Daily standing time, dietary fiber, and intake of unsaturated fatty acids are beneficially associated with hepatic insulin sensitivity in adults with metabolic syndrome.


Journal

Frontiers in endocrinology
ISSN: 1664-2392
Titre abrégé: Front Endocrinol (Lausanne)
Pays: Switzerland
ID NLM: 101555782

Informations de publication

Date de publication:
2024
Historique:
received: 04 08 2023
accepted: 11 06 2024
medline: 11 7 2024
pubmed: 11 7 2024
entrez: 11 7 2024
Statut: epublish

Résumé

Obesity is associated with impaired glucose metabolism and hepatic insulin resistance. The aim was to investigate the associations of hepatic glucose uptake (HGU) and endogenous glucose production (EGP) to sedentary behavior (SB), physical activity (PA), cardiorespiratory fitness, dietary factors, and metabolic risk markers. Forty-four adults with metabolic syndrome (mean age 58 [SD 7] years, BMI ranging from 25-40kg/; 25 females) were included. HGU was measured by positron emission tomography during the hyperinsulinemic-euglycemic clamp. EGP was calculated by subtracting the glucose infusion rate during clamp from the glucose rate of disappearance. SB and PA were measured with hip-worn accelerometers (26 [SD3] days). Fitness was assessed by maximal bicycle ergometry with respiratory gas measurements and dietary intake of nutrients by 4-day food diaries. HGU was not associated with fitness or any of the SB or PA measures. When adjusted for sex, age, and body fat-%, HGU was associated with whole-body insulin sensitivity (β=0.58), water-insoluble dietary fiber (β=0.29), energy percent (E%) of carbohydrates (β=-0.32), saccharose (β=-0.32), mono- and polyunsaturated fatty acids (β=0.35, β=0.41, respectively). EGP was associated with whole-body insulin sensitivity (β=-0.53), and low-density lipoprotein cholesterol [β=-0.31], and when further adjusted for accelerometry wear time, EGP was associated with standing [β=-0.43]. (p-value for all< 0.05). Standing more, consuming a diet rich in fiber and unsaturated fatty acids, and a lower intake of carbohydrates, especially sugar, associate beneficially with hepatic insulin sensitivity. Habitual SB, PA, or fitness may not be the primary modulators of HGU and EGP. However, these associations need to be confirmed with intervention studies.

Sections du résumé

Background UNASSIGNED
Obesity is associated with impaired glucose metabolism and hepatic insulin resistance. The aim was to investigate the associations of hepatic glucose uptake (HGU) and endogenous glucose production (EGP) to sedentary behavior (SB), physical activity (PA), cardiorespiratory fitness, dietary factors, and metabolic risk markers.
Methods UNASSIGNED
Forty-four adults with metabolic syndrome (mean age 58 [SD 7] years, BMI ranging from 25-40kg/; 25 females) were included. HGU was measured by positron emission tomography during the hyperinsulinemic-euglycemic clamp. EGP was calculated by subtracting the glucose infusion rate during clamp from the glucose rate of disappearance. SB and PA were measured with hip-worn accelerometers (26 [SD3] days). Fitness was assessed by maximal bicycle ergometry with respiratory gas measurements and dietary intake of nutrients by 4-day food diaries.
Results UNASSIGNED
HGU was not associated with fitness or any of the SB or PA measures. When adjusted for sex, age, and body fat-%, HGU was associated with whole-body insulin sensitivity (β=0.58), water-insoluble dietary fiber (β=0.29), energy percent (E%) of carbohydrates (β=-0.32), saccharose (β=-0.32), mono- and polyunsaturated fatty acids (β=0.35, β=0.41, respectively). EGP was associated with whole-body insulin sensitivity (β=-0.53), and low-density lipoprotein cholesterol [β=-0.31], and when further adjusted for accelerometry wear time, EGP was associated with standing [β=-0.43]. (p-value for all< 0.05).
Conclusions UNASSIGNED
Standing more, consuming a diet rich in fiber and unsaturated fatty acids, and a lower intake of carbohydrates, especially sugar, associate beneficially with hepatic insulin sensitivity. Habitual SB, PA, or fitness may not be the primary modulators of HGU and EGP. However, these associations need to be confirmed with intervention studies.

Identifiants

pubmed: 38989003
doi: 10.3389/fendo.2024.1272886
pmc: PMC11233550
doi:

Substances chimiques

Dietary Fiber 0
Fatty Acids, Unsaturated 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1272886

Informations de copyright

Copyright © 2024 Laine, Sjöros, Garthwaite, Honka, Löyttyniemi, Eskola, Saarenhovi, Kallio, Koivumäki, Vähä-Ypyä, Sievänen, Vasankari, Hirvonen, Laitinen, Houttu, Kalliokoski, Saunavaara, Knuuti and Heinonen.

Déclaration de conflit d'intérêts

JK received consultancy fees from GE Healthcare and AstraZeneca and speaker fees from GE Healthcare, Bayer, Lundbeck, Boehringer-Ingelheim, and Merck, outside of the submitted work. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be constructed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.

Auteurs

Saara Laine (S)

Turku PET Centre, University of Turku, Åbo Akademi University and Turku University Hospital, Turku, Finland.

Tanja Sjöros (T)

Turku PET Centre, University of Turku, Åbo Akademi University and Turku University Hospital, Turku, Finland.

Taru Garthwaite (T)

Turku PET Centre, University of Turku, Åbo Akademi University and Turku University Hospital, Turku, Finland.

Miikka-Juhani Honka (MJ)

Turku PET Centre, University of Turku, Åbo Akademi University and Turku University Hospital, Turku, Finland.

Eliisa Löyttyniemi (E)

Department of Biostatistics, University of Turku, Turku, Finland.

Olli Eskola (O)

Turku PET Centre, University of Turku, Åbo Akademi University and Turku University Hospital, Turku, Finland.

Maria Saarenhovi (M)

Turku PET Centre, University of Turku, Åbo Akademi University and Turku University Hospital, Turku, Finland.
Department of Clinical Physiology and Nuclear Medicine, University of Turku and Turku University Hospital, Turku, Finland.

Petri Kallio (P)

Department of Clinical Physiology and Nuclear Medicine, University of Turku and Turku University Hospital, Turku, Finland.
Paavo Nurmi Center, University of Turku, Turku, Finland.

Mikko Koivumäki (M)

Turku PET Centre, University of Turku, Åbo Akademi University and Turku University Hospital, Turku, Finland.

Henri Vähä-Ypyä (H)

The UKK Institute for Health Promotion Research, Tampere, Finland.

Harri Sievänen (H)

The UKK Institute for Health Promotion Research, Tampere, Finland.

Tommi Vasankari (T)

The UKK Institute for Health Promotion Research, Tampere, Finland.
Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.

Jussi Hirvonen (J)

Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Department of Radiology, University of Turku and Turku University Hospital, Turku, Finland.

Kirsi Laitinen (K)

Institute of Biomedicine, University of Turku, Turku, Finland.

Noora Houttu (N)

Institute of Biomedicine, University of Turku, Turku, Finland.

Kari Kalliokoski (K)

Turku PET Centre, University of Turku, Åbo Akademi University and Turku University Hospital, Turku, Finland.

Virva Saunavaara (V)

Turku PET Centre, University of Turku, Åbo Akademi University and Turku University Hospital, Turku, Finland.
Department of Medical Physics, Division of Medical Imaging, Turku University Hospital, Turku, Finland.

Juhani Knuuti (J)

Turku PET Centre, University of Turku, Åbo Akademi University and Turku University Hospital, Turku, Finland.

Ilkka H A Heinonen (IHA)

Turku PET Centre, University of Turku, Åbo Akademi University and Turku University Hospital, Turku, Finland.

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Classifications MeSH