Recent studies in rats suggest that vasopressin and the resulting urinary concentrating activity reduce the capacity of the kidney to excrete sodium. The present study investigates the influence of the level of hydration on the excretion of a sodium load in humans. Eight healthy male volunteers (18-35 yr) were studied twice, in random order, under either low (LowH) or high (HighH) hydration. They drank throughout the study either 0.25 (LowH) or 2.0 ml water/kg body wt (HighH) every 30 min. After 1 h equilibration, urine was collected for 2 h before (basal) and 10 h after the NaCl load (5 g NaCl in 250 ml, infused intravenously over 30 min). Differences in excretory patterns between LowH and HighH were mostly confined to the first 4 h after the load. The increase in Na excretion after the load was more intense under HighH than under LowH (+ 10.9 +/- 2.6 vs. + 5.8 +/- 2.7 mmol/h in the first 4 postload h; P
excrete
It forms all or part of: ascertain; certain; concern; concert; crime; criminal; crisis; critic; criterion; decree; diacritic; discern; disconcert; discreet; discriminate; endocrine; excrement; excrete; garble; hypocrisy; incertitude; recrement; recriminate; riddle (n.2) "coarse sieve;" secret; secretary.
Infectious prion diseases-scrapie of sheep and chronic wasting disease (CWD) of several species in the deer family-are transmitted naturally within affected host populations. Although several possible sources of contagion have been identified in excretions and secretions from symptomatic animals, the biological importance of these sources in sustaining epidemics remains unclear. Here we show that asymptomatic CWD-infected mule deer (Odocoileus hemionus) excrete CWD prions in their faeces long before they develop clinical signs of prion disease. Intracerebral inoculation of irradiated deer faeces into transgenic mice overexpressing cervid prion protein (PrP) revealed infectivity in 14 of 15 faecal samples collected from five deer at 7-11 months before the onset of neurological disease. Although prion concentrations in deer faeces were considerably lower than in brain tissue from the same deer collected at the end of the disease, the estimated total infectious dose excreted in faeces by an infected deer over the disease course may approximate the total contained in a brain. Prolonged faecal prion excretion by infected deer provides a plausible natural mechanism that might explain the high incidence and efficient horizontal transmission of CWD within deer herds, as well as prion transmission among other susceptible cervids.
In animals, the main excretory products are carbon dioxide, ammonia (in ammoniotelics), urea (in ureotelics), uric acid (in uricotelics), guanine (in Arachnida), and creatine. The liver and kidneys clear many substances from the blood (for example, in renal excretion), and the cleared substances are then excreted from the body in the urine and feces.[5]
Aquatic animals usually excrete ammonia directly into the external environment, as this compound has high solubility and there is ample water available for dilution. In terrestrial animals ammonia-like compounds are converted into other nitrogenous materials, i.e. urea, that are less harmful as there is less water in the environment and ammonia itself is toxic. This process is called detoxification.[6]
Birds excrete their nitrogenous wastes as uric acid in the form of a paste. Although this process is metabolically more expensive, it allows more efficient water retention and it can be stored more easily in the egg. Many avian species, especially seabirds, can also excrete salt via specialized nasal salt glands, the saline solution leaving through nostrils in the beak.
In insects, a system involving Malpighian tubules is used to excrete metabolic waste. Metabolic waste diffuses or is actively transported into the tubule, which transports the wastes to the intestines. The metabolic waste is then released from the body along with fecal matter.
There are two kidneys, each about the size of a fist, located on either side of the spine at the lowest level of the rib cage. Each kidney contains up to a million functioning units called nephrons. A nephron consists of a filtering unit of tiny blood vessels called a glomerulus attached to a tubule. When blood enters the glomerulus, it is filtered and the remaining fluid then passes along the tubule. In the tubule, chemicals and water are either added to or removed from this filtered fluid according to the body's needs, the final product being the urine we excrete.
The kidneys perform their life-sustaining job of filtering and returning to the bloodstream about 200 quarts of fluid every 24 hours. About two quarts are removed from the body in the form of urine, and about 198 quarts are recovered. The urine we excrete has been stored in the bladder for anywhere from 1 to 8 hours.
This time, Zhouyao injected two additional forms of RNA into the developing zebrafish, one of which would prevent the larvae from producing the zebrafish Hiat1a protein and another to block production of the Hiat1b protein, and then tracked how much ammonia the larvae were able to expel from their bodies. The embryos that could not produce zebrafish Hiat1b suffered a 30% reduction in their ability to excrete ammonia. And, when Zimmer checked the level of ammonia excretion near to the developing gill, it was significantly reduced. Zebrafish Hiat1b definitely contributes to the larvae's ability to excrete ammonia.
Zinc is an essential metal involved in a wide range of biological processes, and aberrant zinc metabolism is implicated in human diseases. The gastrointestinal tract of animals is a critical site of zinc metabolism that is responsible for dietary zinc uptake and distribution to the body. However, the role of the gastrointestinal tract in zinc excretion remains unclear. Zinc transporters are key regulators of zinc metabolism that mediate the movement of zinc ions across membranes. Here, we identified a comprehensive list of 14 predicted Cation Diffusion Facilitator (CDF) family zinc transporters in Caenorhabditis elegans and demonstrated that zinc is excreted from intestinal cells by one of these CDF proteins, TTM-1B. The ttm-1 locus encodes two transcripts, ttm-1a and ttm-1b, that use different transcription start sites. ttm-1b expression was induced by high levels of zinc specifically in intestinal cells, whereas ttm-1a was not induced by zinc. TTM-1B was localized to the apical plasma membrane of intestinal cells, and analyses of loss-of-function mutant animals indicated that TTM-1B promotes zinc excretion into the intestinal lumen. Zinc excretion mediated by TTM-1B contributes to zinc detoxification. These observations indicate that ttm-1 is a component of a negative feedback circuit, since high levels of cytoplasmic zinc increase ttm-1b transcript levels and TTM-1B protein functions to reduce the level of cytoplasmic zinc. We showed that TTM-1 isoforms function in tandem with CDF-2, which is also induced by high levels of cytoplasmic zinc and reduces cytoplasmic zinc levels by sequestering zinc in lysosome-related organelles. These findings define a parallel negative feedback circuit that promotes zinc homeostasis and advance the understanding of the physiological roles of the gastrointestinal tract in zinc metabolism in animals.
At the organismal level, the gastrointestinal tract is the major site of zinc metabolism that mediates dietary zinc uptake and distribution to the body [18], [19]. In humans, dietary zinc is absorbed into enterocytes across the apical plasma membrane by the action of ZIP4 [13]. Loss-of-function mutations of ZIP4 cause the recessive genetic disease acrodermatitis enteropathica, which is characterized by symptoms of zinc deficiency [8]. ZIP4 expression is highly responsive to dietary zinc levels, which regulates zinc influx into enterocytes [20]. Zinc absorbed in enterocytes is transported by ZnT1 across the basolateral plasma membrane to allow distribution to other tissues [21]. ZnT1 expression is also responsive to dietary zinc levels and induced in high zinc conditions [21], [22]. ZnT1 is essential for viability, since ZnT1-deficient mice display embryonic lethality [23]. Zinc excretion is not as well characterized as zinc absorption. Zinc is excreted in the feces, and a major source of fecal zinc is pancreatic and biliary secretion of zinc containing enzymes [18]. However, the primary role of these enzymes is likely to be digestion rather than zinc homeostasis. The role of enterocytes in zinc excretion via zinc transporters is only beginning to emerge. The ZnT5 variant B is localized to the apical membrane of enterocytes and is reported to function in both zinc efflux and influx [24], [25]. Additional zinc transporters are localized to intracellular compartments in enterocytes. For example, ZnT5A, ZnT6, ZnT7 and ZIP7 are localized to the Golgi complex, and ZnT2 and ZnT4 are localized to endosomal or lysosomal vesicles [19]. These proteins might be involved in zinc excretion through the secretory pathway, although in vivo evidence for this function has not been well established. 2ff7e9595c
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