Nuklearmedizin 2025; 64(01): 88-89
DOI: 10.1055/s-0045-1804403
Abstracts │ NuklearMedizin 2025
Wissenschaftliche Poster
Varia

Beta cell mass as quantified by exendin PET/CT imaging is similar in individuals with and without remission of type 2 diabetes after Roux-en-Y Gastric Bypass

S Tokgöz
1   Radboudumc, Nijmegen, Niederlande
,
L Deden
1   Radboudumc, Nijmegen, Niederlande
2   Rijnstate , Arnhem, Niederlande
,
A Hofboer
2   Rijnstate , Arnhem, Niederlande
,
E Hazebroek
2   Rijnstate , Arnhem, Niederlande
,
R Meijer
1   Radboudumc, Nijmegen, Niederlande
,
B E de Galan
1   Radboudumc, Nijmegen, Niederlande
,
C Tack
1   Radboudumc, Nijmegen, Niederlande
,
M Boss
1   Radboudumc, Nijmegen, Niederlande
,
M Gotthardt
1   Radboudumc, Nijmegen, Niederlande
› Author Affiliations
 

Ziel/Aim: In people with type 2 diabetes (T2D) and obesity, persistent weight loss can be obtained by bariatric surgery, such as Roux-en-Y Gastric Bypass (RYGB), with potential remission of diabetes through restoration of insulin sensitivity and -secretion. RYGB has been reported to improve beta cell function in individuals with T2D, but the effects on beta cell mass are still unclear. In this study, we aimed to compare the differences in beta cell mass in individuals with and without remission of T2D after RYGB using [68Ga]Ga-NODAGA-exendin-4 PET/CT imaging.

Methodik/Methods: Age- and BMI-matched individuals with (n=8) and without (n=9) remission of type 2 diabetes up to 4 years after RYGB underwent a combined arginine stimulation test (AST) and oral glucose tolerance test (OGTT) to determine beta cell function. Subsequently, the total pancreatic tracer uptake corrected for injected dose (kBq/MBq), representing beta cell mass, was quantified using PET/CT imaging after infusion with 100±5.6 MBq of [68Ga]Ga-NODAGA-exendin-4.

Ergebnisse/Results: Individuals without remission of T2D after RYGB had a longer T2D duration before RYGB compared to individuals with remission (18±8 vs 8±6 years; p=0.0096). Beta cell function was lower in individuals without remission of T2D after RYGB compared to individuals with remission (AST: AUCC-peptide:AUCglucose 0.053 (0.037-0.096) vs 0.16 (0.11-0.24), p=0.0016; OGTT: AUCC-peptide:AUCglucose 0.032 (0.023-0.054) vs 0.15 (0.11-0.24), p=0.0052). In contrast, our data show similar beta cell mass in individuals with and without remission of T2D (3.6 (2.9-5.1) vs 3.8 (1.2-4.4) kBq/MBq, p=0.81). Beta cell mass inversely correlated with BMI (r=-0.53, p=0.030). However, beta cell mass did not correlate with either beta cell function (AST r=0.11, p=0.68, OGTT r=0.13, p=0.62) or diabetes duration (r=0.086, p=0.74).

Schlussfolgerungen/Conclusions: Individuals with T2D who show remission after RYGB have better beta cell function compared to those not achieving remission, but do not differ with respect to beta cell mass. Using Exendin PET imaging, we demonstrate that RYGB does not increase beta cell mass but reactivates nonfunctional beta cells. These data underpin the ability of non-invasive imaging techniques to elucidate pathophysiological processes.



Publication History

Article published online:
12 March 2025

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