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VSL#3 resets insulin signaling and protects against NASH and atherosclerosis in a model of genetic dyslipidemia and intestinal inflammation

PloS one, 2012-09, Vol.7 (9), p.e45425-e45425 [Tạp chí có phản biện]

Mencarelli et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2012 Mencarelli et al 2012 Mencarelli et al ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0045425 ;PMID: 23029000

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Nhan đề:
VSL#3 resets insulin signaling and protects against NASH and atherosclerosis in a model of genetic dyslipidemia and intestinal inflammation
Tác giả: Mencarelli, Andrea ; Cipriani, Sabrina ; Renga, Barbara ; Bruno, Angela ; D'Amore, Claudio ; Distrutti, Eleonora ; Fiorucci, Stefano
Sanz, Yolanda
Chủ đề: Acids ; Adipose tissue ; Animal tissues ; Animals ; Aorta ; Apolipoprotein E ; Apolipoproteins E - genetics ; Apolipoproteins E - metabolism ; Arteriosclerosis ; Atherosclerosis ; Atherosclerosis - prevention & control ; Bile ; Biology ; Blood levels ; Cardiovascular disease ; Cholesterol ; Colitis ; Conditioning ; Dextran ; Dextran sulfate ; Diabetes ; Diet ; Disorders ; Drinking water ; Dyslipidemia ; Dyslipidemias - diet therapy ; Ethanol ; Fatty Liver - prevention & control ; Fibroblasts ; Growth factors ; Histopathology ; Immune system ; Inflammation ; Inflammation - diet therapy ; Insulin ; Insulin resistance ; Insulin Resistance - physiology ; Intervention ; Intestinal microflora ; Intestine ; Intestines - pathology ; Lesions ; Lipids ; Liver ; Liver diseases ; Low level ; Male ; Medicine ; Metabolic disorders ; Metabolic syndrome ; Mice ; Mice, Knockout ; Microbiota ; Muridae ; Nuclear receptors ; Permeability ; Plaques ; Probiotics ; Probiotics - therapeutic use ; Receptors ; Rodents ; Serum lipids ; Signal Transduction ; Signaling ; Signs and symptoms ; Sodium ; Steatosis ; Sulfate ; Sulfates ; Vitamin D
Là 1 phần của: PloS one, 2012-09, Vol.7 (9), p.e45425-e45425
Mô tả: Signals generated by the inflammed intestine are thought to contribute to metabolic derangement. The intestinal microbiota contributes to instructing the immune system beyond the intestinal wall and its modulation is a potential target for treating systemic disorders. To investigate the pathogenetic role of low grade intestinal inflammation in the development of steatohepatitis and atherosclerosis in a model of genetic dyslipidemia and to test the therapeutic potential of a probiotics intervention in protecting against development of these disorders. ApoE(-/-) mice were randomized to receive vehicle or VSL#3, a mixture of eight probiotics, at the dose of 20×10(9) colony-forming units/kg/day for three months alone or in combination with 0.2% of dextran sulfate sodium (DSS) in drinking water. Administering DSS to ApoE(-/-) mice failed to induce signs and symptoms of colitis but increased intestinal permeability to dextran FITC and, while had no effect on serum lipids, increased the blood levels of markers of liver injury and insulin resistance. DSS administration associated with low level inflammation of intestinal and mesenteric adipose tissues, caused liver histopathology features of steatohepatitis and severe atherosclerotic lesions in the aorta. These changes were prevented by VSL#3 intervention. Specifically, VSL#3 reversed insulin resistance, prevented development of histologic features of mesenteric adipose tissue inflammation, steatohepatitis and reduced the extent of aortic plaques. Conditioned media obtained from cultured probiotics caused the direct transactivation of peroxisome proliferator-activated receptor-γ, Farnesoid-X-receptors and vitamin D receptor. Low grade intestinal inflammation drives a transition from steatosis to steatohepatitis and worsens the severity of atherosclerosis in a genetic model of dyslipidemia. VSL#3 intervention modulates the expression of nuclear receptors, corrects for insulin resistance in liver and adipose tissues and protects against development of steatohepatitis and atherosclerosis.
Nơi xuất bản: United States: Public Library of Science
Ngôn ngữ: English
Số nhận dạng: ISSN: 1932-6203
EISSN: 1932-6203
DOI: 10.1371/journal.pone.0045425
PMID: 23029000
Nguồn: AUTh Library subscriptions: ProQuest Central
GFMER Free Medical Journals
MEDLINE
PubMed Central
Directory of Open Access Journals
Public Library of Science

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VSL#3 resets insulin signaling and protects against NASH and atherosclerosis in a model of genetic dyslipidemia and intestinal inflammation

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