Synonyms for colonocytes or Related words with colonocytes
Examples of "colonocytes"
Butyrates are important as food for cells lining the mammalian colon (
). Without butyrates for energy, colon cells undergo autophagy (self digestion) and die.
Butyric acid is important as an energy (ATP) source for cells lining the mammalian colon (
). Without butyric acid for energy, colon cells undergo upregulated autophagy (i.e., self-digestion).
The major SCFAs in humans are butyrate, propionate, and acetate, where butyrate is the major energy source for
, propionate is destined for uptake by the liver, and acetate enters the peripheral circulation to be metabolized by peripheral tissues.
Glutaminolysis takes place in all proliferating cells, such as lymphocytes, thymocytes,
, adipocytes and especially in tumor cells. In tumor cells the citric acid cycle is truncated due to an inhibition of the enzyme aconitase (EC 220.127.116.11) by high concentrations of reactive oxygen species (ROS) Aconitase catalyzes the conversion of citrate to isocitrate.
Short-chain fatty acids, which include butyrate, are produced by beneficial colonic bacteria (probiotics) that feed on, or ferment prebiotics, which are plant products that contain adequate amounts of dietary fiber. These short-chain fatty acids benefit the
(cells of the colon) by increasing energy production and cell proliferation, and may protect against colon cancer.
Colestyramine is commonly used to treat diarrhea resulting from bile acid malabsorption. It was first used for this in Crohn's disease patients who had undergone ileal resection. The terminal portion of the small bowel (ileum) is where bile acids are reabsorbed. When this section is removed, the bile acids pass into the large bowel and cause diarrhea due to stimulation of chloride/fluid secretion by the
resulting in a secretory diarrhea. Colestyramine prevents this increase in water by making the bile acids insoluble and osmotically inactive.
Butyrate that is produced in the colon through microbial fermentation of dietary fiber is primarily absorbed and utilized by
and the liver for the generation of ATP during energy metabolism; however, some butyrate is absorbed in the distal colon, which is not connected to the portal vein, thereby allowing for the systemic distribution of butyrate to multiple organ systems through the circulatory system. Butyrate that has reached systemic circulation can readily cross the blood-brain barrier via monocarboxylate transporters (i.e., certain members of the SLC16A group of transporters). Other transporters that mediate the passage of butyrate across lipid membranes include SLC5A8 (SMCT1), SLC27A1 (FATP1), and SLC27A4 (FATP4).
Butyrate produces different effects in healthy and cancerous cells; this is known as the "butyrate paradox". In particular, butyrate inhibits colonic tumor cells and promotes healthy colonic epithelial cells. The signaling mechanism is not well understood. A review suggested that the chemopreventive benefits of butyrate depend in part on the amount, time of exposure with respect to the tumorigenic process, and type of fat in the diet. The production of volatile fatty acids such as butyrate from fermentable fibers may contribute to the role of dietary fiber in colon cancer. Short-chain fatty acids, which include butyric acid, are produced by beneficial colonic bacteria (probiotics) that feed on, or ferment prebiotics, which are plant products that contain adequate amounts of dietary fiber. These short-chain fatty acids benefit the
by increasing energy production and cell proliferation, and may protect against colon cancer.
A tumor-specific LACTB2-NCOA2 fusion originating from intra-chromosomal rearrangement of chromosome 8 has been identified at both DNA and RNA levels. Unlike conventional oncogenic chimeric proteins, the fusion product lacks functional domain from respective genes, indicative of an amorphic rearrangement. This chimeric LACTB2-NCOA2 transcript was detected in 6 out of 99 (6.1%) colorectal cancer (CRC) cases, where NCOA2 was significantly downregulated. Enforced expression of wild-type NCOA2 but not the LACTB2-NCOA2 fusion protein impaired the pro-tumorigenic phenotypes of CRC cells, whereas knockdown of endogenous NCOA2 in normal
had opposite effects. Mechanistically, NCOA2 inhibited Wnt/β-catenin signaling through simultaneously upregulating inhibitors and downregulating stimulators of Wnt/β-catenin pathway. NCOA2 is a novel negative growth regulatory gene repressing the Wnt/β-catenin pathway in CRC, where recurrent fusion with LACTB2 contributes to its disruption.
Like other short-chain fatty acids (SCFAs), butyrate is an agonist at the free fatty acid receptors FFAR2 and FFAR3, which function as nutrient sensors which help regulate energy balance; unlike the other SCFAs, butyrate is also an agonist of niacin receptor 1 (NIACR1, aka GPR109A). Butyric acid is utilized by mitochondria, particularly in
and by the liver, to generate adenosine triphosphate (ATP) during fatty acid metabolism. Butyric acid is also an HDAC inhibitor (specifically, HDAC1, HDAC2, HDAC3, and HDAC8), a drug that inhibits the function of histone deacetylase enzymes, thereby favoring an acetylated state of histones in cells. Histone acetylation loosens the structure of chromatin by reducing the electrostatic attraction between histones and DNA. In general, it is thought that transcription factors will be unable to access regions where histones are tightly associated with DNA (i.e., non-acetylated, e.g., heterochromatin). Therefore, butyric acid is thought to enhance the transcriptional activity at promoters, which are typically silenced or downregulated due to histone deacetylase activity.
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