Higher fasting fibroblast growth factor 21 was associated with a greater decline in postprandial blood pressure.

Blood pressure Cardiovascular disease Fibroblast growth factor 21 Oral glucose tolerance test Postprandial hypotension

Journal

Diabetes & metabolic syndrome
ISSN: 1878-0334
Titre abrégé: Diabetes Metab Syndr
Pays: Netherlands
ID NLM: 101462250

Informations de publication

Date de publication:
Feb 2023
Historique:
received: 22 11 2022
revised: 16 01 2023
accepted: 20 01 2023
pubmed: 2 2 2023
medline: 22 3 2023
entrez: 1 2 2023
Statut: ppublish

Résumé

A fall in blood pressure (BP) following a meal is well known and is usually a transient phenomenon, due to appropriate cardiovascular adjustments. Older individuals and those with high BP experience a greater postprandial fall that can manifest as postprandial hypotension (PPH). Fibroblast growth factor 21 (FGF21) is positively associated with BP, and is known to increase after meal ingestion. We explored whether fasting FGF21 or its postprandial change would be associated with meal induced BP change, after accounting for several covariates. Eighty-three Western Australian adults were studied. Supine resting BP was recorded and an oral glucose test was administered. Serial measurements of systolic BP (SBP) and diastolic BP (DBP) were then made in duplicate every 30 min up to 120 min. Fasting and 120 min blood samples were analysed for FGF21 and clinical chemistry. Multiple linear regression analyses of the incremental area under curve of postprandial SBP and DBP was conducted on 12 known determinants. The final parsimonious model based on backward regression of postprandial SBP included fasting SBP, gender, fasting insulin and fasting FGF21 (β = -0.009 (95% confidence interval (CI): 0.017, -0.002, P = 0.015)). For postprandial DBP these included fasting DBP, gender, fasting glucose, fasting insulin and fasting FGF21 (β = -0.005; 95% CI: 0.010, -0.001, P = 0.021). A higher fasting FGF21, independent of glucose and insulin, was associated with a greater postprandial decline in SBP and in DBP.

Sections du résumé

BACKGROUND BACKGROUND
A fall in blood pressure (BP) following a meal is well known and is usually a transient phenomenon, due to appropriate cardiovascular adjustments. Older individuals and those with high BP experience a greater postprandial fall that can manifest as postprandial hypotension (PPH). Fibroblast growth factor 21 (FGF21) is positively associated with BP, and is known to increase after meal ingestion. We explored whether fasting FGF21 or its postprandial change would be associated with meal induced BP change, after accounting for several covariates.
METHODS METHODS
Eighty-three Western Australian adults were studied. Supine resting BP was recorded and an oral glucose test was administered. Serial measurements of systolic BP (SBP) and diastolic BP (DBP) were then made in duplicate every 30 min up to 120 min. Fasting and 120 min blood samples were analysed for FGF21 and clinical chemistry. Multiple linear regression analyses of the incremental area under curve of postprandial SBP and DBP was conducted on 12 known determinants.
RESULTS RESULTS
The final parsimonious model based on backward regression of postprandial SBP included fasting SBP, gender, fasting insulin and fasting FGF21 (β = -0.009 (95% confidence interval (CI): 0.017, -0.002, P = 0.015)). For postprandial DBP these included fasting DBP, gender, fasting glucose, fasting insulin and fasting FGF21 (β = -0.005; 95% CI: 0.010, -0.001, P = 0.021).
CONCLUSIONS CONCLUSIONS
A higher fasting FGF21, independent of glucose and insulin, was associated with a greater postprandial decline in SBP and in DBP.

Identifiants

pubmed: 36724701
pii: S1871-4021(23)00016-4
doi: 10.1016/j.dsx.2023.102720
pii:
doi:

Substances chimiques

fibroblast growth factor 21 0
Glucose IY9XDZ35W2
Insulin 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

102720

Informations de copyright

Copyright © 2023 Research Trust of DiabetesIndia (DiabetesIndia) and National Diabetes Obesity and Cholesterol Foundation (N-DOC). Published by Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare no conflict of interest.

Auteurs

Jane Yu Ying Ong (JYY)

Department of Health, WA Health, Perth, Australia.

Kaveri Pathak (K)

Curtin School of Population Health, Faculty of Health Science, Curtin University, Perth, Western Australia, Australia.

Yun Zhao (Y)

Curtin School of Population Health, Faculty of Health Science, Curtin University, Perth, Western Australia, Australia.

Emily Calton (E)

Curtin School of Population Health, Faculty of Health Science, Curtin University, Perth, Western Australia, Australia.

Christopher M Reid (CM)

Curtin School of Population Health, Faculty of Health Science, Curtin University, Perth, Western Australia, Australia; School of Public Health & Preventive Medicine, Monash University, Melbourne, Victoria, Australia.

Mario J Soares (MJ)

Curtin School of Population Health, Faculty of Health Science, Curtin University, Perth, Western Australia, Australia. Electronic address: m.soares@curtin.edu.au.

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