Przyswajanie biotyny i cynku - jak zwiększyć?
Olga - 18-07-07 21:21
Przyswajanie biotyny i cynku - jak zwiększyć?
Szukam dla mnie niezwykle ważnej informacji, a mianowicie - co wpływa na przyswajanie cynku i biotyny. Nie możemy nigdzie znaleźć z weterynarzem sposobu, jak wpłynąć na to, aby organizm zaczął przyswajać cynk i biotynę a nie wydalał te związki bez wiązania. Będę wdzięczna za informacje na ten temat.
bura4 - 20-07-07 19:00
Cytat:
Napisane przez Olga Szukam dla mnie niezwykle ważnej informacji, a mianowicie - co wpływa na przyswajanie cynku i biotyny. Nie możemy nigdzie znaleźć z weterynarzem sposobu, jak wpłynąć na to, aby organizm zaczął przyswajać cynk i biotynę a nie wydalał te związki bez wiązania. Będę wdzięczna za informacje na ten temat. Przyswajanie cynku blokuje duża ilość wapnia w diecie i magnezu. Poszukam coś więcej...
DRUGS
Antibiotics: Antibiotic use may decrease the biotin contribution to the body made by the microflora of the large intestine.
Anticonvulsants (carbamazepine, phenytoin, phenobarbital, primidone): Carbamazepine, phenytoin and phenobarbital can accelerate biotin metabolism and may cause reduced biotin status. Long-term use of carbamazepine, phenytoin, phenobarbital and primidone has been associated with reduced plasma concentrations of biotin.
NUTRITIONAL SUPPLEMENTS
Pantothenic Acid: High-doses of pantothenic acid may inhibit the absorption of biotin produced by the microflora in the large intestine. Pantothenic acid and biotin appear to use the same uptake carrier in colonocytes.
http://jn.nutrition.org/cgi/content/full/128/12/2783S
Absolute dietary deficiencies of zinc are considered rare in dogs and have not been reported in cats. However, a relative deficiency may occur in some dogs when the availability of dietary zinc is reduced through nutrient interactions or cases in which intestinal absorption of zinc is impaired as a result of disease or genetic factors. A defect in zinc metabolism has been implicated in lethal acrodermatitis of English bull terriers, which gives rise to severe systemic as well as cutaneous signs that resemble experimental zinc deficiency. This disease is inherited as an autosomal recessive trait, is unresponsive to zinc supplementation and is usually fatal, with an average survival time of 7 mo for affected puppies (Jezyk et al. 1986).
Absorption of zinc can be inhibited by excessive levels of dietary calcium, iron and copper, which compete with zinc for intestinal absorption sites. Dietary phytate, which is found in cereal-based diets, chelates zinc, and high levels may also hinder intestinal zinc absorption. Historically, most cases of zinc-responsive dermatosis in dogs were associated with the feeding of poor quality, cereal-or soy-based dry foods, whose effects may have been exacerbated in some animals with a simultaneous inherent defect of zinc absorption. Prolonged enteritis or other malabsorption syndromes may also prevent normal zinc absorption and may precipitate clinical signs of deficiency, particularly when combined with other predisposing factors.
Clinically, two zinc-responsive dermatologic syndromes are recognized, although there is considerable overlap between the two. Syndrome I is associated with defective intestinal absorption of zinc and occurs predominantly in Alaskan malamutes and Siberian huskies, although other breeds may also be affected. A genetic disorder of decreased capacity for zinc absorption has been identified in Alaskan malamutes. In some Siberian huskies, hypothyroidism and low serum zinc may occur concurrently, although the significance of this is not clear (Kunkle 1980, Scott et al. 1995). The appearance of lesions frequently coincides with the onset of adulthood and during periods of stress; it may be linked to higher metabolic requirements in these dogs. Although dietary interactions may limit zinc absorption in some affected animals, the condition occurs in many cases despite feeding a nutritionally complete and balanced diet. Oral zinc supplementation, together with dietary correction, where appropriate, brings rapid resolution of signs in most cases. Supplementation with zinc sulfate [10 mg/(kg · d)] or zinc methionate [1.7 mg/(kg · d)] is usually adequate, but lifelong therapy is normally required, and the dosage may be adjusted for long-term maintenance (Scott et al. 1995). Some cases, especially Siberian huskies, do not respond to oral supplementation and may require the intravenous administration of zinc sulfate (10-15 mg/kg) at weekly intervals for 4 wk, followed by maintenance injections every 1-6 mo to prevent a relapse.
Syndrome II is usually seen in rapidly growing puppies, particularly of the giant breeds, and may correspond with a high metabolic requirement for zinc in affected animals. The condition occurs when the diet is absolutely or relatively deficient in zinc, and is most likely to be seen when the diet is high in phytate or is oversupplemented with calcium. Lesions resolve within 2-6 wk after dietary correction, but the response time can be hastened by oral supplementation with zinc. In these cases, supplementation may be discontinued once the clinical signs are in remission.
http://www.lincolnbiotech.com/p0000047.htm
"Process of zinc absorption"
Absorption and clearance of zinc from the plasma occurs quickly after ingestion by way of homeostatic
control. Both extracellular and intracellular factors determine the amount of dietary zinc that reaches
the plasma from the intestinal lumen. Zinc in ionic form does not cross the membranes off mucosal
cells in significant amounts. To cross these lipoid barriers, zinc must first form complexes with
organic molecules known as zinc binding ligands (ZBL).
Amino acids form complexes with zinc and other cations which can cross the mocosal cell membrane
readily. The mucosal cell contains proteins known as metallothioneins, which bind zinc ions.
Intracellular concentrations of these proteins can change rapidly in response to an animal's zinc
status and dietary zinc intake. Increased intracellular concentrations of zinc metallothionein is
in reserve for transport. Zinc metallothioneins provide the mechanism of homeostatic control governing
the amount of zinc that reaches the bloodstream. Absorption of zinc ions from the intestinal lumen into
the mucosal cells is controlled by several factors:
-Solubility of dietary zinc source. Zinc oxide is relatively insoluable in water, and its rates
of dissolution depends on the PH of the contents of the gastrointestinal tract. Zinc sulfate and
zinc chloride are readily soluble in water, and provide ionic zinc; however, they irritate
gastrointestinal membranes.
-Presence of ZBL's, which form complexes with amino acids to be absorbed. The amount of zinc absorbed
depends upon the fraction of zinc ions present as absorbable complexes.
-Presence of chelating agent, which form unabsorbable complexes. Absorption of dietary zinc is
adversely affected by high dietary levels of phytates, calcium, phosphorous and fibre. Also, trace
minerals such as copper and iron in high levels compete for ligands, leaving less ZBL to form complexes
with zinc ions.
"Problems with conventional zinc compounds"
Synthetically chelated zinc products are usually excreted in the urine shortly after ingestion. As
a result, most of the zinc and many other heavy metals are wasted. Zinc chelated with hydrolyzed protein
is bound by more than one amino acid and must be altered by the body before it can be absorbed.
Inorganic compounds such as zinc oxide and zinc sulfate cannot be used by the body as sources of zinc
until complexes have been formed with specific organic compounds in the gastrointestinal tract.
Sometimes these complexing compounds are not present in sufficient concentrations for adequate zinc
absorption. Giving an animal excessive amounts of organic zinc compounds can create an imbalance or
deficiency of other metals like copper or iron.
Tu o huskych ale tez warto poczytac
http://www.siberianhuskyhealthfounda...deficiency.asp
bura4 - 20-07-07 19:12
Poza tym warto zainwestowac w cynk chelatowany, tylko taki pomogl mojej suce na cynkozalezna dermatoze w wieku mlodzienczym...
Olga - 20-07-07 22:58
O dziękuję bardzo :) A czy cynk chelatanowy jest ludzkim czy zwierzęcym suplementem?
Wapnia mamy mało w diecie, musimy coś na cito zaradzić.
mamy problem ze wzrostem puszki kopytowej u kopytnego, szukam rozwiązania jak zmobilizowac ją do jakiegoś wzrostu, chociaz minimalnego bo jest bardzo kiepsko.
bura4 - 20-07-07 23:06
Cytat:
Napisane przez Olga O dziękuję bardzo :) A czy cynk chelatanowy jest ludzkim czy zwierzęcym suplementem?
Wapnia mamy mało w diecie, musimy coś na cito zaradzić.
mamy problem ze wzrostem puszki kopytowej u kopytnego, szukam rozwiązania jak zmobilizowac ją do jakiegoś wzrostu, chociaz minimalnego bo jest bardzo kiepsko. Chelatowany cynk tak to jest zwierzęcy też. Popytaj ludzików z firmy FITMIN oni mieli też koniowe. Ich "psi" preparat uratował mi sukę co się wydrapywała do mięsa.....
wiki1 - 21-07-07 15:00
Jezeli chodzi o preparaty wiem ze skuteczna sa końskie, w suplementach diety cynk jest chaletowany.
wiki1 - 21-07-07 15:03
Na przyswajanie cynku i biotyny maja wpływ:
-pomiędzy cynkiem i miedzią istnieje anatagonizm pomiedzy wchałanianiem i wykorzystaniem
-cynk jest wchałaniany w dwunastnicy z roztworów ok w 60% przy jego deficycie rośnie stopień wchalaniania
-czynnikiem decydującym o wchanianu cynku jest rozpuszczalność związków cynku, podstawowymi inhibitorami wchałaniania cynku sa kwas fitynowy wiąze on cynk i wapn w trudno rozpuszczalne zwiazki nie sa one trawione
-wysoki poziom wapnia w diecie powoduje zmniejszenia wchaniania cynku
-najlepsza dostepność cynku pochodzi z pasz tj maczki zwierzęce i produkty mleczne
- jeżeli8 zostanie przekroczony poziom cynku potzrebnego w organiazmie to powoduj to wzrost stezenia glukozy
Jezeli chodzi o biotyne to wystepuje ona w wiekszej ilości w wątrobie i drożdzach
Synergistycznie działa z biotyna kwas foliowy, wit C, kw pantotenowy zaś antagonostami są awidyna i antybiotyki ktore wit H wiążą
bura4 - 24-07-07 15:12
http://www.horsenutrition.com.au/zinc.html
http://www.petalia.com.au/templates/...?story_no=1656
http://www.ncbi.nlm.nih.gov/sites/en...&dopt=Abstract
http://home.att.net/~horsenutrition101/protein.html
To pare końskich linków...zanotowane.pl doc.pisz.pl pdf.pisz.pl reyes.pev.pl
Olga - 18-07-07 21:21
Przyswajanie biotyny i cynku - jak zwiększyć?
Szukam dla mnie niezwykle ważnej informacji, a mianowicie - co wpływa na przyswajanie cynku i biotyny. Nie możemy nigdzie znaleźć z weterynarzem sposobu, jak wpłynąć na to, aby organizm zaczął przyswajać cynk i biotynę a nie wydalał te związki bez wiązania. Będę wdzięczna za informacje na ten temat.
bura4 - 20-07-07 19:00
Cytat:
Napisane przez Olga Szukam dla mnie niezwykle ważnej informacji, a mianowicie - co wpływa na przyswajanie cynku i biotyny. Nie możemy nigdzie znaleźć z weterynarzem sposobu, jak wpłynąć na to, aby organizm zaczął przyswajać cynk i biotynę a nie wydalał te związki bez wiązania. Będę wdzięczna za informacje na ten temat. Przyswajanie cynku blokuje duża ilość wapnia w diecie i magnezu. Poszukam coś więcej...
DRUGS
Antibiotics: Antibiotic use may decrease the biotin contribution to the body made by the microflora of the large intestine.
Anticonvulsants (carbamazepine, phenytoin, phenobarbital, primidone): Carbamazepine, phenytoin and phenobarbital can accelerate biotin metabolism and may cause reduced biotin status. Long-term use of carbamazepine, phenytoin, phenobarbital and primidone has been associated with reduced plasma concentrations of biotin.
NUTRITIONAL SUPPLEMENTS
Pantothenic Acid: High-doses of pantothenic acid may inhibit the absorption of biotin produced by the microflora in the large intestine. Pantothenic acid and biotin appear to use the same uptake carrier in colonocytes.
http://jn.nutrition.org/cgi/content/full/128/12/2783S
Absolute dietary deficiencies of zinc are considered rare in dogs and have not been reported in cats. However, a relative deficiency may occur in some dogs when the availability of dietary zinc is reduced through nutrient interactions or cases in which intestinal absorption of zinc is impaired as a result of disease or genetic factors. A defect in zinc metabolism has been implicated in lethal acrodermatitis of English bull terriers, which gives rise to severe systemic as well as cutaneous signs that resemble experimental zinc deficiency. This disease is inherited as an autosomal recessive trait, is unresponsive to zinc supplementation and is usually fatal, with an average survival time of 7 mo for affected puppies (Jezyk et al. 1986).
Absorption of zinc can be inhibited by excessive levels of dietary calcium, iron and copper, which compete with zinc for intestinal absorption sites. Dietary phytate, which is found in cereal-based diets, chelates zinc, and high levels may also hinder intestinal zinc absorption. Historically, most cases of zinc-responsive dermatosis in dogs were associated with the feeding of poor quality, cereal-or soy-based dry foods, whose effects may have been exacerbated in some animals with a simultaneous inherent defect of zinc absorption. Prolonged enteritis or other malabsorption syndromes may also prevent normal zinc absorption and may precipitate clinical signs of deficiency, particularly when combined with other predisposing factors.
Clinically, two zinc-responsive dermatologic syndromes are recognized, although there is considerable overlap between the two. Syndrome I is associated with defective intestinal absorption of zinc and occurs predominantly in Alaskan malamutes and Siberian huskies, although other breeds may also be affected. A genetic disorder of decreased capacity for zinc absorption has been identified in Alaskan malamutes. In some Siberian huskies, hypothyroidism and low serum zinc may occur concurrently, although the significance of this is not clear (Kunkle 1980, Scott et al. 1995). The appearance of lesions frequently coincides with the onset of adulthood and during periods of stress; it may be linked to higher metabolic requirements in these dogs. Although dietary interactions may limit zinc absorption in some affected animals, the condition occurs in many cases despite feeding a nutritionally complete and balanced diet. Oral zinc supplementation, together with dietary correction, where appropriate, brings rapid resolution of signs in most cases. Supplementation with zinc sulfate [10 mg/(kg · d)] or zinc methionate [1.7 mg/(kg · d)] is usually adequate, but lifelong therapy is normally required, and the dosage may be adjusted for long-term maintenance (Scott et al. 1995). Some cases, especially Siberian huskies, do not respond to oral supplementation and may require the intravenous administration of zinc sulfate (10-15 mg/kg) at weekly intervals for 4 wk, followed by maintenance injections every 1-6 mo to prevent a relapse.
Syndrome II is usually seen in rapidly growing puppies, particularly of the giant breeds, and may correspond with a high metabolic requirement for zinc in affected animals. The condition occurs when the diet is absolutely or relatively deficient in zinc, and is most likely to be seen when the diet is high in phytate or is oversupplemented with calcium. Lesions resolve within 2-6 wk after dietary correction, but the response time can be hastened by oral supplementation with zinc. In these cases, supplementation may be discontinued once the clinical signs are in remission.
http://www.lincolnbiotech.com/p0000047.htm
"Process of zinc absorption"
Absorption and clearance of zinc from the plasma occurs quickly after ingestion by way of homeostatic
control. Both extracellular and intracellular factors determine the amount of dietary zinc that reaches
the plasma from the intestinal lumen. Zinc in ionic form does not cross the membranes off mucosal
cells in significant amounts. To cross these lipoid barriers, zinc must first form complexes with
organic molecules known as zinc binding ligands (ZBL).
Amino acids form complexes with zinc and other cations which can cross the mocosal cell membrane
readily. The mucosal cell contains proteins known as metallothioneins, which bind zinc ions.
Intracellular concentrations of these proteins can change rapidly in response to an animal's zinc
status and dietary zinc intake. Increased intracellular concentrations of zinc metallothionein is
in reserve for transport. Zinc metallothioneins provide the mechanism of homeostatic control governing
the amount of zinc that reaches the bloodstream. Absorption of zinc ions from the intestinal lumen into
the mucosal cells is controlled by several factors:
-Solubility of dietary zinc source. Zinc oxide is relatively insoluable in water, and its rates
of dissolution depends on the PH of the contents of the gastrointestinal tract. Zinc sulfate and
zinc chloride are readily soluble in water, and provide ionic zinc; however, they irritate
gastrointestinal membranes.
-Presence of ZBL's, which form complexes with amino acids to be absorbed. The amount of zinc absorbed
depends upon the fraction of zinc ions present as absorbable complexes.
-Presence of chelating agent, which form unabsorbable complexes. Absorption of dietary zinc is
adversely affected by high dietary levels of phytates, calcium, phosphorous and fibre. Also, trace
minerals such as copper and iron in high levels compete for ligands, leaving less ZBL to form complexes
with zinc ions.
"Problems with conventional zinc compounds"
Synthetically chelated zinc products are usually excreted in the urine shortly after ingestion. As
a result, most of the zinc and many other heavy metals are wasted. Zinc chelated with hydrolyzed protein
is bound by more than one amino acid and must be altered by the body before it can be absorbed.
Inorganic compounds such as zinc oxide and zinc sulfate cannot be used by the body as sources of zinc
until complexes have been formed with specific organic compounds in the gastrointestinal tract.
Sometimes these complexing compounds are not present in sufficient concentrations for adequate zinc
absorption. Giving an animal excessive amounts of organic zinc compounds can create an imbalance or
deficiency of other metals like copper or iron.
Tu o huskych ale tez warto poczytac
http://www.siberianhuskyhealthfounda...deficiency.asp
bura4 - 20-07-07 19:12
Poza tym warto zainwestowac w cynk chelatowany, tylko taki pomogl mojej suce na cynkozalezna dermatoze w wieku mlodzienczym...
Olga - 20-07-07 22:58
O dziękuję bardzo :) A czy cynk chelatanowy jest ludzkim czy zwierzęcym suplementem?
Wapnia mamy mało w diecie, musimy coś na cito zaradzić.
mamy problem ze wzrostem puszki kopytowej u kopytnego, szukam rozwiązania jak zmobilizowac ją do jakiegoś wzrostu, chociaz minimalnego bo jest bardzo kiepsko.
bura4 - 20-07-07 23:06
Cytat:
Napisane przez Olga O dziękuję bardzo :) A czy cynk chelatanowy jest ludzkim czy zwierzęcym suplementem?
Wapnia mamy mało w diecie, musimy coś na cito zaradzić.
mamy problem ze wzrostem puszki kopytowej u kopytnego, szukam rozwiązania jak zmobilizowac ją do jakiegoś wzrostu, chociaz minimalnego bo jest bardzo kiepsko. Chelatowany cynk tak to jest zwierzęcy też. Popytaj ludzików z firmy FITMIN oni mieli też koniowe. Ich "psi" preparat uratował mi sukę co się wydrapywała do mięsa.....
wiki1 - 21-07-07 15:00
Jezeli chodzi o preparaty wiem ze skuteczna sa końskie, w suplementach diety cynk jest chaletowany.
wiki1 - 21-07-07 15:03
Na przyswajanie cynku i biotyny maja wpływ:
-pomiędzy cynkiem i miedzią istnieje anatagonizm pomiedzy wchałanianiem i wykorzystaniem
-cynk jest wchałaniany w dwunastnicy z roztworów ok w 60% przy jego deficycie rośnie stopień wchalaniania
-czynnikiem decydującym o wchanianu cynku jest rozpuszczalność związków cynku, podstawowymi inhibitorami wchałaniania cynku sa kwas fitynowy wiąze on cynk i wapn w trudno rozpuszczalne zwiazki nie sa one trawione
-wysoki poziom wapnia w diecie powoduje zmniejszenia wchaniania cynku
-najlepsza dostepność cynku pochodzi z pasz tj maczki zwierzęce i produkty mleczne
- jeżeli8 zostanie przekroczony poziom cynku potzrebnego w organiazmie to powoduj to wzrost stezenia glukozy
Jezeli chodzi o biotyne to wystepuje ona w wiekszej ilości w wątrobie i drożdzach
Synergistycznie działa z biotyna kwas foliowy, wit C, kw pantotenowy zaś antagonostami są awidyna i antybiotyki ktore wit H wiążą
bura4 - 24-07-07 15:12
http://www.horsenutrition.com.au/zinc.html
http://www.petalia.com.au/templates/...?story_no=1656
http://www.ncbi.nlm.nih.gov/sites/en...&dopt=Abstract
http://home.att.net/~horsenutrition101/protein.html
To pare końskich linków...