9 research outputs found

    Oral administration of short chain fatty acids could attenuate fat deposition of pigs

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    <div><p>Short chain fatty acids (SCFAs) are the main products of indigestible carbohydrates that are fermented by microbiota in the hindgut. This study was designed to investigate the effects of oral SCFAs administration on the lipid metabolism of weaned pigs. A total of 21 barrows were randomly allocated into three groups, including control group (orally infused with 200 mL physiological saline per day), low dose SCFAs group (orally infused with 200 mL SCFAs containing acetic acid 20.04 mM, propionic acid 7.71 mM and butyric acid 4.89 mM per day), and high dose SCFAs group (orally infused with 200 mL SCFAs containing acetic acid 40.08 mM, propionic acid 15.42 mM and butyric acid 9.78 mM per day). The results showed that the average daily feed intake of SCFAs groups were lower than that of control group (<i>P</i><0.05). Oral administration of SCFAs decreased the concentrations of triglyceride (TG), total cholesterol (TC), high density lipoprotein-cholesterol and insulin (<i>P</i><0.05), and increased the leptin concentration in serum (<i>P</i><0.05). The total fat, as well as TC and TG levels in liver, was decreased by oral SCFAs administration (<i>P</i><0.05). In addition, SCFAs down-regulated the mRNA expressions of fatty acid synthase (FAS) and sterol regulatory element binding protein 1c (<i>P</i><0.05), and enhanced the mRNA expression of carnitine palmitoyltransferase-1α (CPT-1α) in liver (<i>P</i><0.05). SCFAs also decreased FAS, acetyl-CoA carboxylase (ACC) and peroxisome proliferator activated receptor σ mRNA expressions in longissimus dorsi (<i>P</i><0.05). And in abdominal fat, SCFAs reduced FAS and ACC mRNA expressions (<i>P</i><0.05), and increased CPT-1α mRNA expression (<i>P</i><0.05). These results suggested that oral administration of SCFAs could attenuate fat deposition in weaned pigs via reducing lipogenesis and enhancing lipolysis of different tissues.</p></div

    Effects of SCFAs on mRNA expressions for key factors related to lipid metabolism in longissimus dorsi over the experimental period of weaned pigs.

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    <p>SCFAs (L): acetic acid 20.04 mM, propionic acid 7.71 mM and butyric acid 4.89 mM; SCFAs (H) :acetic acid 40.08 mM, propionic acid 15.42 mM and butyric acid 9.78 mM. FAS fatty acid synthase; ACC acetyl-CoA carboxylase; PPAR peroxisome proliferator activated receptor; SREBP-1C sterol regulatory element binding protein 1C; LPL lipoprotein lipase; CPT-1α carnitine palmitoyltransferase-1α; LIPE lipase hormone- sensitive. <sup>a-b</sup>Within a row, means without a common superscript differ (P<0.05).</p

    Effects of SCFAs on mRNA expressions for key factors related to lipid metabolism in abdominal fat over the experimental period of weaned pigs.

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    <p>SCFAs (L): acetic acid 20.04 mM, propionic acid 7.71 mM and butyric acid 4.89 mM; SCFAs (H) :acetic acid 40.08 mM, propionic acid 15.42 mM and butyric acid 9.78 mM. FAS fatty acid synthase; ACC acetyl-CoA carboxylase; PPAR peroxisome proliferator activated receptor; SREBP-1C sterol regulatory element binding protein 1C; LPL lipoprotein lipase; CPT-1α carnitine palmitoyltransferase-1α; LIPE lipase hormone- sensitive. <sup>a-b</sup>Within a row, means without a common superscript differ (P<0.05).</p

    Genome-wide association analysis identifies novel blood pressure loci and offers biological insights into cardiovascular risk

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    Elevated blood pressure is the leading heritable risk factor for cardiovascular disease worldwide. We report genetic association of blood pressure (systolic, diastolic, pulse pressure) among UK Biobank participants of European ancestry with independent replication in other cohorts, leading to discovery and validation of 107 novel loci. We also identify new independent variants at 11 previously reported blood pressure loci. Combined with results from a range of in-silico functional analyses and wet bench experiments, our findings highlight new biological pathways for blood pressure regulation enriched for genes expressed in vascular tissues and identify potential therapeutic targets for hypertension. Results from genetic risk score models raise the possibility of a precision medicine approach through early lifestyle intervention to offset the impact of blood pressure raising variants on future cardiovascular disease risk
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