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Objective <p>Previous studies have shown that patient characteristics, such as fasting blood glucose, can modulate hepatic <sup>18</sup>F-fluorodeoxyglucose (FDG) uptake; however, the drug-specific effects of different antidiabetic agents on hepatic and whole-body FDG distribution remain poorly understood. Therefore, in this study, we aimed to evaluate the impact of biguanide therapy, as well as insulin and other antidiabetic medications, on hepatic FDG uptake and dynamic positron emission tomography (PET) kinetic parameters [the static mean standardized uptake value normalized by lean body mass (SULmean), dynamic metabolic rate of glucose (Ki), and the FDG distribution volume (DV)] in patients with diabetes, using a multiparametric dynamic FDG-PET/computed tomography (CT) protocol.</p> Methods <p>This retrospective study included 107 patients with diabetes who underwent dynamic whole-body FDG-PET/CT after a 4-h fast and drug withdrawal between January 2022 and May 2025. Patients with hepatic structural abnormalities or artifacts were excluded. PET kinetic parameters (SULmean, Ki, and DV) were measured in the liver and analyzed for associations with clinical variables, including biguanide and insulin therapy, via multivariate regression.</p> Results <p>Among the 107 patients included, 44 and 9 received biguanide and insulin, respectively. Multivariate regression showed that biguanide therapy, but not insulin use or other clinical variables, was significantly associated with increased hepatic SULmean (p = 0.037). No clinical variables were significantly associated with Ki or DV in the corresponding models. These findings suggest that biguanide therapy elevates static hepatic FDG uptake, whereas hepatic glucose metabolic dynamics, as assessed by Ki and DV, did not show significant alterations associated with the antidiabetic medications evaluated in our cohort under standard pre-scan preparation.</p> Conclusions <p>Our study demonstrates that biguanide therapy increases static hepatic FDG accumulation without interfering with the underlying glucose metabolic dynamics (Ki and DV). The observed increase in SULmean is numerically significant but visually minimal; thus, its impact on routine diagnostic interpretation is likely minimal.</p>

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Impact of biguanide therapy on hepatic 18F-fluorodeoxyglucose-positron emission tomography quantitative parameters in patients with diabetes: a dynamic positron emission tomography study

  • 期刊论文

  • 发表日期：

    2026年6月29日

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  • Akiko Tomiyama,
  • Yu Iwabuchi,
  • Kai Tonda,
  • Yoshiki Owaki,
  • Arashi Fujita,
  • Ryosuke Sakurai,
  • Atsushi Shimizu,
  • Maho Kurihara,
  • Kogo Togo,
  • Yuki Iwaita,
  • Takehiro Nakahara,
  • Tohru Shiga,
  • Yoshitake Yamada,
  • Masahiro Jinzaki

摘要

Objective

Previous studies have shown that patient characteristics, such as fasting blood glucose, can modulate hepatic 18F-fluorodeoxyglucose (FDG) uptake; however, the drug-specific effects of different antidiabetic agents on hepatic and whole-body FDG distribution remain poorly understood. Therefore, in this study, we aimed to evaluate the impact of biguanide therapy, as well as insulin and other antidiabetic medications, on hepatic FDG uptake and dynamic positron emission tomography (PET) kinetic parameters [the static mean standardized uptake value normalized by lean body mass (SULmean), dynamic metabolic rate of glucose (Ki), and the FDG distribution volume (DV)] in patients with diabetes, using a multiparametric dynamic FDG-PET/computed tomography (CT) protocol.

Methods

This retrospective study included 107 patients with diabetes who underwent dynamic whole-body FDG-PET/CT after a 4-h fast and drug withdrawal between January 2022 and May 2025. Patients with hepatic structural abnormalities or artifacts were excluded. PET kinetic parameters (SULmean, Ki, and DV) were measured in the liver and analyzed for associations with clinical variables, including biguanide and insulin therapy, via multivariate regression.

Results

Among the 107 patients included, 44 and 9 received biguanide and insulin, respectively. Multivariate regression showed that biguanide therapy, but not insulin use or other clinical variables, was significantly associated with increased hepatic SULmean (p = 0.037). No clinical variables were significantly associated with Ki or DV in the corresponding models. These findings suggest that biguanide therapy elevates static hepatic FDG uptake, whereas hepatic glucose metabolic dynamics, as assessed by Ki and DV, did not show significant alterations associated with the antidiabetic medications evaluated in our cohort under standard pre-scan preparation.

Conclusions

Our study demonstrates that biguanide therapy increases static hepatic FDG accumulation without interfering with the underlying glucose metabolic dynamics (Ki and DV). The observed increase in SULmean is numerically significant but visually minimal; thus, its impact on routine diagnostic interpretation is likely minimal.