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Postprandial Responses to a Standardised Meal in Hypertension: The Mediatory Role of Visceral Fat Mass

Research output: Contribution to journalArticlepeer-review

Bano Louca, Sarah Berry, Kate Bermingham, Paul W. Franks, Jonathan Wolf, Tim Spector, Ana M. Valdes, Philip Chowienczyk, Cristina Menni

Original languageEnglish
Article number4499
Pages (from-to)4499
Issue number21
PublishedNov 2022

Bibliographical note

Funding Information: This work was supported by the Chronic Disease Research Foundation, ZOE, and in part by the Wellcome Trust [Grant number: 212904/Z/18/Z]. For the purpose of open access, the authors have applied a CC BY public copyright licence to any Author Accepted Manuscript version arising from this submission. TwinsUK receives funding from the Wellcome Trust, the European Commission H2020 grants SYSCID (contract #733100); the National Institute for Health Research (NIHR) Clinical Research Facility and the Biomedical Research Centre based at Guy’s and St Thomas’ NHS Foundation Trust in partnership with King’s College London, the Chronic Disease Research foundation, the UKRI Medical Research Council (MRC)/British Heart Foundation Ancestry and Biological Informative Markers for Stratification of Hypertension (AIM-HY; MR/M016560/1), and Zoe. C.M. is funded by the Chronic Disease Research Foundation and by the UKRI Medical Research Council (MRC) AIM-HY project grant (MR/M016560/1). P.L. is supported by the Chronic Disease Research Foundation (CDRF–15/2018). A.M.V. is supported by the National Institute for Health Research Nottingham Biomedical Research Centre. Publisher Copyright: © 2022 by the authors.

King's Authors


Postprandial insulinaemia, triglyceridaemia and measures of inflammation are thought to be more closely associated with cardiovascular risk than fasting measures. Although hypertension is associated with altered fasting metabolism, it is unknown as to what extent postprandial lipaemic and inflammatory metabolic responses differ between hypertensive and normotensive individuals. Linear models adjusting for age, sex, body mass index (BMI), visceral fat mass (VFM) and multiple testing (false discovery rate), were used to investigate whether hypertensive cases and normotensive controls had different fasting and postprandial (in response to two standardised test meal challenges) lipaemic, glycaemic, insulinaemic, and inflammatory (glycoprotein acetylation (GlycA)) responses in 989 participants from the ZOE PREDICT-1 nutritional intervention study. Compared to normotensive controls, hypertensive individuals had significantly higher fasting and postprandial insulin, triglycerides, and markers of inflammation after adjusting for age, sex, and BMI (effect size: Beta (Standard Error) ranging from 0.17 (0.08), p = 0.04 for peak insulin to 0.29 (0.08), p = 4.4 × 10 −4 for peak GlycA). No difference was seen for postprandial glucose. When further adjusting for VFM effects were attenuated. Causal mediation analysis suggests that 36% of the variance in postprandial insulin response and 33.8% of variance in postprandial triglyceride response were mediated by VFM. Hypertensive individuals have different postprandial insulinaemic and lipaemic responses compared to normotensive controls and this is partially mediated by visceral fat mass. Consequently, reducing VFM should be a key focus of health interventions in hypertension. Trial registration: The registration identifier is NCT03479866.

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