Mitogen Stimulation of Lymphocytes in Pigs with Hereditary Vitamin C Deficiency

Recently an inherited vitamin G deficiency in the pigs presumably based on an autosomal recessive gene was decribed* Homozygotes are in contrast to heterozygotes and normal pigs unable to synthesize ascorbic acid. In an experiment comprising 3 littermate pigs, 2 homozygous and 1 heterozygous for the vitamin C deficiency gene, the influence of ascorbic acid depletion, and repletion on mitogen stimulation of peripheral blood lymphocytes was studied. Ascorbic acid depletion of the vitamin C dependent pigs resulted in a rapid decline in plasma ascorbic acid. Response of lymphocytes to stimular tion with Concanavalin A (Con A) and phytohemagglutinin M (PHA) decreased more slowly reaching a minimum, which coincidedi with the occurrence of the first clinical symptoms of scurvy. Following resupplementation with vitamin C the plasma content of ascorbic acid rapidly returned to normal, while the lymphocyte response to Con A and PHA stimulation only gradually approached the initial values. The repletion with ascorbic acid caused a transitory increase in the response to pokeweed mitogen (PWM) stimulation. The significance of these findings in relation to the cellular immune system in normal pigs is discussed.     

Consequences of dietary calcium and phosphorus depletion and repletion feeding sequences on growth performance and body composition of growing pigs

The effect of a calcium (Ca) and phosphorus (P) depletion and repletion strategy was studied in four consecutive feeding phases of 28 days each. In all, 60 castrated male pigs (14±1.6 kg initial BW) received 60% (low (L) diet; depletion) or 100% (control (C) diet; repletion) of their Ca and digestible P requirements according to six feeding sequences (CCCC, CCCL, CLCC, CCLC, LCLC and LLLL; subsequent letters indicate the diet received in phases 1, 2, 3 and 4, respectively). Pigs bone mineral content in whole-body (BMCb) and lumbar vertebrae L2 to L4 (BMCv) was measured in every feeding phase by dual-energy X-ray absorptiometry. Growth performance was slightly (<10%) affected by depletion, however, dietary treatments did not affect overall growth. Compared with control pigs, depletion reduced BMCb (34%, 38%, 33% and 22%) and BMCv (46%, 54%, 38% and 26%) in phases 1 to 4, respectively. Depletion increased however digestible P retention efficiency from the second to the fourth phases allowing LLLL pigs to present no differences in BMCb and BMCv gain compared with CCCC pigs in phase 4. Growth performance in repleted compared with control pigs was lower in phase 2, was no different in phase 3 and was lower in CLCC pigs in phase 4. Repletion increased body P and Ca retention efficiency when compared with control pigs (respectively, 8% and 10% for LC v. CC, P<0.01; 8% and 10% for CLC v. CCC, P<0.10; 18% and 25% for CLCC, CCLC, LCLC v. CCCC, P<0.001). Moreover, BMCv gain was higher in CLC pigs (P<0.001) and gains of body P, Ca, BMCb and BMCv in phase 4 were also higher in repleted than in CCCC pigs (respectively, 14%, 20%, 20% and 52%; P⩽0.02). Repletion reduced body P, Ca, BMCb and BMCv masses in phase 2 but no differences were found in phase 4 compared with control pigs. Lumbar vertebrae L2 to L4 bone mineral content was more sensitive to depletion and repletion sequences than BMCb especially in the first phase probably due to a higher proportion of metabolically active trabecular bone in vertebrae than in the whole skeleton. Dietary Ca was, however, oversupply in L compared with C diets (3.1 v. 2.5 Ca:digestible P ratio, respectively) suggesting that P has probably driven the regulations. Phosphorus and Ca depletion and repletion increases dietary P utilization efficiency and can help to reduce dietary P supply, but the underlying mechanisms need elucidation before its practical application.     

Elevated bone collagenolytic activity and hyperplasia of parafollicular light cells of the thyroid gland in parathormone-treated grey-lethal mice

Summary By application of light and electron microscopy, histochemistry, tracer procedures and a collagenolytic assay procedure, it was established that the osteolytic response of grey-lethal mice to acute parathormone (PTH) therapy was decidedly more vigorous than that elicited from their normal littermates.Time and calcium dependency studies conducted on a cell-free extract obtained from PTH-treated grey-lethal mouse bone indicated that the collagenolytic factor present in the preparation was collagenase.The osteoclasts seen in osteopetrotic mouse bone eighteen hours after PTH injection were characteristically intensely basophilic and possessed secretory inclusions apparently derived from their nuclei. Karyorrhexis was of common occurrence in these cells.Histologic evidence indicated that osteocytes promote resorption of bone matrix in anticipation of becoming fused into osteoclasts.A large proportion of the epithelial cells in the thyroid glands of the PTH-treated grey-lethal mice was identified as parafollicular, light cells.Osteopetrosis may be considered a congenital endocrinopathy, the primary lesion of which is hyperplasia of the calcitonin-producing parafollicular cells of the thyroid gland.Aided by a grant from The National Foundation.     

Difference between the thyroid gland of normal and hypomyelinated jimpy mice--a light microscopic study

A light microscopic quantitative analysis was performed on normal and jimpy male mice for studying the difference between the structures of the thyroid glands of the two animals. The results of this analysis showed that the thyroid gland of the normal mice consisted of numerous homogenous round follicles with cuboidal follicular cells, separated by thin interlobular and interfollicular connective tissue and a few adipose tissue. The thyroid gland of jimpy mice consisted of a few, small follicles surrounded by columnar follicular cells and intraepithelial capillaries, separated by thick connective tissue and abundant adipose tissue. The number of thyroid follicles are significantly less in the jimpy mice than in the normal mice. Another striking difference is that almost every follicular cell surrounding the follicular lumen of jimpy mice is accompanied by an intraepithelial capillary. In addition, the ratio of the number of intraepithelial capillaries to the number of the thyroid follicular cells are significantly higher in the jimpy mice than in the normal mice. The S-follicles or ultimobranchial cysts of the thyroid gland are well developed in the jimpy mice. The parafollicular cells are normal in appearance. Morphological evidence suggested that the thyroid follicular cells of the jimpy mice are very active in the transport, synthesis and release of thyroglobulin, and secretion of thyroid hormones. But owing to the significantly decreased number of thyroid follicles, the inadequate secretion of the thyroid hormones result in the hypothyroidism and the hypomyelination of the jimpy mice.     

Lymphocyte propionyl-CoA carboxylase and accumulation of odd-chain fatty acid in plasma and erythrocytes are useful indicators of marginal biotin deficiency small star,filled

BACKGROUND: Recent studies indicate marginal biotin deficiency is more common than previously thought. That conclusion's validity rests on two indicators of biotin status that depend on renal function.OBJECTIVE: Assessing the validity of two indicators of biotin status that do not depend upon renal function: 1) activity of the biotin-dependent enzyme propionyl-CoA carboxylase (PCC) in lymphocytes and 2) accumulation of odd-chain fatty acids in the lipids of plasma and erythrocytes.DESIGN: Marginal biotin deficiency was induced in 11 healthy adults by egg-white feeding for 28 days. Blood and 24-h urine samples were collected before commencing the diet and twice weekly thereafter. After depletion, biotin status was restored with a general diet with or without 80 &mgr;g/day or 328 nmol/day biotin supplement. Activity of PCC was determined by an optimized NaH 14CO(3) incorporation assay. Fatty acid composition was determined by gas chromatography.RESULTS: With time on the egg-white diet, lymphocyte PCC activity decreased significantly (P <0.0001); C15:0 and C17:0 content increased significantly in the lipids of plasma and erythrocytes (P <0.015). In eight of 11 subjects, lymphocyte PCC activity returned to normal within three weeks of resuming general diets with or without biotin supplement. With repletion, C15:0 and C17:0 in plasma lipids decreased (P <0.02), but odd-chain content of erythrocytes did not decrease significantly.CONCLUSIONS: Lymphocyte PCC activity is an early and sensitive indicator of marginal biotin deficiency. Odd-chain fatty acids accumulate in blood lipids more gradually during marginal deficiency and return to normal more gradually after biotin repletion.     

Zinc-deficient rats have more limited bone recovery during repletion than diet-restricted rats

The objective of this study was to investigate the effects of dietary zinc deficiency and diet restriction on bone development in growing rats, and to determine whether any adverse effects could be reversed by dietary repletion. Weanling rats were fed either a zinc-deficient diet ad libitum (ZD; <1 mg zinc/kg) or nutritionally complete diet (30 mg zinc/kg) either ad libitum (CTL) or pair-fed to the intake of the ZD group (DR; diet-restricted) for 3 weeks (deficiency phase) and then all groups were fed the zinc-adequate diet ad libitum for 3, 7, or 23 days (repletion phase). Excised femurs were analyzed for bone mineral density (BMD) using dual-energy x-ray absorptiometry, and plasma was analyzed for markers of bone formation (osteocalcin) and resorption (Ratlaps). After the deficiency phase, ZD had lower body weight and reduced femur BMD, zinc, and phosphorus concentrations compared with DR; and these parameters were lower in DR compared with CTL. Femur calcium concentrations were unchanged among the groups. Reduced plasma osteocalcin in ZD and elevated plasma Ratlaps in DR suggested that zinc deficiency limits bone formation while diet restriction accelerates bone resorption activity. After 23 days of repletion, femur size, BMD, and zinc concentrations remained lower in ZD compared with DR and CTL. Body weight and femur phosphorus concentrations remained lower in both ZD and DR compared with CTL after repletion. There were no differences in plasma osteocalcin concentrations after the repletion phase, but the plasma Ratlaps concentrations remained elevated in DR compared with CTL. In summary, both ZD and DR lead to osteopenia during rapid growth, but the mechanisms appear to be due to reduced modeling in ZD and higher turnover in DR. Zinc deficiency was associated with a greater impairment in bone development than diet restriction, and both deficiencies limited bone recovery during repletion in growing rats.     

“Calcium receptors” on eukaryotic cells with special reference to the osteoclast

There is a growing list of cells that are capable of detecting and responding to changes in the concentration of extracellular calcium. The two classic examples of this behaviour are the calcitonin-secreting parafollicular cells of the thyroid and parathyroid hormone-secreting chief cells of the parathyroid gland. A more recent addition to this list is the renin-secreting juxtaglomerular cell of the kidney. Particularly intriguing has been independently the discovery by two laboratories, that the resorptive cell of bone, the osteoclast, is capable of detecting changes in ambient calcium. A common theme amongst all these so called calcium-responsive cells is that extracellular calcium increases elevate intracellular calcium levels, and this intracellular signal is either stimulatory or inhibitory to the functional response. But how these cells detect changes in the concentration of extracellular calcium, and how these recognition events are subsequently transformed into intracellular signals that regulate cell function are somewhat less clear. The commentary reveals some recent developments that seemingly provide insights into these mechanisms, with special reference to the osteoclast.     

Single cellular origin of somatostatin and calcitonin in the rat thyroid gland

Summary Immunostaining of thin serial paraffin sections has shown that somatostatin is present in the same parafollicular cells as calcitonin in the adult rat thyroid gland. The number of cells containing both peptides is much smaller than the number containing calcitonin but not somatostatin.     

Response of blood serum constituents to production of and recovery from a kwashiorkor-like syndrome in the young pig.

Twenty-six 3-week-old genetically obese pigs were fed in two experiments to determine the serum chemistry profile during severe protein malnutrition and repletion. Severe protein deficiency was produced in pigs fed the high-fat, low-protein diet (growth failure, rough hair, low serum total protein and albumin). In Experiment 1, blood was sampled from the anterior vena cava of each pig five times during depletion and three times during repletion to determine serum total cholesterol, high density lipoprotein (HDL)-cholesterol, triglycerides, total protein, albumin, glucose, Ca, inorganic P, Mg, Na, K, Cl, total bilirubin, urea N, creatinine, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyltransferase. In Experiment 2, blood was sampled weekly for 8 weeks for serum total cholesterol, HDL-cholesterol, triglycerides, albumin, glucose, Ca, P, Mg and alkaline phosphatase. HDL-cholesterol was increased (P less than 0.01) and albumin was decreased (P less than 0.01) in protein-deficient pigs in both experiments. Creatinine, total bilirubin, gamma-glutamyltransferase, alanine aminotransferase, and aspartate aminotransferase were elevated in protein-deficient pigs compared with controls after 7 weeks of depletion. Inorganic P (P less than 0.01), Ca (P less than 0.01), and Mg (P less than 0.05) concentrations were depressed in protein-depleted pigs compared with controls in both experiments. After 8 weeks of repletion in Experiment 1, all elements except inorganic P were similar in the two groups. Short-term, severe, protein malnutrition affected lipid, electrolyte, and structural mineral metabolism and indices of liver function in the absence of parasites, diarrhea, and infection. The effects were reversed after 8 weeks of repletion. We conclude that the elevated serum cholesterol in protein deficiency is related primarily to an increase in the HDL fraction.     

Lymphocyte propionyl-CoA carboxylase and accumulation of odd-chain fatty acid in plasma and erythrocytes are useful indicators of marginal biotin deficiency☆

Background: Recent studies indicate marginal biotin deficiency is more common than previously thought. That conclusion’s validity rests on two indicators of biotin status that depend on renal function.Objective: Assessing the validity of two indicators of biotin status that do not depend upon renal function: 1) activity of the biotin-dependent enzyme propionyl-CoA carboxylase (PCC) in lymphocytes and 2) accumulation of odd-chain fatty acids in the lipids of plasma and erythrocytes.Design: Marginal biotin deficiency was induced in 11 healthy adults by egg-white feeding for 28 days. Blood and 24-h urine samples were collected before commencing the diet and twice weekly thereafter. After depletion, biotin status was restored with a general diet with or without 80 μg/day or 328 nmol/day biotin supplement. Activity of PCC was determined by an optimized NaH ¹⁴CO₃ incorporation assay. Fatty acid composition was determined by gas chromatography.Results: With time on the egg-white diet, lymphocyte PCC activity decreased significantly (P <0.0001); C15:0 and C17:0 content increased significantly in the lipids of plasma and erythrocytes (P <0.015). In eight of 11 subjects, lymphocyte PCC activity returned to normal within three weeks of resuming general diets with or without biotin supplement. With repletion, C15:0 and C17:0 in plasma lipids decreased (P <0.02), but odd-chain content of erythrocytes did not decrease significantly.Conclusions: Lymphocyte PCC activity is an early and sensitive indicator of marginal biotin deficiency. Odd-chain fatty acids accumulate in blood lipids more gradually during marginal deficiency and return to normal more gradually after biotin repletion.     

Osteocyte-Derived Insulin-Like Growth Factor I Is Not Essential for the Bone Repletion Response in Mice

The present study sought to evaluate the functional role of osteocyte-derived IGF-I in the bone repletion process by determining whether deficient expression of Igf1 in osteocytes would impair the bone repletion response to one week of dietary calcium repletion after two weeks of dietary calcium deprivation. As expected, the two-week dietary calcium depletion led to hypocalcemia, secondary hyperparathyroidism, and increases in bone resorption and bone loss in both Igf1 osteocyte conditional knockout (cKO) mutants and WT control mice. Thus, conditional disruption of Igf1 in osteocytes did not impair the calcium depletion-induced bone resorption. After one week of calcium repletion, both cKO mutants and WT littermates showed an increase in endosteal bone formation attended by the reduction in osteoclast number, indicating that deficient Igf1 expression in osteocytes also did not have deleterious effects on the bone repletion response. The lack of an effect of deficient osteocyte-derived IGF-I expression on bone repletion is unexpected since previous studies show that these Igf1 osteocyte cKO mice exhibited impaired developmental growth and displayed complete resistance to bone anabolic effects of loading. These studies suggest that there is a dichotomy between the mechanisms necessary for anabolic responses to mechanical loading and the regulatory hormonal and anabolic skeletal repletion following low dietary calcium challenge. In conclusion, to our knowledge this study has demonstrated for the first time that osteocyte-derived IGF-I, which is essential for anabolic bone response to mechanical loading, is not a key regulatory factor for bone repletion after a low calcium challenge.     

Kinetics of tissue RRR-alpha-tocopherol depletion and repletion. Effect of cold exposure

Vitamin E was estimated in plasma and tissues of rats kept for three months on a low vitamin E diet or a high vitamin E diet. Some of the animals from each group were switched to the opposite diet, and the kinetics of uptake and depletion of vitamin E were followed 3, 8, and 15 days after the diet change. Some rats were also submitted to cold exposure (6 degrees C) for three days. During repletion plasma, red blood cells, liver, spleen, and adrenal gland were the only tissues that responded rapidly to the diet change; after three days, their vitamin E levels corresponded to that of the new diet. Heart, brain, lung, muscle, and thymus were slow in reacting to diet change. Fifteen days after the change in diet, white adipose tissue did not respond. The rate of repletion for all tissues was more rapid than the rate of depletion, but liver was the only tissue that after three days had vitamin E levels corresponding to the low-vitamin diet. Cold exposure for three days did not produce any significant change in the vitamin E content of any tissue, indicating that despite high oxygen consumption by the animal, vitamin E was not consumed or mobilized.     

Effect of a low calcium diet on the ultrastructure of the parathyroid gland of chicks

Summary The effect of a low calcium diet on the ultrastructure of the parathyroid gland in the chick was examined. Two-week-old White Leghorn chicks were fed a low calcium diet (calcium content 0.63%) for two weeks. In these chicks, the parathyroid glands are grossly enlarged. Hypertrophy and hyperplasia of the chief cells are evident. The plasma membranes between adjacent cells are relatively straight but interdigitate in some places. Chief cells contain occasional membrane-limited secretory granules (150–350 m in diameter) and with contents of variable electron density. Secretory granules are distributed randomly but some are closely applied to the plasma membrane. There is an increase in the development of the rough-surfaced endoplasmic reticulum. The Golgi complex is enlarged and consists of cisternae arranged in concentric layers, smooth-surfaced and coated vesicles and condensing vacuoles. Dilatations of the cisternae at several points are observed. Mitochondria and filaments are also encountered. These morphological features suggest that low calcium intake stimulates the synthetic activity of the chief cells of the chick parathyroid.     

The parathyroid gland of the woodchuck (Marmota monax): a study of seasonal variations in the chief cells

The ultrastructure of the parathyroid chief cell in the woodchuck, Marmota monax, was studied during the four seasons of the year. Spring chief cells have stacks of granular endoplasmic reticulum, prominent multiple Golgi zones and many clumped mitochondria. Summer cells resemble those seen in the spring but the mitochondria are associated with stacks of granular endoplasmic reticulum. Multiple areas of stacked granular endoplasmic reticulum characterize the fall chief cells. Their Golgi zones are large and are associated with many dense core secretory granules. Lipoid vacuoles are frequently noted. Winter chief cells have secretory granules and phagolysosomes (dense bodies). Some of these cells contain stacked arrays of granular endoplasmic reticulum associated with mitochondria, others have only short segments. The above morphological findings are discussed in relation to those in other hibernators, the parafollicular (C) cell, and to the cyclic seasonal activities of the woodchuck.     

Impairments in pyridoxine-dependent sulphur amino acid metabolism are highly sensitive to the degree of vitamin B6 deficiency and repletion in the pig

The objectives of the current study included the characterization of the temporal changes in indices of sulphur amino acid metabolism in piglets in response to vitamin B6 deficiency and repletion with graded levels of pyridoxine hydrochloride. In Experiment 1, 12 piglets (average initial weight = 5.3 kg; n = 6 per group) were fed a semi-purified diet containing either 0 (deficiency group) or 3 mg (control group) pyridoxine·HCl/kg diet, using a pair-feeding design, for 6 weeks. Piglets consuming vitamin B6-deficient diets exhibited decreased average daily gains on the 4th week and feed conversion efficiency from the 4th week until the end of the trial (P < 0.05). Plasma pyridoxal-5'-phosphate (PLP), in pigs consuming vitamin B6-deficient diets, was significantly lower than controls throughout the experiment (P < 0.01), reaching a nadir of 14% of the control animals' value by the end of the trial. Indices of sulphur amino acid metabolism, including activities of hepatic cystathionine-β-synthase (CBS), cystathionine-γ-lyase (CGL) and serine hydroxymethyltransferase, as well as hepatic-free cysteine concentrations were markedly decreased after 6 weeks of B6 deficiency (P < 0.05). Total hepatic mRNA expressions for CBS and CGL were not affected. Concurrently, hepatic-free homocysteine concentrations increased by more than eight-fold (P < 0.01) at the end of the trial. An examination of plasma total homocysteine and cysteine concentrations revealed significant (P < 0.05) differences between treatments, with evidence of an abrupt shift in concentrations at 3 weeks post-initiation of dietary treatments (>25-fold increase in homocysteine; halving of cysteine values). At the end of Experiment 1, vitamin B6 deficiency significantly increased plasma methionine and serine levels, but decreased plasma glycine concentrations (P < 0.05). In Experiment 2, 20 pigs of 14 days old (initial BW = 5.0 kg) were subjected to a 4-week vitamin B6 depletion protocol, based on results obtained in Experiment 1. After the depletion period and assessment of baseline status (four pigs), remaining pigs were allocated to one of four dietary vitamin B6 repletion treatments: 0.75, 1.5, 2.25 and 3 mg/kg diet as pyridoxine·HCl (n = 4 per level) for 14 days. Significant dose-dependent increases in plasma PLP and cysteine, and decreases in homocysteine were observed, and these were sensitive to the duration of repletion. In conclusion, data from the current studies support the use of both plasma PLP and homocysteine as sensitive indices of vitamin B6 status in the pig. Additionally, the observed patterns of responses in vitamin B6-sensitive metabolites are supportive of an inclusion level of 2.25 mg/kg diet, as pyridoxine·HCl, in diets for young pigs.     

Origin of cholinesterase-containing follicle cells and parafollicular cells of the developing thyroid gland in the rat

Summary The location of cholinesterase-containing cells in the thyroid gland and its precursors (median thyroid primordium and ultimobranchial bodies) has been investigated light-microscopically in rat embryos from the 13 to the 20th day of gestation.From the 13th to the 16th day of gestation the median thyroid primordium and the ultimobranchial bodies are distinct from each other. Cholinesterase-containing cells are found in both. On the 17th–18th day of gestation the reacting ultimobranchial cells spread into the median thyroid primordium where they take up a parafollicular position. At the 19th–20th day of gestation the distribution of cholinesterase-containing cells is as in the adult rat. The results seem to show that cholinesterase-containing follicular cells derive from the median thyroid primordium and cholinesterase-containing parafollicular cells from the ultimobranchial body.     

Fine structure of the fetal rat thyroid and parathyroid glands at term and during prolonged gestation

Summary The fine structure of the fetal rat thyroid and parathyroid glands was studied at term and during prolonged gestation, which was induced by subcutaneous injections of progesterone to the mothers from gestational days 20 through 24. At term, the follicular and parafollicular cells of the thyroid as well as cells of the parathyroid exhibited well developed cytoplasmic organelles. Morphological changes were not detected in either of the endocrine glands during prolonged gestation. The results are discussed in relationship to 1) thyroid follicular cell activity during stress and 2) the function of thyroid parafollicular and parathyroid cells in calcium homeostasis.Supported by the Medical Research Council of Canada Grant No. MA4740.     

Maternal Vitamin C Deficiency during Pregnancy Persistently Impairs Hippocampal Neurogenesis in Offspring of Guinea Pigs

While having the highest vitamin C (VitC) concentrations in the body, specific functions of VitC in the brain have only recently been acknowledged. We have shown that postnatal VitC deficiency in guinea pigs causes impairment of hippocampal memory function and leads to 30% less neurons. This study investigates how prenatal VitC deficiency affects postnatal hippocampal development and if any such effect can be reversed by postnatal VitC repletion. Eighty pregnant Dunkin Hartley guinea pig dams were randomized into weight stratified groups receiving High (900 mg) or Low (100 mg) VitC per kg diet. Newborn pups (n = 157) were randomized into a total of four postnatal feeding regimens: High/High (Control); High/Low (Depleted), Low/Low (Deficient); and Low/High (Repleted). Proliferation and migration of newborn cells in the dentate gyrus was assessed by BrdU labeling and hippocampal volumes were determined by stereology. Prenatal VitC deficiency resulted in a significant reduction in postnatal hippocampal volume (P<0.001) which was not reversed by postnatal repletion. There was no difference in postnatal cellular proliferation and survival rates in the hippocampus between dietary groups, however, migration of newborn cells into the granular layer of the hippocampus dentate gyrus was significantly reduced in prenatally deficient animals (P<0.01). We conclude that a prenatal VitC deficiency in guinea pigs leads to persistent impairment of postnatal hippocampal development which is not alleviated by postnatal repletion. Our findings place attention on a yet unrecognized consequence of marginal VitC deficiency during pregnancy.     

Concomitant depletion of dopamine and secretory granules from cells in the ultimobranchial gland of vitamin D2-treated chicken

Summary The ultimobranchial gland (UBG) is a rich source of the polypeptide hormone calcitonin, which is present in a cell system analogous to the mammalian parafollicular cells (C cells) of the thyroid gland. Both types of cells are argyrophilic and, ultrastructurally, they are furnished with numerous electron-dense granules considered to contain the hormone. In the chicken, the main cells of the UBG contain large amounts of dopamine. The possible functional relationship between this amine and the hormone has been studied by a combination of fluorescence and electron microscopy of the UBG from chickens treated with vitamin D₂. This stimulus produced a depletion of dopamine and a pronounced degranulation of the UBG cells, concomitant with a loss in their argyrophilia. Administration of l-3,4-dihydroxyphenylalanine (l-DOPA) to vitamin D₂-treated animals was followed by a reappearance of dopamine in the cytoplasm of the UBG cells, whereas electron-dense granules or argyrophilia were not restored. It is suggested that this concomitant depletion of dopamine and the secretory granules from the UBG cells reflects a participation of the amine in the secretion of the polypeptide hormone.