Effects of liraglutide on intrapancreatic fat deposition in patients with type 2 diabetes.

Diabetes Ectopic fat GLP-1 Medication Pancreas

Journal

Clinical nutrition ESPEN
ISSN: 2405-4577
Titre abrégé: Clin Nutr ESPEN
Pays: England
ID NLM: 101654592

Informations de publication

Date de publication:
Feb 2024
Historique:
received: 27 11 2023
revised: 01 12 2023
accepted: 05 12 2023
medline: 15 1 2024
pubmed: 15 1 2024
entrez: 14 1 2024
Statut: ppublish

Résumé

Ectopic fat deposition is associated with worsening of glycemic control. This study was conducted to determine whether liraglutide reduces ectopic fat deposition, especially in pancreas, in patients with type 2 diabetes (T2D). We retrospectively recruited T2D patients who underwent abdominal unenhanced CT scans both before and after administration of liraglutide (N = 13) or glimepiride (N = 29). Using CT values of pancreas (P), liver (L) and spleen (S), we defined the indices of intrapancreatic and liver fat as P-S value and L-S value, respectively. Increase of each value suggests the reduction of each fat deposition. The values of HbA1c (p = 0.0017) and body weight (p = 0.0081) decreased, and L-S (p = 0.0024) increased significantly after administration of liraglutide compared with those at baseline. Similarly, P-S tended to increase in the liraglutide group (p = 0.0547) and increased significantly in the liraglutide subgroup with fatty pancreas (p = 0.0303), defined as having baseline P-S less than -5. In the glimepiride group, P-S did not increase regardless of baseline P-S. Among patients with fatty pancreas, administration of liraglutide tended to be a significant factor for the change in P-S after adjustment for the change in HbA1c (p = 0.1090) and the change in visceral fat area (p = 0.1030). Intrapancreatic fat deposition was decreased after treatment with liraglutide, but not glimepiride, in T2D patients with fatty pancreas. Liraglutide might reduce intrapancreatic fat deposition independently of decreases in HbA1c and visceral fat volume.

Sections du résumé

BACKGROUND & AIMS OBJECTIVE
Ectopic fat deposition is associated with worsening of glycemic control. This study was conducted to determine whether liraglutide reduces ectopic fat deposition, especially in pancreas, in patients with type 2 diabetes (T2D).
METHODS METHODS
We retrospectively recruited T2D patients who underwent abdominal unenhanced CT scans both before and after administration of liraglutide (N = 13) or glimepiride (N = 29). Using CT values of pancreas (P), liver (L) and spleen (S), we defined the indices of intrapancreatic and liver fat as P-S value and L-S value, respectively. Increase of each value suggests the reduction of each fat deposition.
RESULTS RESULTS
The values of HbA1c (p = 0.0017) and body weight (p = 0.0081) decreased, and L-S (p = 0.0024) increased significantly after administration of liraglutide compared with those at baseline. Similarly, P-S tended to increase in the liraglutide group (p = 0.0547) and increased significantly in the liraglutide subgroup with fatty pancreas (p = 0.0303), defined as having baseline P-S less than -5. In the glimepiride group, P-S did not increase regardless of baseline P-S. Among patients with fatty pancreas, administration of liraglutide tended to be a significant factor for the change in P-S after adjustment for the change in HbA1c (p = 0.1090) and the change in visceral fat area (p = 0.1030).
CONCLUSIONS CONCLUSIONS
Intrapancreatic fat deposition was decreased after treatment with liraglutide, but not glimepiride, in T2D patients with fatty pancreas. Liraglutide might reduce intrapancreatic fat deposition independently of decreases in HbA1c and visceral fat volume.

Identifiants

pubmed: 38220377
pii: S2405-4577(23)02230-1
doi: 10.1016/j.clnesp.2023.12.005
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

208-213

Informations de copyright

Copyright © 2023 The Author(s). Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest JK and IS have received lecture fees from Novo Nordisk Pharma Ltd. IS has received research funds from Novo Nordisk Pharma Ltd. Other authors have no conflict of interest to declare.

Auteurs

Tsukasa Kuriyama (T)

Division of Diabetes, Department of Internal Medicine, Itami City Hospital, Itami, Hyogo, Japan; Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.

Chisaki Ishibashi (C)

Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.

Junji Kozawa (J)

Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan; Department of Diabetes Care Medicine, Graduate School of Medicine, Osaka University, Suita, Japan. Electronic address: kjunji@endmet.med.osaka-u.ac.jp.

Megu Y Baden (MY)

Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan; Department of Lifestyle Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.

Tomomi Horii (T)

Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.

Akiko Niki (A)

Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.

Harutoshi Ozawa (H)

Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan; Department of Diabetes Care Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.

Yoshiya Hosokawa (Y)

Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.

Yukari Fujita (Y)

Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.

Katsuhiko Sadahiro (K)

Division of Diabetes, Department of Internal Medicine, Itami City Hospital, Itami, Hyogo, Japan.

Tomomi Satoh (T)

Division of Diabetes, Department of Internal Medicine, Itami City Hospital, Itami, Hyogo, Japan.

Tomoya Hamaguchi (T)

Division of Diabetes, Department of Internal Medicine, Itami City Hospital, Itami, Hyogo, Japan.

Iichiro Shimomura (I)

Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.

Classifications MeSH