American Diabetes Association
BC Online Appendix Final 2104_cx01.pdf (356.26 kB)

Effects of Gastric Bypass Surgery on the Brain; Simultaneous Assessment of Glucose Uptake, Blood Flow, Neural Activity and Cognitive Function during Normo- and Hypoglycemia

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Version 2 2021-04-16, 22:32
Version 1 2021-03-04, 19:01
posted on 2021-04-16, 22:32 authored by Kristina E. Almby, Martin H. Lundqvist, Niclas Abrahamsson, Sofia Kvernby, Markus Fahlström, Maria J. Pereira, Malin Gingnell, F. Anders Karlsson, Giovanni Fanni, Magnus Sundbom, Urban Wiklund, Sven Haller, Mark Lubberink, Johan Wikström, Jan W. Eriksson
While Roux-en-Y Gastric Bypass (RYGB) surgery in obese individuals typically improves glycemic control and prevents diabetes, it also frequently causes hypoglycemia. Previous work showed attenuated counter-regulatory responses following RYGB. The underlying mechanisms as well as the clinical consequences are unclear.

In this study, 11 non-diabetic subjects with severe obesity were investigated pre- and post-RYGB during hyperinsulinemic hypoglycemic clamps. Assessments were made of hormones, cognitive function, cerebral blood flow by arterial spin labeling, brain glucose metabolism by FDG PET and activation of brain networks by functional MRI. Post- vs pre-surgery, we found a general increase of cerebral blood flow but a decrease of total brain FDG uptake during normoglycemia. During hypoglycemia, there was a marked increase in total brain FDG uptake and this was similar for post- and pre-surgery, whereas hypothalamic FDG uptake was reduced. During hypoglycemia, attenuated responses of counterregulatory hormones and improvements in cognitive function were seen post-surgery. In early hypoglycemia, there was increased activation post- vs pre-surgery of neural networks in CNS regions implicated in glucose regulation such as the thalamus and hypothalamus. The results suggest adaptive responses of the brain that contribute to lowering of glycemia following RYGB, and the underlying mechanisms should be further elucidated.


The study was funded by grants from the Swedish Diabetes Foundation, EXODIAB – Excellence of Diabetes Research in Sweden, the Ernfors Foundation, TREATMENT (EC H2020-MSCA-ITN-721236), the NovoNordisk foundation and ALF (Swedish Government research grants to Uppsala University Hospital).