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Brain glucose uptake is associated with endogenous glucose production in obese patients before and after bariatric surgery and predicts metabolic outcome at follow-up

Ele Ferrannini; Paulina Salminen; Miikka-Juhani Honka; Lauri Nummenmaa; Jarna C. Hannukainen; Minna Soinio; Patricia Iozzo; Marco Bucci; Heidi Immonen; Pirjo Nuutila; Eleni Rebelos

Brain glucose uptake is associated with endogenous glucose production in obese patients before and after bariatric surgery and predicts metabolic outcome at follow-up

Ele Ferrannini
Paulina Salminen
Miikka-Juhani Honka
Lauri Nummenmaa
Jarna C. Hannukainen
Minna Soinio
Patricia Iozzo
Marco Bucci
Heidi Immonen
Pirjo Nuutila
Eleni Rebelos
Katso/Avaa
Publisher's version (1.536Mb)
Lataukset: 

Blackwell Publishing Ltd
doi:10.1111/dom.13501
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Julkaisun pysyvä osoite on:
https://urn.fi/URN:NBN:fi-fe2021042719895
Tiivistelmä

Aims: To investigate further the finding that insulin enhances brain
glucose uptake (BGU) in obese but not in lean people by combining BGU
with measures of endogenous glucose production (EGP), and to explore the
associations between insulin-stimulated BGU and peripheral markers,
such as metabolites and inflammatory markers. Materials and methods: A
total of 20 morbidly obese individuals and 12 lean controls were
recruited from the larger randomized controlled SLEEVEPASS study. All
participants were studied under fasting and euglycaemic
hyperinsulinaemic conditions using fluorodeoxyglucose-positron emission
tomography. Obese participants were re-evaluated 6 months after
bariatric surgery and were followed-up for ~3 years. Results: In obese
participants, we found a positive association between BGU and EGP during
insulin stimulation. Across all participants, insulin-stimulated BGU
was associated positively with systemic inflammatory markers and plasma
levels of leucine and phenylalanine. Six months after bariatric surgery,
the obese participants had achieved significant weight loss. Although
insulin-stimulated BGU was decreased postoperatively, the association
between BGU and EGP during insulin stimulation persisted. Moreover, high
insulin-stimulated BGU at baseline predicted smaller improvement in
fasting plasma glucose at 2 and 3 years of follow-up. Conclusions: Our
findings suggest the presence of a brain-liver axis in morbidly obese
individuals, which persists postoperatively. This axis might contribute
to further deterioration of glucose homeostasis.

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