Gland Wet Weight Research Articles

Response of Chick Parathyroid Glands to the Vitamin D Metabolites, 1,25-Dihydroxycholecalciferol and 24,25-Dihydroxycholecalciferol

Under conditions of chronic hypocalcemia, e.g. in vitamin D depletion, the parathyroid glands undergo marked hypertrophy and hyperplasia. Seven days of treatment ( 100 lU/day; 6.5 nmoles ) with cholecalciferol (CC) decreased parathyroid gland weight significantly from vitamin D depleted controls while increasing serum Ca from 6.3 to 8.6 mg/100 ml. 1,25-Dihydroxycholecalciferol (1.3 nmoles/day) also increased serum Ca to 8.6, but had no effect on gland weight. Both CC and 1,25dihydroxycholecalciferol stimulated the production of intestinal calcium binding protein. This same dose of 1,25-dihydroxycholecalciferol in com bination with small amounts of 24R,25-dihydroxycholecalciferol was as effective as CC in reducing parathyroid gland weight, but 24R,25-dihydroxycholecalciferol alone had no effect on gland weight or on calcium binding protein synthesis. When chicks received a twoto four-fold larger dose of 1,25-dihydroxycholecalciferol, parathyroid gland weight was sig nificantly reduced relative to vitamin D depleted controls. A time course of the action of CC indicated that 4 days treatment was sufficient for sig nificant parathyroid gland size reduction. Decreases in gland wet weight caused by CC were paralleled by decreases in dry weight, and loss of DNA and protein. It is concluded that parathyroid gland regression, involving loss of cells, occurs within a few days of treatment with vitamin D metab olites and that gland regression does not obligatorily follow an increase in serum Ca. At low doses, 1,25-dihydroxycholecalciferol requires the presence of 24R,25-dihydroxycholecalciferoI to cause gland regression (but not in testinal calcium binding protein production), whereas it is effective alone at higher doses. These results suggest that the dihy droxy lated vitamin D metabolites may play a role in modulating parathyroid gland as well as intestinal function. J. Nutr. 107: 1918-1926, 1977. INDEXING

Relation between mammary gland development and body weight.

Mammary gland indices including deoxyribonucleic acid, dry fat-free tissue, and wet weight were correlated with body weight in species having a range of 20,000 fold in body weight. Included were mice, hamsters, rats, guinea pigs, rabbits, sheep, and cattle. From limited data accumulated at Missouri, the relation of deoxyribonucleic acid of mammary gland (Y, mg) to bodyweight (X, g) was Y = .53X-79 at the peak of lactation, Y = .29X-82 at the end of pregnancy, and Y = .056X-84 at the beginning of pregnancy. Comparing mammary dry fat-free tissue (mg) to body weight resulted in: Y = 20X-80, Y = 9.7X-85, and Y = 2.6X-91 in the same order while equations for mammary gland wet weight (mg) and body weight were: Y = 135X-82, Y = 123X-79, and Y = 38X-85. The composite value for regression (b) when all data were combined was .80. These mammary indices relate to but are slightly higher than metabolic body weight which is accepted generally as body weight to the three-quarter power.

Isolation of a “proline-rich” protein from rat parotid glands following isoproterenol treatment

Prolonged treatment of rats with isoproterenol induces both hypertrophy and hyperplasia of the parotid glands. Daily injections of 5 mg dl-isoproterenol resulted in a 4–6 fold increase in gland wet weight within 7 days. The protein composition of parotid gland homogenates and saliva, as monitored by disc gel electrophoresis, was markedly altered. In particular, the concentration of a proline-rich protein increased dramatically. This protein was purified by Sephadex G-100 chromatography and preparative disc gel electrophoresis and was found to be comprised mainly of four amino acids (moles/100 moles): Pro, 29.5; Glx, 19.3; Gly, 17.1; Asx, 11.9. The molecular weight as determined by sedimentation equilibrium is about 25,000. When [ 14C] glucosamine was injected intraperitoneally, a small amount of label was incorporated into the proline-rich protein. Upon stopping the isoproterenol treatment, the parotid glands and the polyacrylamide disc gel patterns of the soluble proteins both return to normal within 10 to 14 days.

Time course of active amylase accumulation by rat submaxillary gland during continuous pilocarpine stimulation.

Administration of pilocarpine for varying periods results in a continuous orderly increase in the amylase levels of rat submaxillary glands without prior depletion or accompanying appreciable changes in gland wet weight. This amylase increase with time appears to occur in two phases: the first phase is characterized by a possible brief initial lag followed by a period of logarithmic increase leading to a plateau within 90 minutes. A second phase of rapid rise occurs within 3 hours. The S-shaped curve of the first phase suggests the time course of an autocatalytic process and may indicate a) synthesis, or b) activation of a precursor or bound enzyme form. Sodium oleate, urea, trypsin, n-butanol, heat and ph activate precursors of other enzymes but neither activated nor significantly inhibited amylase of gland homogenates. Atropine in vivo effected complete inhibition of the pilocarpine-induced amylase accumulation. Amylase accumulation under these conditions suggests enzyme synthesis.