Revealing the Pathogenesis of Salt-Sensitive Hypertension in Dahl Salt-Sensitive Rats through Integrated Multi-Omics Analysis.

Salt-induced renal metabolism dysfunction is an important mechanism of salt-sensitive hypertension. Given that the gut-liver axis is the first hit of a high-salt diet (HSD), we aimed to identify the extra-renal mechanism from hepatic metabolism and gut microbiota, and attempted to relieve the salt-induced metabolic dysfunctions by curcumin. Untargeted metabolomics analysis was performed to identify the changes in hepatic metabolic pathways, and integrated analysis was employed to reveal the relationship between hepatic metabolic dysfunction and gut microbial composition.

Benincasa hispida extracts positively regulated high salt-induced hypertension in Dahl salt-sensitive rats: Impact on biochemical profile and metabolic patterns.

Salt-induced hypertension is one of the major issues worldwide and one of the main factors involved in heart and kidney failure. The objective of this study was to investigate the potential role of Benincasa hispida extracts on high salt-induced hypertension in Dahl-salt sensitive (D-SS) rats and to find out the metabolic and biochemical pattern involved in the reduction of hypertension. Twenty-six Dahl salt-sensitive (D-SS) rats were selected and divided into four groups.

β-Aminoisobutyric acid supplementation attenuated salt-sensitive hypertension in Dahl salt-sensitive rats through prevention of insufficient fumarase.

The human Dietary Approaches to Stop Hypertension-Sodium Trial has shown that β-aminoisobutyric acid (BAIBA) may prevent the development of salt-sensitive hypertension (SSHT). However, the specific antihypertensive mechanism remains unclear in the renal tissues of salt-sensitive (SS) rats. In this study, BAIBA (100 mg/kg/day) significantly attenuated SSHT via increased nitric oxide (NO) content in the renal medulla, and it induced a significant increase in NO synthesis substrates (L-arginine and malic acid) in the renal medulla.

Reconstruction and analysis of correlation networks based on GC-MS metabolomics data for hypercholesterolemia.

Background And Aims: Hypercholesterolemia is characterized by the elevation of plasma total cholesterol level, especially low-density lipoprotein (LDL) cholesterol. This disease is usually caused by a mutation in genes such as LDL receptor, apolipoprotein B, or proprotein convertase subtilisin/kexin type 9. However, a considerable number of patients with hypercholesterolemia do not have any mutation in these candidate genes.

Protective effect of oral histidine on hypertension in Dahl salt-sensitive rats induced by high-salt diet.

Aims: Salt-sensitive hypertension is a risk factor for cardiovascular disease. Previous studies have shown that insufficient arginine in the kidney caused by metabolic imbalance is an important factor in salt-sensitive hypertension. Whether the high nitrogen content of histidine can affect the balance of nitrogen metabolism in Dahl salt-sensitive (SS) rats.

High salt diet contributes to hypertension by weakening the medullary tricarboxylic acid cycle and antioxidant system in Dahl salt-sensitive rats.

High salt diet (HSD, 8% NaCl) contributes to salt-sensitive hypertension, this study aimed to determine the effect of HSD on salt-sensitive hypertension by combining proteomic with metabolomics methods. Salt-sensitive rats were fed on HSD and normal salt diet (NSD, 0.4% NaCl) for two weeks before further analysis.

Revealing metabolic pathways relevant to prediabetes based on metabolomics profiling analysis.

Aims: Dahl salt-sensitive (SS) rats develop similar prediabetes lesion characteristics, such as impaired glucose tolerance (IGT), when compared with the salt resistant rat. In this study, we evaluate the risk of high glucose intake during prediabetes and reveal the metabolic pathways relevant to the pathophysiology of prediabetes to diabetes using the SS rat model and compared this with the salt-resistant consomic SS.13BN rat model.

Functional analysis of the interferon-stimulated response element of porcine circovirus type 2 and its role during viral replication in vitro and in vivo.

Background: Porcine circovirus type 2 (PCV2) is associated with post-weaning multi-systemic wasting syndrome (PMWS) in young weaned pigs. Immune stimulation was found to activate the replication of PCV2 and exacerbate the clinical outcome of the infection. Proper amount of interferon-α (IFN-α) is able to enhance PCV2 infection and production in Porcine kidney-15 (PK-15) cells when administered after inoculation.