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Haematology and oncology
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
9.9 Which of the following is/are features of haemolytic anaemias?Reticulocytosis.Raised haptoglobin.Raised conjugated bilirubin.Hypochromic erythrocytes.Urobilin in urine.
Liver Diseases
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Approximately 300 mg of bilirubin is produced daily from the breakdown of hemoglobin. Minor amounts are synthetized directly and bound to albumin in the liver and bone marrow. Bilirubin is transported in the blood from the reticuloendothelial system to the liver. At the surface of the liver cell it is released from albumin and internalized. Within the cell, bilirubin is attached to ligandin and carried to the endoplasmic reticulum, where it is conjugated with glucuronic acid. The conjugated bilirubin is excreted into the intestines via the bile. Further conversion of bilirubin in the large intestines into urobilinogen, to urobilin and stercobilinogen, and then to stercobilin, is mainly bacterial. Some of these bile pigments are reabsorbed from the gut and again taken up by the liver. About 90 to 350 mg of urobilin is excreted daily in the feces and less than 4 mg is eliminated by the kidney (Figure 17).
Absorption of Macromolecules by Mammalian Intestinal Epithelium
Published in Shayne C. Gad, Toxicology of the Gastrointestinal Tract, 2018
The feces normally are about three-fourths water and one-fourth solid matter which is itself is composed of about 30% inorganic matter, 2%–3% protein, and 30% undigested roughage of the food and dried constituents of digestive juices, such as bile pigment and sloughed epithelial cells. The large amount of fat derives mainly from fat formed by bacteria and fat in the sloughed epithelial cells. The brown color of feces is caused by stercobilin and urobilin, derivatives of bilirubin. The odor is caused principally by the products of bacterial action; these products vary from one individual or species to another, depending on colonic bacterial flora and on the type of food eaten.
Fumarate hydratase as a therapeutic target in renal cancer
Published in Expert Opinion on Therapeutic Targets, 2020
Priyanka Kancherla, Michael Daneshvar, Rebecca A. Sager, Mehdi Mollapour, Gennady Bratslavsky
In an effort to identify metabolic biomarkers, Zheng et al. aimed to develop a metabolic signature of FH-deficient renal cell carcinoma using an FH-deficient mouse model [78]. The authors identified the urinary metabolites most characteristic of FH loss to be fumarate, urobilin, a product of heme degradation, and 2-SC, as expected based on the known metabolic derangements associated with FH loss presented in this review. Additionally, argininosuccinate, a urea cycle metabolite, was also identified. This metabolic signature was replicated in the spent culture media of UOK262 cells compared to UOK262 cells with re-constituted FH expression. The authors suggest that the generation of argininosuccinate serves as a means by which FH-deficient cells excrete accumulated fumarate. Reversal of the urea cycle enzyme argininosuccinate lyase generates argininosuccinate from arginine and excess fumarate, causing cells to become dependent on exogenous arginine. The authors aim to exploit this weakness for therapeutic benefit. They demonstrated that arginine deprivation using pegylated arginine deiminase inhibited cellular proliferation in FH-deficient cells. Their findings suggest a role for argininosuccinate and arginine deprivation in the diagnosis and treatment of HLRCC [78].
Balance of saccharolysis and proteolysis underpins improvements in stool quality induced by adding a fiber bundle containing bound polyphenols to either hydrolyzed meat or grain-rich foods
Published in Gut Microbes, 2019
Matthew I. Jackson, Dennis E. Jewell
Heme is catabolized to biliverdin before enzymatic reduction to bilirubin and excretion in bile. Urobilins are microbial metabolites of bilirubin, and fecal levels are higher in human subjects with irritable bowel syndrome who respond to low fermentable substrate foods, implying that urobilins are markers for specific microbial activity associated with bowel pathophysiology.42 Indeed, bile pigment deconjugation and enterohepatic recirculation has been shown to be mediated most strongly by only a few bacterial commensals,43 and levels of urobilins are decreased in human Crohn’s-type inflammatory bowel disease.44 In this study, levels of urobilins were more strongly impacted when fiber was added to GR food than to HM food. On balance, urobilinoids were decreased by inclusion of fiber into either food; 2 of 3 detected urobilinoids were decreased on either HM or GR foods. Biliverdin was not changed on either HM Fiber or GR Fiber, whereas bilirubins themselves were decreased by inclusion of fiber into GR but not HM food. The decreased bile pigment effects appear to be microbiome mediated, as fiber per se would be expected to entrap and promote excretion of luminal bile pigments, increasing fecal levels. There may be instances where modulation of microbiome urobilin postbiotic production has physiological utility, and dietary fiber from natural sources could be a safe dietary way to effect this change.