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ORIGINAL RESEARCH article

Front. Endocrinol.
Sec. Diabetes: Molecular Mechanisms
Volume 16 - 2025 | doi: 10.3389/fendo.2025.1460253

Changes in pancreatic levodopa uptake in patients with obesity and new-onset type 2 diabetes: An 18F-FDOPA PET-CT study

Provisionally accepted
Yeongkeun Kwon Yeongkeun Kwon 1,2,3Hanseok Yoon Hanseok Yoon 4Jane Ha Jane Ha 5Hyeonseong Lee Hyeonseong Lee 6Kisoo Pahk Kisoo Pahk 7*Hyun Woo Kwon Hyun Woo Kwon 7*Sungeun Kim Sungeun Kim 7*Sungsoo Park Sungsoo Park 1,2,3
  • 1 Center for Obesity and Metabolic Diseases, Korea University Anam Hospital, Seoul, Republic of Korea
  • 2 Division of Foregut Surgery, College of Medicine, Korea University, Seoul, Republic of Korea
  • 3 College of Medicine, Korea University, Seoul, Republic of Korea
  • 4 Division of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, Seoul, Republic of Korea
  • 5 Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States
  • 6 Gangneung Institute of Natural Products, Korea Institute of Science and Technology (KIST), Gangneung, Gangwon, Republic of Korea
  • 7 Department of Nuclear Medicine, College of Medicine, Korea University, Seoul, Republic of Korea

The final, formatted version of the article will be published soon.

    Levodopa (L-3,4-dihydroxyphenylalanine)g, a dopamine precursor that circulates in the peripheral region, is involved in pancreatic glycemic control. Although previous animal studies have shown that peripheral levodopa is correlated with insulin secretion in pancreatic beta cells, the mechanism by which the pancreas uses levodopa differently in humans with obesity and type 2 diabetes remains unknown. Our study aimed to observe how the pancreas uptakes and utilizes levodopa differently under obese and diabetic conditions.18 F-fluoro-L-dopa positron emission tomography-computed tomography ( 18 F-FDOPA PET-CT) was used to visualize how the human body uses levodopa under obese and diabetic conditions and presented its clinical implications. 10 patients were divided into 3 groups: 1) Group A, normal weight without type 2 diabetes; 2) Group B, obese without type 2 diabetes; and 3) Group C, obese with new-onset type 2 diabetes. All patients' lifestyle modification was conducted prior to 18 F-FDOPA PET-CT, and plasma samples were collected to confirm changes in amino acid metabolites.Pancreatic levodopa uptake increased in obese patients with insulin resistance, whereas it decreased in obese patients with new-onset type 2 diabetes [standardized uptake value (SUV) mean in participants with normal weight, 2.6 ± 0.7; SUVmean in patients with obesity, 3.6 ± 0.1; SUVmean in patients with obesity and new-onset type 2 diabetes, 2.6 ± 0.1, P = 0.02].This suggested that the alterations in the functional capacity of pancreatic beta cells to take up circulating levodopa are potentially linked to the insulin resistance and the pathogenesis of type 2 diabetes. The differences in the uptake values between the groups implied that pancreatic levodopa uptake could be an early indicator of type 2 diabetes.

    Keywords: Obesity, type 2 diabetes, 18 F-FDOPA PET-CT, Levodopa, insulin secretion

    Received: 05 Jul 2024; Accepted: 23 Jan 2025.

    Copyright: © 2025 Kwon, Yoon, Ha, Lee, Pahk, Kwon, Kim and Park. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Kisoo Pahk, Department of Nuclear Medicine, College of Medicine, Korea University, Seoul, 136-701, Republic of Korea
    Hyun Woo Kwon, Department of Nuclear Medicine, College of Medicine, Korea University, Seoul, 136-701, Republic of Korea
    Sungeun Kim, Department of Nuclear Medicine, College of Medicine, Korea University, Seoul, 136-701, Republic of Korea

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