 4%) both before and after surgery. CONCLUSIONS: Bariatric surgery leads to sustained weight loss and improves tissue-specific glucose metabolism in morbidly obese patients. We conclude that 1) enhanced visceral fat accumulation is a feature of T2D, 2) severe obesity compromises muscle insulin sensitivity more than fat insulin sensitivity, and 3) fat mass expansion is a sink for plasma glucose.
OBJECTIVE: We investigated fat distribution and tissue-specific insulin-stimulated glucose uptake (GU) in seven fat compartments (visceral and subcutaneous) and skeletal muscle in morbidly obesepatients with (T2D) and without (ND) type 2 diabetes before and 6 months after bariatric surgery. RESEARCH DESIGN AND METHODS: A total of 23 obesepatients (BMI 43.0 ± 3.6 kg/m(2); 9 T2D and 14 ND) were recruited from a larger, randomized multicenter SLEEVEPASS study. MRI (for fat distribution) and [(18)F]-fluorodeoxyglucose PET (for GU) studies were performed for the obesepatients before and 6 months postsurgery; 10 lean subjects served as control subjects and were studied once. RESULTS: At baseline, visceral fat GU was 30 ± 7% of muscle GU in control subjects and 57 ± 5% in obesepatients. Visceral and deep subcutaneous fat were more abundant (despite same total fat mass) and less insulin sensitive in T2D than ND; in both, GU was impaired compared with control subjects. Postsurgery, visceral fat mass decreased (∼40%) more than subcutaneous fat (7%). Tissue-specific GU was improved, but not normalized, at all sites in T2D and ND alike. The contribution of visceral fat to whole-body GU was greater in T2D than ND but decreased similarly with surgery. Subcutaneous fat made a fourfold greater contribution to whole-body GU in obese versus lean subjects (15% vs. 4%) both before and after surgery. CONCLUSIONS: Bariatric surgery leads to sustained weight loss and improves tissue-specific glucose metabolism in morbidly obesepatients. We conclude that 1) enhanced visceral fat accumulation is a feature of T2D, 2) severe obesity compromises muscle insulin sensitivity more than fat insulin sensitivity, and 3) fat mass expansion is a sink for plasma glucose.
Authors: Derek K Hagman; Ilona Larson; Jessica N Kuzma; Gail Cromer; Karen Makar; Katya B Rubinow; Karen E Foster-Schubert; Brian van Yserloo; Peter S Billing; Robert W Landerholm; Matthew Crouthamel; David R Flum; David E Cummings; Mario Kratz Journal: Metabolism Date: 2017-02-02 Impact factor: 8.694
Authors: Sanna M Honkala; Jarkko Johansson; Kumail K Motiani; Jari-Joonas Eskelinen; Kirsi A Virtanen; Eliisa Löyttyniemi; Juhani Knuuti; Pirjo Nuutila; Kari K Kalliokoski; Jarna C Hannukainen Journal: J Cereb Blood Flow Metab Date: 2017-09-29 Impact factor: 6.200