Non-alcoholic fatty liver disease and hypertension: coprevalent or correlated?

Abstract

NAFLD and HT are associated independent of traditional cardiovascular risk factors. Insulin resistance appears to be the main linking mechanism. Although RAAS inhibitors are the most beneficial treatment option for HT in patients with NAFLD, randomized studies on the administration of these agents in HT patients with NAFDL are warranted to provide optimal treatment options in these high cardiovascular risk individuals.

Higher Sodium Intake Assessed by 24 Hour Urinary Sodium Excretion Is Associated with Non-Alcoholic Fatty Liver Disease: The PREVEND Cohort Study

“…It is also evident that a higher sodium intake increases systemic blood pressure [44]. Interestingly, high blood pressure may also independently contribute to the development of NAFLD, even in the absence of obesity and MetS [51]. In turn, a bi-directional effect has been proposed where NAFLD represents an important risk factor for the development of hypertension, possibly involving insulin resistance [51].…”

“…Interestingly, high blood pressure may also independently contribute to the development of NAFLD, even in the absence of obesity and MetS [51]. In turn, a bi-directional effect has been proposed where NAFLD represents an important risk factor for the development of hypertension, possibly involving insulin resistance [51]. From a clinical perspective our study supports the contention that it is important to take sodium intake into account when evaluating the adverse impact of NAFLD on the incidence of cardiovascular disease, hypertension and diabetes [6,9,52].…”

The Comparation of Anthropometric and Metabolic Indices in the Regulation and Prediction of Fatty Liver: a population-based cross-sectional study in China

“…BFM and VFA are often reported markers in athletes related articles or are used to explore the relationship between insulin resistance and excessive visceral fat accumulation [31,32]. Additionally, elevated data strongly suggests that advanced blood lipids, blood pressure and blood sugar could also be lead to more severe histological changes and poorer clinical outcomes [14,22,33]. Once FL is established, insulin resistance can promote the progression to the more severe state of liver endangerment like non-alcoholic steatohepatitis.…”

Mean Arterial Pressure Is Related to Incident Nonalcoholic Fatty Liver Disease among the Nonobese Female with Normal Low-Density Lipoprotein Cholesterol Levels: A Large Cohort Study in China

“…Owing to the epidemic of obesity, the prevalence of NAFLD has been increasing dramatically and was reported approximately 25-30% of the general population worldwide [1,2], including Asia-Pacific region which was thought to be a nonepidemic area in the past [3]. Furthermore, it has been demonstrated that NAFLD is a significant risk factor for developing hypertension, type 2 diabetes mellitus, and cardiovascular disease [4][5][6]. Therefore, it is quite interesting to identify individuals at a high risk of developing NAFLD.…”

“…The specific mechanism about the relationship between MAP and the incident NAFLD remains unclear. Considering that MAP is a combination of two components of BP: SBP and DBP, the proposed pathophysiologic mechanisms like insulin resistance, sympathetic nervous system activity, and arterial stiffness which are in regard to the relationship between increased BP and NAFLD [4] may serve as possible explanations that MAP independently increased the risk of incident NAFLD. For example, insulin resistance increases BP through enhancing salt absorption and activating the sympathetic nervous system [19], and hypertension is a predictor of insulin resistance in turn [20,21], whereas insulin resistance leads to liver endothelial dysfunction and then promotes NAFLD [20,22].…”