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High-salt intake negatively regulates fat deposition in mouse.

ABSTRACT: High-salt (HS) intake contributes to hypertension and cardiopathy, but the effect of HS on fat deposition is controversial. Feed intake, fat mass, the percentage of abdominal fat, heat production, rate of oxygen consumption and the respiratory exchange ratio of mice on a HS diet were significantly decreased (P?0.05?M). Abdominal fat mRNA profiles and protein measurements showed that 5 known genes involved in lipolysis were up-regulated significantly and 9 genes related to lipogenesis were down-regulated in HS mice. Abundant genes and some proteins (ATP2a1, AGT, and ANGPTL4) related to calcium ion metabolism or the renin-angiotensin system (RAS) were differentially expressed between HS and NS mice. Of special interest, CREB1 phosphorylation (S133 and S142), a key factor involved in calcium signaling and other pathways, was up-regulated in HS mice. By IPA analysis, a network mediated by calcium was established providing the molecular mechanisms underlying the negative effect of HS on fat deposition.

SUBMITTER: Cui H

PROVIDER: S-EPMC5435674 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature

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High-salt intake negatively regulates fat deposition in mouse.

Cui Huanxian H Yang Shuyan S Zheng Maiqing M Liu Ranran R Zhao Guiping G Wen Jie J

Scientific reports 20170517 1

High-salt (HS) intake contributes to hypertension and cardiopathy, but the effect of HS on fat deposition is controversial. Feed intake, fat mass, the percentage of abdominal fat, heat production, rate of oxygen consumption and the respiratory exchange ratio of mice on a HS diet were significantly decreased (P < 0.01 or 0.05) compared with mice on a normal-salt (NS) diet. An in vitro experiment with differentiating pre-adipocytes showed reduced fat deposition in the presence of high concentratio ...[more]

PMID: 28515432

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Project description:Salt stress is one of the major abiotic factors that affect the metabolism, growth and development of plants, and soybean [Glycine max (L.) Merr.] germination is sensitive to salt stress. Thus, to ensure the successful establishment and productivity of soybeans in saline soil, the genetic mechanisms of salt tolerance at the soybean germination stage need to be explored. In this study, a population of 184 recombinant inbred lines (RILs) was utilized to map quantitative trait loci (QTLs) related to salt tolerance. A major QTL related to salt tolerance at the soybean germination stage named qST-8 was closely linked with the marker Sat_162 and detected on chromosome 8. Interestingly, a genome-wide association study (GWAS) identified several single nucleotide polymorphisms (SNPs) significantly associated with salt tolerance in the same genetic region on chromosome 8. Resequencing, bioinformatics and gene expression analyses were implemented to identify the candidate gene Glyma.08g102000, which belongs to the cation diffusion facilitator (CDF) family and was named GmCDF1. Overexpression and RNA interference of GmCDF1 in soybean hairy roots resulted in increased sensitivity and tolerance to salt stress, respectively. This report provides the first demonstration that GmCDF1 negatively regulates salt tolerance by maintaining K+-Na+ homeostasis in soybean. In addition, GmCDF1 affected the expression of two ion homeostasis-associated genes, salt overly sensitive 1 (GmSOS1) and Na+/H+ exchanger 1 (GmNHX1), in transgenic hairy roots. Moreover, a haplotype analysis detected ten haplotypes of GmCDF1 in 31 soybean genotypes. A candidate-gene association analysis showed that two SNPs in GmCDF1 were significantly associated with salt tolerance and that Hap1 was more sensitive to salt stress than Hap2. The results demonstrated that the expression level of GmCDF1 was negatively correlated with salt tolerance in the 31 soybean accessions (r = -0.56, P < 0.01). Taken together, these results not only indicate that GmCDF1 plays a negative role in soybean salt tolerance but also help elucidate the molecular mechanisms of salt tolerance and accelerate the breeding of salt-tolerant soybean.

Project description:High-protein diets are known to reduce adiposity in the context of high carbohydrate and Western diets. However, few studies have investigated the specific high-protein effect on lipogenesis induced by a high-sucrose (HS) diet or fat deposition induced by high-fat feeding. We aimed to determine the effects of high protein intake on the development of fat deposition and partitioning in response to high-fat and/or HS feeding. A total of thirty adult male Wistar rats were assigned to one of the six dietary regimens with low and high protein, sucrose and fat contents for 5 weeks. Body weight (BW) and food intake were measured weekly. Oral glucose tolerance tests and meal tolerance tests were performed after 4th and 5th weeks of the regimen, respectively. At the end of the study, the rats were killed 2 h after ingestion of a calibrated meal. Blood, tissues and organs were collected for analysis of circulating metabolites and hormones, body composition and mRNA expression in the liver and adipose tissues. No changes were observed in cumulative energy intake and BW gain after 5 weeks of dietary treatment. However, high-protein diets reduced by 20 % the adiposity gain induced by HS and high-sucrose high-fat (HS-HF) diets. Gene expression and transcriptomic analysis suggested that high protein intake reduced liver capacity for lipogenesis by reducing mRNA expressions of fatty acid synthase (fasn), acetyl-CoA carboxylase a and b (Acaca and Acacb) and sterol regulatory element binding transcription factor 1c (Srebf-1c). Moreover, ketogenesis, as indicated by plasma β-hydroxybutyrate levels, was higher in HS-HF-fed mice that were also fed high protein levels. Taken together, these results suggest that high-protein diets may reduce adiposity by inhibiting lipogenesis and stimulating ketogenesis in the liver. Adult male Wistar rats were fed diets with varying amounts of protein, carbohydrates and fat for 5 weeks. At the end of the experiment, rats were killed and tanscriptome analysis was performed on pooled liver samples.

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High-salt intake negatively regulates fat deposition in mouse.

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High-salt intake negatively regulates fat deposition in mouse.

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