**1. Introduction**

Hypertension is the most prevalent modifiable risk factor for cardiovascular morbidity and mortality affecting over 1.3 billion people around the world [1]. Studies have shown that hypertension clusters with metabolic factors including glucose intolerance, hyperinsulinaemia, and dyslipidaemia [2]. Indeed, results from the prospective follow-up study, Pressioni Arteriose Monitorate E Loro Associazioni (PAMELA), suggest that elevated blood pressure (BP) is the most common component of the metabolic syndrome (MetS), with 95.4% of participants with MetS having elevated BP, and up to 80% of individuals with MetS being hypertensive [3,4]. Moreover, hypertensive individuals that fulfil the criteria for MetS have up to a 73% increased age and risk factor-adjusted risk for cardiovascular

**Citation:** Louca, P.; Berry, S.E.; Bermingham, K.; Franks, P.W.; Wolf, J.; Spector, T.D.; Valdes, A.M.; Chowienczyk, P.; Menni, C. Postprandial Responses to a Standardised Meal in Hypertension: The Mediatory Role of Visceral Fat Mass. *Nutrients* **2022**, *14*, 4499. https://doi.org/10.3390/nu14214499

Academic Editors: Omorogieva Ojo and Amanda R. Amorim Adegboye

Received: 18 September 2022 Accepted: 18 October 2022 Published: 26 October 2022

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events [5]. Hypertension may also be linked with the onset of new MetS [6]; it is strongly associated with insulin resistance, a component of MetS, independently of other risk factors, including obesity [7]. Mechanisms behind this may centre around the hormonal actions of insulin, which can regulate renal sodium clearance [8], a key mechanism involved in BP regulation. The increased cardiovascular risk associated with MetS and hypertension may also be linked to endothelial dysfunction and atherosclerosis [2].

Although previous research has explored fasting metabolism in hypertensive individuals, the majority of the population spend most of their waking hours in a postprandial state [9,10] and postprandial glycaemia, insulinaemia, lipaemia, and inflammation are thought to be more closely associated with cardiovascular risk than fasting levels [11], it is therefore of utmost importance to understand postprandial metabolic responses in hypertensive individuals. Hypertensive individuals have been found to have higher postprandial triglyceride levels [12], and postprandial hypertriglyceridaemia also correlates with levels of visceral adiposity [13], and causal links have been shown in murine models [14,15]. Additionally, postprandial glucose disposal in the presence of insulin resistance may promote hypertension through various atherogenic processes [2].

However, a comprehensive exploration of the fasting and postprandial differences in metabolic markers (triglycerides, insulin, glucose, and inflammation), between hypertensive and normotensive individuals, when challenged by a standardised mixed-nutrient meal, is lacking. Here, we investigate whether individuals with hypertension have a different postprandial response compared to normotensive controls. We further explore whether visceral fat mass (VFM), thought to be a key marker of glucose homeostasis and lipid metabolism, is a mediator of associations between hypertension and postprandial insulin and triglyceride response in the ZOE UK PREDICT 1 study [9]—a single-arm, randomized cross-over trial of standardized meal interventions designed to quantify and predict individual variations in postprandial responses (NCT03479866).
