Calcium Metabolism In Birds Research Articles

Parathyroid and ultimobranchial glands: Calcium metabolism in birds

Calcium is essential for normal metabolic processes in birds. Several hormonal systems exist to regulate calcium levels. These include calcitonin from the ultimobranchial glands, parathyroid hormone from parathyroid tissue, vitamin D, and the reproductive hormones, especially estrogens. These systems interact closely to keep plasma and tissue calcium levels at a steady state. Calcium disorders may be caused by a number of factors, and can lead to a variety of clinical problems in pet birds. The physiology of calcium metabolism in avian species is discussed along with common disease states arising from derangements in calcium homeostasis.

Effects on PCBs on liver ultrastructure and monooxygenase activities in Japanese quail.

The effect of environmental pollutants such as PCBs and DDT on avian species is well documented. It is proven that chronic high level PCB intoxication perturbs calcium metabolism in birds, affecting eggshell thickness. PCBs have an impact on the liver. which accumulates high levels of toxicants. These induce drug-metabolizing enzyme activities in quail (Coturnix coturnix), herring gull (larus argentatus), and partridge (Prdix perdix). As these enzymes can degrade endogeneous molecules such as steroids, xenobiotics like PCBs can severely hinder birds` reproductive performance. PCBs induce damage such as regression of the testes, decreased sperm concentration, and altered embryonic development resulting in death or malformation of chicks. More ever, ultrastructural alterations linked with induction of these enzymes have been observed in the livers of PCB-contaminated chickens and ducks. This study examines the effects of Aroclor 1254 on liver morphology and glycogen content in quail, and related morphological modification to liver monoxygenase activities. 26 refs., 6 figs., 1 tab.

Calcium metabolism in birds: computer simulation of response to 1,25-dihydroxycholecalciferol.

A simulation model of calcium metabolism in the chick has been used to evaluate the response of the systems that regulate plasma calcium to a continuous input of 1,25-dihydroxycholecalciferol [1,25(OH)2D3] from the intestine. The results of simulation showed that the concentration of the vitamin D metabolite in the intestine increased during the first 24 h and thereafter decreased slightly due to suppression of endogenous hormone production. Metabolite accumulation was accompanied by an increase in calcium absorption, with a lag period of about 4 h. Most of the increase in absorbed calcium was excreted in the urine, with a lesser change in net bone calcium uptake. Plasma calcium increased with time, in proportion to the intake of the exogenous hormone. The validity of the predicted steady-state plasma calcium levels, and bone and kidney calcium flows, is discussed. The results of the simulation demonstrate the importance of the vitamin D-intestinal axis in regulation of plasma calcium.

Effect of DDT on calcium uptake and vitamin D metabolism in birds.

THE “thin eggshell phenomenon” has been widely found in nature for several species of raptors1 and has been demonstrated for a number of species in laboratory conditions2. Calcium metabolism in birds is closely linked to the reproductive cycle and is, to a large extent, regulated by two steroids, oestradiol and vitamin D. Avian hepatic liver enzymes induced by chlorinated hydrocarbons have been shown to increase the metabolism of sex hormones both in vitro3 and in vivo4. The structure of vitamin D is sufficiently close to that of the sex hormones investigated to suggest that increased vitamin D metabolism might occur and thus calcium uptake from the gastrointestinal tract be affected. Two groups of experiments were carried out: in vivo studies of 45Ca uptake in zebra finches (Poephila guttata) and in vitro studies of vitamin D metabolism by the hepatic microsomal fractions of ringed turtle doves (ring doves; Streptopelia risoria).

Sensitization by oestradiol to the production of experimental nephrocalcinosis.

EARLIER experiments showed that excessive oral administration of mono- or dibasic-phosphates produces nephrocalcinosis in the rat, and that these renal lesions are aggravated by mineralocorticoids, such as deoxycorticosterone1–3. Recent experiments revealed that, under similar experimental conditions, the nephrocalcinosis produced by oral administration of acid sodium phosphate is not aggravated by methyltestosterone, progesterone, corticosterone, Δ1-cortisol acetate, or Δ1-cortisone acetate, but curiously, œstradiol proved to be even more effective in this respect than deoxycorticosterone. It has long been known that folliculoid or ‘œstrogenic’ hormones exert a pronounced effect on calcium metabolism in birds, presumably because in the avian species the production of calcified egg shells is closely related to the action of sex hormones. In mammals, on the other hand, folliculoids do not exert any comparably pronounced effect upon calcium metabolism, and, therefore, the production of intense nephrocalcinosis by œstradiol (when given in combination with phosphates) was made the subject of a special study.