Acetylation of the Entamoeba histone H4 N-terminal domain is influenced by short-chain fatty acids that enter trophozoites in a pH-dependent manner

Abstract Background Previous studies have reported that gut microbiota, permeability, short-chain fatty acids (SCFAs), and inflammation are altered in Parkinson’s disease (PD), but how these factors are linked and how they contribute to disease processes and symptoms remains uncertain. This study sought to compare and identify associations among these factors in PD patients and controls to elucidate their interrelations and links to clinical manifestations of PD. Methods Stool and plasma samples and clinical data were collected from 55 PD patients and 56 controls. Levels of stool SCFAs and stool and plasma inflammatory and permeability markers were compared between patients and controls and related to one another and to the gut microbiota. Results Calprotectin was increased and SCFAs decreased in stool in PD in a sex-dependent manner. Inflammatory markers in plasma and stool were neither intercorrelated nor strongly associated with SCFA levels. Age at PD onset was positively correlated with SCFAs and negatively correlated with CXCL8 and IL-1β in stool. Fecal zonulin correlated positively with fecal NGAL and negatively with PD motor and non-motor symptoms. Microbiota diversity and composition were linked to levels of SCFAs, inflammatory factors, and zonulin in stool. Certain relationships differed between patients and controls and by sex. Conclusions Intestinal inflammatory responses and reductions in fecal SCFAs occur in PD, are related to the microbiota and to disease onset, and are not reflected in plasma inflammatory profiles. Some of these relationships are distinct in PD and are sex-dependent. This study revealed potential alterations in microbiota-host interactions and links between earlier PD onset and intestinal inflammatory responses and reduced SCFA levels, highlighting candidate molecules and pathways which may contribute to PD pathogenesis and clinical presentation and which warrant further investigation.

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Effect of short-chain fatty acids on the secretory response of the ovine exocrine pancreas

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1983.244.3.g284 ◽

1983 ◽

Vol 244 (3) ◽

pp. G284-G290 ◽

Cited By ~ 2

Author(s):

E. Harada ◽

S. Kato

Keyword(s):

Fatty Acids ◽

Exocrine Pancreas ◽

Short Chain Fatty Acids ◽

Secretory Response ◽

Short Chain ◽

Pancreatic Acinar Cells ◽

Dependent Manner ◽

Amylase Release ◽

Amylase Output ◽

Chain Fatty Acids

The secretory response of the exocrine pancreas to short-chain fatty acids has been studied in anesthetized sheep and in isolated lobules. Butyrate, propionate, and acetate stimulated pancreatic juice flow and protein and amylase output in the anesthetized sheep. The secretory response to butyrate was significantly greater than that of propionate or acetate. Rapid intravenous injection of butyrate (625 mumol/kg) caused a 13-fold rise in the juice flow, 26-fold in protein output, and 37-fold in amylase output above the basal levels within 5 min and declined to basal levels over a period of 30 min. Responses to butyrate (625 mumol/kg) were comparable with those obtained with 2 U/kg pancreozymin (Boots). Detectable responses were obtained with 15 mu/kg butyrate, 125 mumol/kg propionate, and 312.5 mumol/kg acetate. The secretory response to butyrate (625 mumol/kg) was not affected by pretreatment with atropine and hexamethonium. In the isolated lobule preparation, amylase release increased in response to butyrate in a concentration-dependent manner, reaching a maximal level at 1 mM and declining at 100 mM. It is concluded that short-chain fatty acids act directly on pancreatic acinar cells to stimulate secretion. The physiological implications of these findings are considered.

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Relationships of gut microbiota, short-chain fatty acids, inflammation, and the gut barrier in Parkinson's disease

10.21203/rs.3.rs-63018/v2 ◽

2021 ◽

Author(s):

Velma T Aho ◽

Madelyn Crawford Houser ◽

Pedro AB Pereira ◽

Jianjun Chang ◽

Knut Rudi ◽

...

Keyword(s):

Parkinson’S Disease ◽

Fatty Acids ◽

Parkinson's Disease ◽

Gut Microbiota ◽

Intestinal Inflammation ◽

Disease Onset ◽

Short Chain Fatty Acids ◽

Short Chain ◽

Dependent Manner ◽

Chain Fatty Acids

Abstract Background Previous studies have reported that gut microbiota, permeability, short-chain fatty acids (SCFAs), and inflammation are altered in Parkinson’s disease (PD), but how these factors are linked and contribute to disease processes and symptoms remains uncertain. This study sought to compare and identify associations among these factors in PD patients and controls to elucidate their interrelations and links to clinical manifestations of PD. Methods Stool and plasma samples and clinical data were collected from 55 PD patients and 56 controls. Levels of stool SCFAs and stool and plasma inflammatory and permeability markers were compared between patients and controls and related to one another and to the gut microbiota. Results Calprotectin was increased and SCFAs decreased in stool in PD in a sex-dependent manner. Inflammatory markers in plasma and stool were neither intercorrelated nor strongly associated with SCFA levels. Age at PD onset was positively correlated with SCFAs and negatively correlated with CXCL8 and IL-1β in stool. Fecal zonulin correlated positively with fecal NGAL and negatively with PD motor and non-motor symptoms. Microbiota diversity and composition were linked to levels of stool SCFAs, inflammation, and zonulin. Certain relationships differed between patients and controls and by sex. Conclusions Intestinal inflammatory responses and reductions in fecal SCFAs occur in PD, are related to the microbiota and to disease onset, and are not reflected in plasma inflammatory profiles. Some of these relationships are PD- and sex-dependent. Alterations in microbiota-host interactions and links between intestinal inflammation and reduced SCFA levels and earlier PD onset warrant further investigation.

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Relationships of gut microbiota, short-chain fatty acids, inflammation, and the gut barrier in Parkinson's disease

10.21203/rs.3.rs-63018/v1 ◽

2020 ◽

Author(s):

Velma T Aho ◽

Madelyn Crawford Houser ◽

Pedro AB Pereira ◽

Jianjun Chang ◽

Knut Rudi ◽

...

Keyword(s):

Parkinson’S Disease ◽

Fatty Acids ◽

Parkinson's Disease ◽

Gut Microbiota ◽

Intestinal Inflammation ◽

Disease Onset ◽

Short Chain Fatty Acids ◽

Short Chain ◽

Dependent Manner ◽

Chain Fatty Acids

Abstract Background: Previous studies have reported that gut microbiota, permeability, short-chain fatty acids (SCFAs), and inflammation are altered in Parkinson’s disease (PD), but how these factors are linked and contribute to disease processes and symptoms remains uncertain. This study sought to compare and identify associations among these factors in PD patients and controls to elucidate their interrelations and links to clinical manifestations of PD.Methods: Stool and plasma samples and clinical data were collected from 55 PD patients and 56 controls. Levels of stool SCFAs and stool and plasma inflammatory and permeability markers were compared between patients and controls and related to one another and to the gut microbiota.Results: Calprotectin was increased and SCFAs decreased in stool in PD in a sex-dependent manner. Inflammatory markers in plasma and stool were neither intercorrelated nor strongly associated with SCFA levels. Age at PD onset was positively correlated with SCFAs and negatively correlated with CXCL8 and IL-1β in stool. Fecal zonulin correlated positively with fecal NGAL and negatively with PD motor and non-motor symptoms. Microbiota diversity and composition were linked to levels of stool SCFAs, inflammation, and zonulin. Certain relationships differed between patients and controls and by sex.Conclusions: Intestinal inflammatory responses and reductions in fecal SCFAs occur in PD, are related to the microbiota and to disease onset, and are not reflected in plasma inflammatory profiles. Some of these relationships are PD- and sex-dependent. Alterations in microbiota-host interactions and links between intestinal inflammation and reduced SCFA levels and earlier PD onset warrant further investigation.

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Cholic acid accumulation and its diminution by short-chain fatty acids in bifidobacteria

Microbiology ◽

10.1099/mic.0.26376-0 ◽

2003 ◽

Vol 149 (8) ◽

pp. 2031-2037 ◽

Cited By ~ 45

Author(s):

Peter Kurdi ◽

Hiroshi Tanaka ◽

Hendrik W. van Veen ◽

Kozo Asano ◽

Fusao Tomita ◽

...

Keyword(s):

Fatty Acids ◽

Cholic Acid ◽

Short Chain Fatty Acids ◽

Weak Acid ◽

Short Chain ◽

Bile Acid Metabolism ◽

Dependent Manner ◽

Human Bile ◽

Chain Fatty Acids

Cholic acid (CA) transport was investigated in nine intestinal Bifidobacterium strains. Upon energization with glucose, all of the bifidobacteria accumulated CA. The driving force behind CA accumulation was found to be the transmembrane proton gradient (ΔpH, alkaline interior). The levels of accumulated CA generally coincided with the theoretical values, which were calculated by the Henderson–Hasselbalch equation using the measured internal pH values of the bifidobacteria, and a pK a value of 6·4 for CA. These results suggest that the mechanism of CA accumulation is based on the diffusion of a hydrophobic weak acid across the bacterial cell membrane, and its dissociation according to the ΔpH value. A mixture of short-chain fatty acids (acetate, propionate and butyrate) at the appropriate colonic concentration (117 mM in total) reduced CA accumulation in Bifidobacterium breve JCM 1192T. These short-chain fatty acids, which are weak acids, reduced the ΔpH, thereby decreasing CA accumulation in a dose-dependent manner. The bifidobacteria did not alter or modify the CA molecule. The probiotic potential of CA accumulation in vivo is discussed in relation to human bile acid metabolism.

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Acetate and Propionate Short Chain Fatty Acids Stimulate Adipogenesis via GPCR43

Endocrinology ◽

10.1210/en.2005-0545 ◽

2005 ◽

Vol 146 (12) ◽

pp. 5092-5099 ◽

Cited By ~ 335

Author(s):

Yeon-Hee Hong ◽

Yukihiko Nishimura ◽

Daisuke Hishikawa ◽

Hiroaki Tsuzuki ◽

Hisae Miyahara ◽

...

Keyword(s):

Fatty Acids ◽

Short Chain Fatty Acids ◽

Short Chain ◽

Dependent Manner ◽

Adipose Tissues ◽

Isolated Adipocytes ◽

High Level ◽

Interfering Rna ◽

G Protein Coupled ◽

Chain Fatty Acids

It has recently been discovered that G protein-coupled receptors (GPCR) 41 and 43 are characterized by having the short chain fatty acids acetate and propionate as their ligands. The objective of this study was to investigate the involvement of GPCR41, GPCR43, and their ligands in the process of adipogenesis. We measured the levels of GPCR41 and GPCR43 mRNA in both adipose and other tissues of the mouse. GRP43 mRNA expression was higher in four types of adipose tissue than in other tissues, whereas GPCR41 mRNA was not detected in any adipose tissues. A high level of GPCR43 expression was found in isolated adipocytes, but expression level was very low in stromal-vascular cells. Expression of GPCR43 was up-regulated in adipose tissues of mice fed a high-fat diet compared with those fed a normal-fat diet. GPCR43 mRNA could not be detected in confluent and undifferentiated 3T3-L1 adipocytes; however, the levels rose with time after the initiation of differentiation. GPCR41 expression was not detected in confluent and differentiated adipocytes. Acetate and propionate treatments increased lipids present as multiple droplets in 3T3-L1 adipocytes. Propionate significantly elevated the level of GPCR43 expression during adipose differentiation, with up-regulation of PPAR-γ2. Small interfering RNA mediated a reduction of GPCR43 mRNA in 3T3-L1 cells and blocked the process of adipocyte differentiation. In addition, both acetate and propionate inhibited isoproterenol-induced lipolysis in a dose-dependent manner. We conclude that acetate and propionate short chain fatty acids may have important physiological roles in adipogenesis through GPCR43, but not through GPCR41.

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Relationships of gut microbiota, short-chain fatty acids, inflammation, and the gut barrier in Parkinson’s disease

10.1101/2020.06.15.20131011 ◽

2020 ◽

Author(s):

Velma T. E. Aho ◽

Madelyn C. Houser ◽

Pedro A. B. Pereira ◽

Jianjun Chang ◽

Knut Rudi ◽

...

Keyword(s):

Parkinson’S Disease ◽

Fatty Acids ◽

Parkinson's Disease ◽

Gut Microbiota ◽

Intestinal Inflammation ◽

Disease Onset ◽

Short Chain Fatty Acids ◽

Short Chain ◽

Dependent Manner ◽

Chain Fatty Acids

AbstractBackgroundPrevious studies have reported that gut microbiota, permeability, short-chain fatty acids (SCFAs), and inflammation are altered in Parkinson’s disease (PD), but how these factors are linked and contribute to disease processes and symptoms remains uncertain.ObjectivesThis study sought to compare and identify associations among these factors in PD patients and controls to elucidate their interrelations and links to clinical manifestations of PD.MethodsStool and plasma samples and clinical data were collected from 55 PD patients and 56 controls. Levels of stool SCFAs and stool and plasma inflammatory and permeability markers were compared between patients and controls and related to one another and to the gut microbiota.ResultsCalprotectin was increased and SCFAs decreased in stool in PD in a sex-dependent manner. Inflammatory markers in plasma and stool were neither intercorrelated nor strongly associated with SCFA levels. Age at PD onset was positively correlated with SCFAs and negatively correlated with CXCL8 and IL-1β in stool. Fecal zonulin correlated positively with fecal NGAL and negatively with PD motor and non-motor symptoms. Microbiota diversity and composition were linked to levels of stool SCFAs, inflammation, and zonulin. These relationships differed somewhat between patients and controls and by sex.ConclusionsIntestinal inflammatory responses and reductions in fecal SCFAs occur in PD, are related to the microbiota and to disease onset, and are not reflected in plasma inflammatory profiles. Some of these relationships are PD- and sex-dependent. Alterations in microbiota-host interactions and links between intestinal inflammation and reduced SCFA levels and earlier PD onset warrant further investigation.

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MODIFICATION OF OLIGOSACCHARIDE AND SHORT CHAIN FATTY ACID CONTENT OF COWPEA MILK THROUGH FERMENTATION WITH SELECTED MIXED STARTER CULTURES

10.37512/400 ◽

2019 ◽

Keyword(s):

Fatty Acids ◽

Propionic Acid ◽

Fatty Acid Content ◽

Streptococcus Thermophilus ◽

Short Chain Fatty Acids ◽

Starter Cultures ◽

Lactobacillus Delbrueckii ◽

Short Chain ◽

Dependent Manner ◽

Chain Fatty Acids

Cowpea milk was fermented with three mixed starter cultures containing (i) Lactobacillus acidophilus, Bifidobacterium sp, and Streptococcus thermophilus (ABT) (ii) Lactobacillus delbrueckii subsp. bulgaricus and Streptococcus thermophilus (DT) or (iii) Lactobacillus rhamnosus GR-1 and Streptococcus thermophilus (GT). Effects of these cultures on flatulencecausing raffinose family oligosaccharides and the production of postbiotic short chain fatty acids were determined. The oligosaccharides and short chain fatty acids were determined by high performance liquid chromatography and gas chromatography, respectively. The stachyose content of raw cowpea (1.388±0.23 g/100 g) was higher than raffinose (0.221±0.06 g/100 g), while verbascose was not detected. Cowpea milk fermentation caused 67-100% reduction in raffinose and 20-70% reduction in stachyose in a culture-dependent manner. All the cultures produced propionic acid, butyric acid and valeric acid in differing concentrations but only GT and ABT produced isovaleric acid. The product fermented with DT attained 2430 ppm of propionic acid, which was four times and ten times higher than the concentrations produced by the ABT and GT cultures, respectively. In conclusion, fermentation of cowpea milk with the three starter cultures reduced flatulence-causing oligosaccharides and produced postbiotic short chain fatty acids that might promote health regardless of the survival of the microorganisms in the gut.

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