scholarly journals Supplemental Clostridium butyricum Modulates Lipid Metabolism Through Shaping Gut Microbiota and Bile Acid Profile of Aged Laying Hens

2020 ◽  
Vol 11 ◽  
Author(s):  
Wei-wei Wang ◽  
Jing Wang ◽  
Hai-jun Zhang ◽  
Shu-geng Wu ◽  
Guang-hai Qi
Keyword(s):  
Lipid Metabolism ◽  
Bile Acid ◽  
Gut Microbiota ◽  
Laying Hens ◽  
Clostridium Butyricum

scholarly journals Perinatal High-Salt Diet Induces Gut Microbiota Dysbiosis, Bile Acid Homeostasis Disbalance, and NAFLD in Weanling Mice Offspring

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2135
Author(s):  
Qing Guo ◽  
Yi Tang ◽  
Ying Li ◽  
Ziyuan Xu ◽  
Di Zhang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Bile Acid ◽  
Gut Microbiota ◽  
Lithocholic Acid ◽  
High Salt ◽  
Alcoholic Fatty Liver ◽  
Hepatic Expression ◽  
Tnf Α ◽  
Junction Protein ◽  
Gut Microbiota Dysbiosis

A perinatal high-salt (HS) diet was reported to elevate plasma triglycerides. This study aimed to investigate the hypothesis that a perinatal HS diet predisposed offspring to non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of abnormal lipid metabolism, and the possible mechanism. Female C57BL/6 mice were fed a control diet (0.5% NaCl) or HS diet (4% NaCl) during pregnancy and lactation and their offspring were sacrificed at weaning. The perinatal HS diet induced greater variation in fecal microbial beta-diversity (β-diversity) and increased bacteria abundance of Proteobacteria and Bacteroides. The gut microbiota dysbiosis promoted bile acid homeostasis disbalance, characterized by the accumulation of lithocholic acid (LCA) and deoxycholic acid (DCA) in feces. These alterations disturbed gut barrier by increasing the expression of tight junction protein (Tjp) and occludin (Ocln), and increased systemic lipopolysaccharide (LPS) levels and hepatic inflammatory cytokine secretion (TNF-α and IL-6) in the liver. The perinatal HS diet also inhibited hepatic expression of hepatic FXR signaling (CYP7A1 and FXR), thus triggering increased hepatic expression of pro-inflammatory cytokines (TNF-α and IL-6) and hepatic lipid metabolism-associated genes (SREBP-1c, FAS, ACC), leading to unique characteristics of NAFLD. In conclusion, a perinatal HS diet induced NAFLD in weanling mice offspring; the possible mechanism was related to increased bacteria abundance of Proteobacteria and Bacteroides, increased levels of LCA and DCA in feces, and increased expressions of hepatic FXR signaling.

scholarly journals Gut Microbiota Dysbiosis Is Associated with Elevated Bile Acids in Parkinson’s Disease

Metabolites ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 29
Author(s):  
Peipei Li ◽  
Bryan A. Killinger ◽  
Elizabeth Ensink ◽  
Ian Beddows ◽  
Ali Yilmaz ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Lipid Metabolism ◽  
Bile Acid ◽  
Gut Microbiota ◽  
Bile Acids ◽  
Lithocholic Acid ◽  
Acid Synthesis ◽  
Cholesterol Homeostasis ◽  
Secondary Bile Acid

The gut microbiome can impact brain health and is altered in Parkinson’s disease (PD). The vermiform appendix is a lymphoid tissue in the cecum implicated in the storage and regulation of the gut microbiota. We sought to determine whether the appendix microbiome is altered in PD and to analyze the biological consequences of the microbial alterations. We investigated the changes in the functional microbiota in the appendix of PD patients relative to controls (n = 12 PD, 16 C) by metatranscriptomic analysis. We found microbial dysbiosis affecting lipid metabolism, including an upregulation of bacteria responsible for secondary bile acid synthesis. We then quantitatively measure changes in bile acid abundance in PD relative to the controls in the appendix (n = 15 PD, 12 C) and ileum (n = 20 PD, 20 C). Bile acid analysis in the PD appendix reveals an increase in hydrophobic and secondary bile acids, deoxycholic acid (DCA) and lithocholic acid (LCA). Further proteomic and transcriptomic analysis in the appendix and ileum corroborated these findings, highlighting changes in the PD gut that are consistent with a disruption in bile acid control, including alterations in mediators of cholesterol homeostasis and lipid metabolism. Microbially derived toxic bile acids are heightened in PD, which suggests biliary abnormalities may play a role in PD pathogenesis.

scholarly journals The Role of the Gut Microbiota in Lipid and Lipoprotein Metabolism

2019 ◽  
Vol 8 (12) ◽  
pp. 2227 ◽  
Author(s):  
Yijing Yu ◽  
Fitore Raka ◽  
Khosrow Adeli
Keyword(s):  
Lipid Metabolism ◽  
Bile Acid ◽  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
Metabolic Disorders ◽  
Cell Function ◽  
Lipoprotein Metabolism ◽  
Bile Acid Metabolism ◽  
Treated Animal ◽  
Postprandial Lipid Metabolism

Both environmental and genetic factors contribute to relative species abundance and metabolic characteristics of the intestinal microbiota. The intestinal microbiota and accompanying microbial metabolites differ substantially in those who are obese or have other metabolic disorders. Accumulating evidence from germ-free mice and antibiotic-treated animal models suggests that altered intestinal gut microbiota contributes significantly to metabolic disorders involving impaired glucose and lipid metabolism. This review will summarize recent findings on potential mechanisms by which the microbiota affects intestinal lipid and lipoprotein metabolism including microbiota dependent changes in bile acid metabolism which affects bile acid signaling by bile acid receptors FXR and TGR5. Microbiota changes also involve altered short chain fatty acid signaling and influence enteroendocrine cell function including GLP-1/GLP-2-producing L-cells which regulate postprandial lipid metabolism.

scholarly journals Long-Term Grow-Out Affects Campylobacter jejuni Colonization Fitness in Coincidence With Altered Microbiota and Lipid Composition in the Cecum of Laying Hens

2021 ◽  
Vol 8 ◽  
Author(s):  
Hiroshi Asakura ◽  
Tatsuya Nakayama ◽  
Shiori Yamamoto ◽  
Kazuki Izawa ◽  
Jun Kawase ◽  
...  
Keyword(s):  
Bile Acid ◽  
Gut Microbiota ◽  
Campylobacter Jejuni ◽  
Laying Hens ◽  
Temporal Dynamics ◽  
16S Rrna Gene Sequencing ◽  
Laying Hen ◽  
Bile Acid Metabolism ◽  
Rrna Gene ◽  
Rrna Gene Sequencing

Campylobacter jejuni is one of the leading causes of gastrointestinal illness worldwide and is mainly transmitted from chicken through the food chain. Previous studies have provided increasing evidence that this pathogen can colonize and replicate in broiler chicken during its breeding; however, its temporal kinetics in laying hen are poorly understood. Considering the possible interaction between C. jejuni and gut microbiota, the current study was conducted to address the temporal dynamics of C. jejuni in the cecum of laying hen over 40 weeks, with possible alteration of the gut microbiota and fatty acid (FA) components. Following oral infection with C. jejuni 81-176, inocula were stably recovered from ceca for up to 8 weeks post-infection (p.i.). From 16 weeks p.i., most birds became negative for C. jejuni and remained negative up to 40 weeks p.i. 16S rRNA gene sequencing analyses revealed that most of the altered relative rRNA gene abundances occurred in the order Clostridiales, in which increased relative rRNA gene abundances were observed at >16 weeks p.i. in the families Clostridiaceae, Ruminococcaceae, Lachnospiraceae, and Peptococcaceae. Lipidome analyses revealed increased levels of sterols associated with bile acid metabolisms in the cecum at 16 and/or 24 weeks p.i. compared with those detected at 8 weeks p.i., suggesting that altered microbiota and bile acid metabolism might underlie the decreased colonization fitness of C. jejuni in the gut of laying hens.

scholarly journals Circadian Rhythm Disruption Influenced Hepatic Lipid Metabolism, Gut Microbiota and Promoted Cholesterol Gallstone Formation in Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Chuanqi He ◽  
Weiyi Shen ◽  
Chaobo Chen ◽  
Qihan Wang ◽  
Qifan Lu ◽  
...  
Keyword(s):  
Circadian Rhythm ◽  
Lipid Metabolism ◽  
Bile Acid ◽  
Gut Microbiota ◽  
Cholesterol Metabolism ◽  
Gallstone Formation ◽  
Hepatic Lipid Metabolism ◽  
Hepatic Lipid ◽  
Lithogenic Diet ◽  
Circadian Expression

BackgroundHepatic lipid metabolism regulates biliary composition and influences the formation of cholesterol gallstones. The genes Hmgcr and Cyp7a1, which encode key liver enzymes, are regulated by circadian rhythm-related transcription factors. We aimed to investigate the effect of circadian rhythm disruption on hepatic cholesterol and bile acid metabolism and the incidence of cholesterol stone formation.MethodsAdult male C57BL/6J mice were fed either a lithogenic diet (LD) only during the sleep phase (time-restricted lithogenic diet feeding, TRF) or an LD ad libitum (non-time-restricted lithogenic diet feeding, nTRF) for 4 weeks. Food consumption, body mass gain, and the incidence of gallstones were assessed. Circulating metabolic parameters, lipid accumulation in the liver, the circadian expression of hepatic clock and metabolic genes, and the gut microbiota were analyzed.ResultsTRF caused a dysregulation of the circadian rhythm in the mice, characterized by significant differences in the circadian expression patterns of clock-related genes. In TRF mice, the circadian rhythms in the expression of genes involved in bile acid and cholesterol metabolism were disrupted, as was the circadian rhythm of the gut microbiota. These changes were associated with high biliary cholesterol content, which promoted gallstone formation in the TRF mice.ConclusionDisordered circadian rhythm is associated with abnormal hepatic bile acid and cholesterol metabolism in mice, which promotes gallstone formation.

Combined use of epigallocatechin-3-gallate (EGCG) and caffeine in low doses exhibits marked anti-obesity synergy through regulation of gut microbiota and bile acid metabolism

2021 ◽  
Author(s):  
Ming-zhi Zhu ◽  
Fang Zhou ◽  
Jian Ouyang ◽  
Qi-ye Wang ◽  
Yi-long Li ◽  
...  
Keyword(s):  
Bile Acid ◽  
Synergistic Effect ◽  
Gut Microbiota ◽  
Acid Metabolism ◽  
Bile Acid Metabolism ◽  
Low Doses ◽  
Combined Use

Combined use of epigallocatechin-3-gallate (EGCG) and caffeine in low doses exhibits marked anti-obesity synergy. The synergistic effect may be attributed to regulation of gut microbiota and BA metabolism.

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