A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Weight Loss After Bariatric Surgery Reverses Insulin-Induced Increases in Brain Glucose Metabolism of the Morbidly Obese
Tekijät: Tuulari JJ, Karlsson HK, Hirvonen J, Hannukainen JC, Bucci M, Helmio M, Ovaska J, Soinio M, Salminen P, Savisto N, Nummenmaa L, Nuutila P
Kustantaja: AMER DIABETES ASSOC
Julkaisuvuosi: 2013
Journal: Diabetes
Tietokannassa oleva lehden nimi: DIABETES
Lehden akronyymi: DIABETES
Numero sarjassa: 8
Vuosikerta: 62
Numero: 8
Aloitussivu: 2747
Lopetussivu: 2751
Sivujen määrä: 5
ISSN: 0012-1797
DOI: https://doi.org/10.2337/db12-1460
Tiivistelmä
Obesity and insulin resistance are associated with altered brain glucose metabolism. Here, we studied brain glucose metabolism in 22 morbidly obese patients before and 6 months after bariatric surgery. Seven healthy subjects served as control subjects. Brain glucose metabolism was measured twice per imaging session: with and without insulin stimulation (hyperinsulinemic-euglycemic clamp) using [F-18]fluorodeoxyglucose scanning. We found that during fasting, brain glucose metabolism was not different between groups. However, the hyperinsulinemic clamp increased brain glucose metabolism in a widespread manner in the obese but not control subjects, and brain glucose metabolism was significantly higher during clamp in obese than in control subjects. After follow-up, 6 months postoperatively, the increase in glucose metabolism was no longer observed, and this attenuation was coupled with improved peripheral insulin sensitivity after weight loss. We conclude that obesity is associated with increased insulin-stimulated glucose metabolism in the brain and that this abnormality can be reversed by bariatric surgery. Diabetes 62:2747-2751, 2013
Obesity and insulin resistance are associated with altered brain glucose metabolism. Here, we studied brain glucose metabolism in 22 morbidly obese patients before and 6 months after bariatric surgery. Seven healthy subjects served as control subjects. Brain glucose metabolism was measured twice per imaging session: with and without insulin stimulation (hyperinsulinemic-euglycemic clamp) using [F-18]fluorodeoxyglucose scanning. We found that during fasting, brain glucose metabolism was not different between groups. However, the hyperinsulinemic clamp increased brain glucose metabolism in a widespread manner in the obese but not control subjects, and brain glucose metabolism was significantly higher during clamp in obese than in control subjects. After follow-up, 6 months postoperatively, the increase in glucose metabolism was no longer observed, and this attenuation was coupled with improved peripheral insulin sensitivity after weight loss. We conclude that obesity is associated with increased insulin-stimulated glucose metabolism in the brain and that this abnormality can be reversed by bariatric surgery. Diabetes 62:2747-2751, 2013
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