Dietary Sodium and Nonalcoholic Fatty Liver Disease: A Systematic Review.

(1) Introduction: Restriction in sodium intake is an important strategy for reducing cardiovascular morbidity and mortality, considering the direct influence of high-sodium diet consumption on the development of hypertension and cardiovascular diseases. There are only a few studies dealing with the influence of dietary sodium on the development of nonalcoholic fatty liver disease (NAFLD). In this systematic review, evidence in humans and animal models was compiled in a critical view of the influence of dietary sodium intake patterns on NAFLD markers; (2) Methods: Systematic review of PubMed data. Clinical outcomes included the prevalence/incidence of NAFLD for human studies, and NAFLD markers (hepatic lipogenesis, and markers of steatosis, fibrosis, and inflammation) for animal studies. The protocol was registered at the International Prospective Register of Systematic Review (PROSPERO; CRD42023390447); (3) Results and Conclusion: Seven studies in humans and eight in animals were included. All studies in humans were observational and associated high-sodium intake with NAFLD. However, in animals, both the increased and reduced consumption of sodium negatively influenced markers of liver steatosis, inflammation, and fibrosis.

Effects of Voluntary Sodium Consumption during the Perinatal Period on Renal Mechanisms, Blood Pressure, and Vasopressin Responses after an Osmotic Challenge in Rats.

Cardiovascular control is vulnerable to forced high sodium consumption during the per-inatal period, inducing programming effects, with anatomical and molecular changes at the kidney, brain, and vascular levels that increase basal and induce blood pressure. However, the program- ming effects of the natriophilia proper of the perinatal period on blood pressure control have not yet been elucidated. In order to evaluate this, we studied the effect of a sodium overload challenge (SO) on blood pressure response and kidney and brain gene expression in adult offspring exposed to voluntary hypertonic sodium consumption during the perinatal period (PM-NaCl group). Male PM-NaCl rats showed a more sustained increase in blood pressure after SO than controls (PM-Ctrol). They also presented a reduced number of glomeruli, decreased expression of TRPV1, and increased expression of At1a in the kidney cortex. The relative expression of heteronuclear vaso- pressin (AVP hnRNA) and AVP in the supraoptic nucleus was unchanged after SO in PM-NaCl in contrast to the increase observed in PM-Ctrol. The data indicate that the availability of a rich source of sodium during the perinatal period induces a long-term effect modifying renal, cardiovascular, and neuroendocrine responses implicated in the control of hydroelectrolyte homeostasis.

Effects of high and low salt intake on left ventricular remodeling after myocardial infarction in normotensive rats.

The dietary-sodium restriction is a standard approach following an acute myocardial infarction (MI). We examined the hypothesis in which the use of a high or low-sodium diet would worsen post-infarction left ventricular remodeling in rats and facilitate the development of heart failure. Left coronary artery ligation or sham-operated (SO) was produced in male Wistar rats (250-290 g). After surgery, animals were assigned to one of the three diets: standard amount of sodium (0.3% NaCl, SO and MI groups), a high-sodium diet (0.6% NaCl, SO-High and MI-High groups), or a low-sodium diet (0.03% NaCl, SO-Low and MI-Low groups). Diets were provided for 8 weeks post-surgery. Mortality rate was elevated in high-salt group (MI-Low, 21.4%; MI, 35.3%; MI-High, 47.6%). Contractility parameter was seen to be impaired in MI-Low animals (3195 ± 211 mm Hg/s) compared with MI (3751 ± 200 mm Hg/s). Low-salt diet did not prevent myocardial collagen deposition (MI-Low, 5.2 ± 0.5%; MI, 5.0 ± 0.4%) nor myocyte hypertrophy (MI-Low, 608 ± 41µ(2); MI, 712 ± 53 µm(2)) in left ventricle after MI. High-salt intake increases collagen volume fraction (SO, 3.3 ± 0.4%; SO-High, 4.7 ± 0.4%) in animals sham, but no major changes after MI. Our results show that ventricular remodeling was not altered by immediate introduction of low sodium after MI, and it may be a safe strategy as a therapeutic intervention to avoid volume retention. However, high sodium can be harmful, accelerating the post-infaction ventricular remodeling.