Transport of n-butyrate into human colonic luminal membrane vesicles

Harig, James M.; Ng, E.; Dudeja, Pradeep K.; Brasitus, Thomas A.; Ramaswamy, Krishnamurthy

doi:10.1152/ajpgi.1996.271.3.g415

Cited by 48 publications

(58 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We have no explanation for these apparent genus differences. Experiments with apical membrane vesicles of rat distal colon (Mascolo et al 1991), human colon (Harig et al 1990) and basolateral membrane vesicles of rat distal colon (Reynolds et al 1991) also indicated the presence of a bicarbonatedependent SCFA anion uptake. However, this uptake was not inhibited by amiloride and acetazolamide (Mascolo et al 1991).…”

Section: Discussionmentioning

confidence: 98%

“…Recent studies with apical membrane vesicles of rat distal colon (Mascolo, Rajendran & Binder, 1991) and human colon (Harig, Knaup, Shoshara, Dudeja, Ramaswamy & Brasitus, 1990) and with basolateral membrane vesicles of rat distal colon (Reynolds, Rajendran & Binder, 1991) provided evidence for a SCFA--HCO3-exchange. HCO3-could be gained from the carbonic anhydrase-catalysed conversion of metabolically derived C02.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Functional role of bicarbonate in propionate transport across guinea‐pig isolated caecum and proximal colon.

Engelhardt

Gros

Burmester

et al. 1994

The Journal of Physiology

View full text Add to dashboard Cite

1. Unidirectional fluxes of propionate across isolated epithelia from the guinea-pig caecum and proximal colon were measured under short-circuit current conditions. In the caecum and proximal colon the serosal-to-mucosal propionate flux (J") was higher than mucosal-to-serosal flux(Jlr ), resulting in a net secretory flux of propionate.2. HCO37-CO2-free solution reduced JPr in the caecum and proximal colon markedly; JPr was not (caecum) or little (proximal colon) affected. The subsequent addition of acetazolamide caused a further decrease in Jlr in the proximal colon, but not in the caecum.3. In HC03--containing solutions acetazolamide or ethoxzolamide inhibited Jlr ; Jlr was not affected. A macromolecular carbonic anhydrase inhibitor, prontosil-dextran, had no effect on propionate fluxes, indicating that the intracellular carbonic anhydrase is of importance for short-chain fatty acid transport. 4. Subsequent to carbonic anhydrase inhibition, mucosal addition of amiloride caused a slight further decrease of Jlr in the caecum and proximal colon; jPr was not affected. 5.Results support the view that a considerable proportion of short-chain fatty acids (SCFAs) is absorbed via a SCFA--HC03-exchange.

show abstract

Section: Discussionmentioning

confidence: 98%

mentioning

confidence: 99%

Functional role of bicarbonate in propionate transport across guinea‐pig isolated caecum and proximal colon.

Engelhardt

Gros

Burmester

et al. 1994

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…2 ). Conclusive evidence for the existence of SCFA-HCO 3 Ϫ exchange was obtained from vesicle studies in which it was shown that SCFA-HCO 3 Ϫ exchange was independent of Cl Ϫ -HCO 3 Ϫ exchange and Na + transport (85)(86)(87)(88). The identity of the transporter, however, remains unknown.…”

Section: The Bacterial Pathways Of Anaerobic Scfa Productionmentioning

confidence: 99%

“…2 ). The basolateral SCFA for butyrate, which are 1.5 mM and 17.5 mM for the apical and the basolateral exchanger, respectively ( 87,95 ). Immunoblotting revealed that MCT4 ( SLC16A3 ) and MCT5 ( SLC16A4 ) were localized to the basolateral membrane ( 96 ).…”

Section: The Bacterial Pathways Of Anaerobic Scfa Productionmentioning

confidence: 99%

The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism

Besten

Eunen

Groen

et al. 2013

Journal of Lipid Research

3,786

2,665

View full text Add to dashboard Cite

of the metabolic syndrome, the exact mechanisms underlying the different comorbidities are not yet completely known. Recently, dietary fi bers have raised much interest, as they exert benefi cial effects on body weight, food intake, glucose homeostasis, and insulin sensitivity ( 2-4 ). Epidemiological studies show an association between a higher fi ber intake and a reduced risk of irritable bowel syndrome, infl ammatory bowel disease, cardiovascular disease, diabetes, and colon cancer ( 1 ).Humans lack the enzymes to degrade the bulk of dietary fi bers. Therefore these nondigestible carbohydrates pass the upper gastrointestinal tract unaffected and are fermented in the cecum and the large intestine by the anaerobic cecal and colonic microbiota. Fermentation results in multiple groups of metabolites [elegantly reviewed by Nicholson et al. ( 5 )] of which short-chain fatty acids (SCFAs) are the major group ( 6 ). To the microbial community SCFAs are a necessary waste product, required to balance redox equivalent production in the anaerobic environment of the gut ( 7 ). SCFAs are saturated aliphatic organic acids that consist of one to six carbons of which acetate (C2), propionate (C3), and butyrate (C4) are the most abundant ( у 95%) ( 8 ). Acetate, propionate, and butyrate are present in an approximate molar ratio of 60:20:20 in the colon and stool ( 9-11 ). Depending on the diet, the total concentration of SCFAs decreases from 70 to 140 mM in the proximal colon to 20 to 70 mM in the distal colon ( 12 ). A unique series of measurements in Abstract Short-chain fatty acids (SCFAs), the end products of fermentation of dietary fi bers by the anaerobic intestinal microbiota, have been shown to exert multiple benefi cial effects on mammalian energy metabolism. The mechanisms underlying these effects are the subject of intensive research and encompass the complex interplay between diet, gut microbiota, and host energy metabolism. This review summarizes the role of SCFAs in host energy metabolism, starting from the production by the gut microbiota to the uptake by the host and ending with the effects on host metabolism. There are interesting leads on the underlying molecular mechanisms, but there are also many apparently contradictory results . A coherent understanding of the multilevel network in which SCFAs exert their effects is hampered by the lack of quantitative data on actual fl uxes of SCFAs and metabolic processes regulated by SCFAs. In this review we address questions that, when answered, will bring us a great step forward in elucidating the role of SCFAs in mammalian energy metabolism. -den Besten, G., K. van Eunen, A. K. The decrease in physical exercise and increase in energy intake, especially seen in the Western world, disrupts the energy balance in humans and can lead to a complex of symptoms collectively denoted as the metabolic syndrome. The key characteristics of the metabolic syndrome are obesity, loss of glycemic control, dyslipidemia, and hypertension ( 1 ). Due to the complex multifactorial etiolog...

show abstract

“…Our laboratories had made significant contributions in this important area of research and have been instrumental in establishing the techniques for the purification of the human intestinal plasma membranes (10,12,16) and establishing the existence of carrier-mediated mechanisms of SCFA transport across the human ileal luminal and colonic antipodal plasma membranes (11,13,17). As early as in 1996 (9), we were interested in investigating MCT1 as a potential candidate gene involved in intestinal butyrate uptake; therefore, we submitted an abstract to the American Gastroenterological Association (AGA) in December 1996 and first presented our studies of MCT1 expression in the human tissues including the intestine at the annual AGA meeting in May 1997.…”

Section: The Human Monocarboxylate Transporter Mct1: Gene Structure Amentioning

confidence: 99%

The Human Monocarboxylate Transporter MCT1: Gene Structure and Regulation

Cuff¹,

Shirazi-Beechey²

2005

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

To the Editor:We read with concern the recent paper by Hadjiagapiou et al. (4) that examines the regulation of the monocarboxylate transporter isoform 1 (MCT1) gene promoter in Caco-2 cells and would like to make a number of comments with regard to 1) errors in their data and 2) misquotation and misrepresentation of prior publications by others in this important study area.MCT1 is the prototype of a family of proteins that play an important role in the transport of monocarboxylates across the cell membrane in a variety of cell types (5). MCT1 is particularly prominent in the colonic epithelium where it functions to transport short-chain fatty acids (most notably, butyrate) from the lumen across the colonocyte luminal membrane (7, 8). We demonstrated several years ago that MCT1 abundance is markedly downregulated during the transition from normality to malignancy in the colon and, more recently, that its expression is required for butyrate to exert many of its effects in cultured colonic epithelial cells (1, 6). Not surprisingly, the regulation of MCT1 expression in the intestine is an important area of study. We have previously reported that human colonic MCT1 expression is responsive to its substrate, butyrate, and that this regulation involves the dual control of transcription and mRNA stability (2). We have also determined the site of transcription initiation, isolated the MCT1 gene promoter, and demonstrated the MCT1 gene structure to comprise five exons interrupted by four introns. The first of these introns occurs in the 5'-untranslated region (UTR) encoding DNA, spans greater than 26 kb, and accounts for more than one-half of the entire MCT1 transcription unit (3).Given that the isolation of the human MCT1 gene promoter was first published in full more than three years ago (3) and the sequence submitted to the European Molecular Biology Laboratories database (Accession no. AJ438944), it is surprising that the first part of the paper by Hadjiagapiou et al. focuses on repetition of this isolation. This aside, a major concern is the inaccurate description by Hadjiagapiou et al. of where the MCT1 promoter DNA sequence is located in relation to the genome. The authors specifically and repeatedly state that the transcriptional start site is located only 281 bp upstream from the translational start site (i.e., the MCT1 coding region) and this is reinforced and illustrated by the contiguous DNA sequence shown in their Fig. 1. We want make it clear that these data are incorrect and ignore the large (26 kb) intron that interrupts the MCT1 5Ј-UTR (3). The presence of this intron is clearly indicated by a database blast of the MCT1 5Ј-RACE sequence, which shows that the sequence of the MCT1 message and that of the MCT1 genomic DNA diverge 45 bp upstream of the MCT1 coding region and only reconverge ϳ26 kb upstream in the genomic DNA. Moreover, this arrangement is described prominently in our prior publication detailing the first isolation of the MCT1 gene promoter and determination of the gene structure of human MCT...

show abstract

Transport of n-butyrate into human colonic luminal membrane vesicles

Cited by 48 publications

References 0 publications

Functional role of bicarbonate in propionate transport across guinea‐pig isolated caecum and proximal colon.

Functional role of bicarbonate in propionate transport across guinea‐pig isolated caecum and proximal colon.

The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism

The Human Monocarboxylate Transporter MCT1: Gene Structure and Regulation

Contact Info

Product

Resources

About