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Salt excretion

Similarly, dietary fibers are known to interact with bile acids in the intestinal limien and thus increase bile salt excretion in feces, resulting in decreased munbers... [Pg.159]

RJ Leipold. Description and simulation of a tubular, plug-flow model to predict the effect of bile sequestrants on human bile salt excretion. J Pharm Sci 84 670-672, 1995. [Pg.421]

Hormones are intercellular messengers. They are typically (1) steroids (e.g., estrogens, androgens, and mineral corticoids, which control the level of water and salts excreted by the kidney), (2) polypeptides (e.g., insulin and endorphins), and (3) amino acid derivatives (e.g., epinephrine, or adrenaline, and norepinephrine, or noradrenaline). Hormones maintain homeostasis—the balance of biological activities in the body for example, insulin controls the blood glucose level, epinephrine and norepinephrine mediate the response to the external environment, and growth hormone promotes normal healthy growth and development. [Pg.121]

ATP-dependent process, aided by the bile-salt excretion pump (BSEP) expression in the canalicular membrane. Conjugation increases the aqueous solubility of the bile adds, and renders these bile adds largely impermeable to the cell membranes of the intestine and duodenum hence, they are unable to leave the intestinal lumen. This allows bile-add levels to rise in the lumen, ultimately reaching sufficient concentrations to form micelles, which allow lipid emulsification and subsequent absorption. [Pg.3]

Sodium chloride (hypotonic) - 0.45% Sodium chloride (hypotonic) is primarily a hydrating solution and may be used to assess the status of the kidneys, because more water is provided than is required for salt excretion. It also may be used in the treatment of hyperosmolar diabetes where the use of dextrose is inadvisable and there is a need for large amounts of fluid without an excess of sodium ions. [Pg.35]

This does not mean that analysis of allelopathy in an arid environment should be done differently from that which is customary in a humid environment yet it is important to estimate the extent to which inorganic salts (excreted by the plant or released from its litter) are involved in the allelopathic effect. So far as secondary metabolites are concerned, it should be of interest to compare their production under humid and stressed conditions. It is suggested that for the evaluation of the allelochemical effect, species suppressed in their natural habitat should be preferred over any other standard seeds commonly used for evaluating germination inhibitors. Also, efforts to isolate allelochemicals from soils will assist in the establishment of allelopathy on a more concrete basis than is available at present. [Pg.67]

T FIGURE 10-19 Steroids derived from cholesterol. Testosterone, the male sex hormone, is produced in the testes. Estradiol, one of the female sex hormones, is produced in the ovaries and placenta. Cortisol and aldosterone are hormones synthesized in the cortex of the adrenal gland they regulate glucose metabolism and salt excretion, respectively. Prednisolone and prednisone are synthetic steroids used as antiinflammatory agents. [Pg.359]

Girard, J.-P. (1976). Salt excretion by the perfused head of trout adapted to sea water and its inhibition by adrenaline. Journal of Comparative Physiology 111, 77-91. [Pg.273]

About 500 mg cholesterol is converted every day to bile salts. This may be increased if the patient is given bile salt binding resins, such as cholestyramine, which diminishes bile salt resorption, causing increased bile salt excretion in the feces. Cholestyramine and similar substances are given to individuals with high serum cholesterol levels. Most of the cholesterol that enters the small intestine via bile (see earlier) is also excreted. Fecal cholesterol amounts to about 1 g/day and is a major means of removing cholesterol from the organism. [Pg.498]

Active transport is found in biological desalination and ion separation. Salt excretion by the glands of desert plants and accumulation of potassium in certain bacteria against a very large concentration gradient are some examples of active transport. Active transport is a highly selective process it can be prevented by specific metabolic inhibitors, and is closely related to facilitated transport. [Pg.531]

The bile salt-independent pathway depends on osmotically active solutes such as glutathione and bicarbonate to generate water flow into the canaliculi. It has been shown that bile flow continues at zero bile salt excretion, i.e. a bile salt-independent process. [Pg.39]

The ring structure of cholesterol cannot be degraded in the body. The bile salts excreted in the feces are the major form in which the steroid nucleus is excreted. [Pg.215]

Gibson LE, diSant Agnese PA. Studies of salt excretion in sweat. J Pediatr 1963 62 855-67. [Pg.1016]

Intrahepatic cholestasis of pregnancy is a syndrome of unknown etiology characterized by a 100-fold increase in maternal and fetal blood bile salt levels. Bile salts are produced in both the fetal and maternal liver. The fetus transfers the bile salts across the placenta for disposal. When the function of the maternal gallbladder is slowed, bile salts can accumulate in the liver and bloodstream, ultimately resulting in the classical pruritus symptom. It is believed that pregnancy-related hormones may slow bile salt excretion from the gallbladder. [Pg.306]

Bile binding resin - binds bile salts Excretion... [Pg.164]

Cholestyramine (Questran) Forms insoluble complex with bile salts, excreted in feces. Body compensates by increasing LDL receptors and oxidizing cholesterol to bile acids. LDL > 190 mg/dl (160 with 2 risk factors) provided that 6 month trial of low lipid diet has failed. i Cholesterol, LDL T Triglycerides, VLDL, HDL ... [Pg.80]

A theoretical role for a salt-excreting hormone in hypertension was proposed by Dahl and expanded by Blaustein. O Haddy et al. [Pg.254]

Kidney dysfunction can lead to edema formation as a result of decreased formation of urine and the subsequent imbalance of water and electrolyte (e.g., sodium ion) homeostasis. Retention of salt and water results in an expansion of the extracellular fluid volume and, thus, edema formation. Thus, when salt intake exceeds salt excretion, edema can form. Edema formation also is associated with deceased protein levels in blood, as seen in nephrotic syndrome and liver disease. Cirrhosis of the liver leads to increased lymph in the space of Disse. Eventually, the increased lymph volume results in movement of fluid into the peritoneal cavity and ascites develops. [Pg.1100]

Sturkie, P.D. (1986). Kidneys, extrarenal salt excretion, and urine. [Pg.259]

In studies with mice and rats, increases in urine output and salt excretion were observed after administration of dandelion leaf fluid extract. A dose corresponding to 8 g/ kg of the dried herb demonstrated activity equivalent to 80 mg/kg of the diuretic furosemide (Racz-Kotilla et al. 1974). [Pg.855]

Dissociated jaundice (ictere dissociee) refers to a dissociation of bilirubin and bile salt excretion in which bilirubin is retained, leading to jaundice, but bile salts are excreted in a normal manner so that such patients are icteric but do not have pruritus and no bile salts are detected in blood or urine. The concept was held that only the hepatic cell could selectively retain bilirubin but excrete bile salts and that bile ducts or gallbladder cells could not. The observation of dissociated jaundice was therefore regarded as useful in distinguishing jaundice due to hepatitis or cirrhosis from that caused by bile duct obstruction (74-76). [Pg.73]

Most bile salts excreted in the feces are of the secondary type. Their formation is discussed in Section VII. The daily fecal excretion of bile salts in healthy subjects is highly variable and easily influenced by dietary alterations. Values from several studies are given in Table VIII. Bile salts virtually disappear from the stools during prolonged fasting, and turnover nearly ceases (19). Primary bile salts appear in the stools of patients with diarrhea (1). Patients taking cholestyramine excrete the usual pattern of secondary bile salts (57), so that apparently bacterial dehydroxylation of bile salts can occur in the presence of this resin. Patients with total external bile fistulas have no bile salts in the feces (2) this does not exclude transintestinal excretion of bile salts but makes it unlikely. As mentioned earlier, the predominance of chenodeoxycholic acid in blood and bile is often reflected in a predominance of lithocholate over deoxycholate in the feces (27). [Pg.76]


See other pages where Salt excretion is mentioned: [Pg.213]    [Pg.241]    [Pg.407]    [Pg.41]    [Pg.133]    [Pg.63]    [Pg.65]    [Pg.144]    [Pg.145]    [Pg.405]    [Pg.33]    [Pg.236]    [Pg.787]    [Pg.212]    [Pg.208]    [Pg.994]    [Pg.730]    [Pg.730]    [Pg.385]    [Pg.49]    [Pg.461]    [Pg.21]    [Pg.144]    [Pg.638]    [Pg.64]   
See also in sourсe #XX -- [ Pg.94 ]




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