Sarcopenic obesity and insulin resistance: Application of novel body composition models.


Journal

Nutrition (Burbank, Los Angeles County, Calif.)
ISSN: 1873-1244
Titre abrégé: Nutrition
Pays: United States
ID NLM: 8802712

Informations de publication

Date de publication:
Historique:
received: 27 03 2019
revised: 08 11 2019
accepted: 28 01 2020
pubmed: 13 4 2020
medline: 24 6 2021
entrez: 13 4 2020
Statut: ppublish

Résumé

Sarcopenic obesity (SO) is characterized by the co-occurrence of high adiposity (HA) and low muscle mass (LM) and has been associated with an increased risk for cardiometabolic diseases. The aim of this study was to investigate the association between markers of insulin sensitivity and SO defined by three novel body composition models: body composition phenotypes; truncal fat mass to appendicular skeletal mass (TrFM/ASM) ratio load capacity; and fat mass to fat-free mass (FM/FFM) ratio load capacity. The study included 314 participants 18 to 65 y of age. Body composition was assessed by dual-energy x-ray absorptiometry. The first model includes four phenotypes: low adiposity-high muscle mass (LA-HM), high adiposity-high muscle mass (HA-HM), low adiposity-low muscle mass (LA-LM), and high adiposity-low muscle mass (HA-LM). The second and third load-capacity models stratified participants into three centile groups: <15th, 15th to 84th and ≥85th. A 2-h oral glucose tolerance test was performed and insulin sensitivity was calculated using the Matsuda Index. Glycated hemoglobin and highly sensitive C-reactive protein also were measured. Lower insulin sensitivity was observed in the HA-LM (P < 0.001) and in the ≥85th centile groups of the TrFM/ASM ratio (P < 0.001) and the FM/FFM ratio (P = 0.001) compared with the other body composition phenotypes. The HA-LM and ≥85th centile group of the TrFM/ASM ratio model showed significantly higher (P < 0.001) concentrations of glycated hemoglobin compared with the other phenotypes. SO defined by both the four body composition phenotypes and TrFM/ASM definitions was associated with increased impairment of insulin sensitivity and glycemic control.

Identifiants

pubmed: 32279031
pii: S0899-9007(20)30048-4
doi: 10.1016/j.nut.2020.110765
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

110765

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Auteurs

Eleonora Poggiogalle (E)

Department of Experimental Medicine - Medical Pathophysiology, Food Science and Endocrinology Section, Sapienza University of Rome, Rome, Italy.

Inês Mendes (I)

Human Nutrition Research Centre, Population Health Sciences Institute, Newcastle University, United Kingdom.

Brennick Ong (B)

Human Nutrition Research Centre, Population Health Sciences Institute, Newcastle University, United Kingdom.

Carla M Prado (CM)

Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada.

Gabriele Mocciaro (G)

Human Nutrition Research Centre, Population Health Sciences Institute, Newcastle University, United Kingdom.

Mohsen Mazidi (M)

Department of Twin Research and Genetic Epidemiology, King's College London, St Thomas' Hospital, Strand, London SE1 7EH, United Kingdom.

Carla Lubrano (C)

Department of Experimental Medicine - Medical Pathophysiology, Food Science and Endocrinology Section, Sapienza University of Rome, Rome, Italy.

Andrea Lenzi (A)

Department of Experimental Medicine - Medical Pathophysiology, Food Science and Endocrinology Section, Sapienza University of Rome, Rome, Italy.

Lorenzo Maria Donini (LM)

Department of Experimental Medicine - Medical Pathophysiology, Food Science and Endocrinology Section, Sapienza University of Rome, Rome, Italy.

Mario Siervo (M)

School of Life Sciences, The University of Nottingham Medical School, Queen's Medical Centre, Nottingham, United Kingdom. Electronic address: mario.siervo@nottingham.ac.uk.

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