Obesity-associated intestinal insulin resistance is ameliorated after bariatric surgery View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-01-29

AUTHORS

Jaakko Mäkinen, Jarna C. Hannukainen, Anna Karmi, Heidi M. Immonen, Minna Soinio, Lassi Nelimarkka, Nina Savisto, Mika Helmiö, Jari Ovaska, Paulina Salminen, Patricia Iozzo, Pirjo Nuutila

ABSTRACT

AIMS/HYPOTHESIS: The intestine is the main site for glucose absorption and it has been suggested that it exhibits insulin resistance. Bariatric surgery has been shown to reverse insulin resistance and type 2 diabetes, but its effects on human intestinal metabolism are unknown. Our aim was to evaluate the effects of insulin on intestinal glucose metabolism before and after bariatric surgery. METHODS: Twenty-one morbidly obese individuals undergoing bariatric surgery and ten age-matched healthy individuals were recruited and intestinal and skeletal muscle glucose uptake (GU) was measured using [(18)F]fluoro-2-deoxyglucose and positron emission tomography at fast and during hyperinsulinaemia. MRI was used as anatomical reference. Obese participants were studied again 6 months postoperatively. RESULTS: In contrast to healthy individuals, insulin had no effect on intestinal GU in obese participants with or without diabetes, suggesting that intestinal insulin resistance is present early in morbid obesity. Postoperatively, jejunal GU increased in line with whole-body and muscle GU. Postoperative GU values in the intestine correlated with whole-body insulin sensitivity, indicating that the intestinal mucosa may reflect the overall glycaemic state and potentially mediate obesity-associated insulin resistance. CONCLUSIONS/INTERPRETATION: This study shows that insulin is a potent stimulator of GU in the healthy intestine and that intestinal insulin resistance is ameliorated after bariatric surgery. In our study, obese individuals had intestinal insulin resistance regardless of their glycaemic status. Persistent changes in intestinal glucose metabolism are likely to influence both local processes in the gut and systemic glucose homeostasis. More... »

PAGES

1055-1062

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00125-015-3501-3

DOI

http://dx.doi.org/10.1007/s00125-015-3501-3

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1007547401

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25631620


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