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Diabetes. 2017 May;66(5):1286-1292. doi: 10.2337/db16-1449. Epub 2017 Feb 28.

[11C]5-hydroxy-tryptophan PET for Assessment of Islet Mass During Progression of Type 2 Diabetes.

Author information

1
Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.
2
Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
3
Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
4
Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
5
Antaros Medical AB, Mölndal, Sweden.
6
Department of Immunology, Genetics, and Pathology, Uppsala University, Uppsala, Sweden.
7
Department of Medicinal Chemistry, Uppsala University, Uppsala, Sweden olof.eriksson@pet.medchem.uu.se.

Abstract

[11C]5-hydroxy-tryptophan ([11C]5-HTP) positron emission tomography of the pancreas has been shown to be a surrogate imaging biomarker of pancreatic islet mass. The change in islet mass in different stages of type 2 diabetes (T2D) as measured by noninvasive imaging is currently unknown. Here, we describe a cross-sectional study where subjects at different stages of T2D development with expected stratification of pancreatic islet mass were examined in relation to individuals without diabetes. The primary outcome was the [11C]5-HTP uptake and retention in pancreas, as a surrogate marker for the endogenous islet mass. We found that metabolic testing indicated a progressive loss of β-cell function, but this was not mirrored by a decrease in [11C]5-HTP tracer accumulation in the pancreas. This provides evidence of retained islet mass despite decreased β-cell function. The results herein indicate that β-cell dedifferentiation, and not necessarily endocrine cell loss, constitutes a major cause of β-cell failure in T2D.

TRIAL REGISTRATION:

ClinicalTrials.gov NCT02967354.

PMID:
28246291
DOI:
10.2337/db16-1449
[Indexed for MEDLINE]
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