Carbohydrate metabolism of heat-acclimated hamsters. 3. Control of liver glucose-6-phosphatase.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to R Chayoth.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Active glycogen metabolism has been demonstrated in both normal and glycogen-rich erythrocytes taken from patients with type III glycogen storage disease. Activity of all enzymes catalyzing the reactions required for the synthesis and degradation of glycogen have been demonstrated in the mature erythrocytes. Uniformly labeled glucose-(14)C is incorporated into glycogen in intact cells of both types during incubation. Replacement of the glucose-(14)C by unlabeled glucose in the medium resulted in a significant loss of radioactivity from cellular glycogen. In the absence of the substrate a progressive shortening of outer branches occurred during incubation of intact glucogen-rich cells. Using cells from patients with type III glycogen storage disease, which have sufficient glycogen content to be analyzed by beta-amylolysis, we demonstrated that the glucosyl units are first incorporated in the outer tiers, then transferred to the core where they tend to accumulate due to the absence of amylo-1,6-glucosidase. The glycogen-rich cells have a more rapid rate of glucose utilization upon incubation which is not reflected by a higher lactate production. The increased rate of glucose utilization did not result from an increased rate of glucose incorporation into glycogen in affected cells. The rate of (14)CO(2) production from glucose-1-(14)C during incubation was not significantly different in the two types of cells unless methylene blue was added as an electron acceptor, in which case the glycogen-rich cells oxidized glucose to CO(2) more rapidly.
Explore the source record for details and available documents.
Adult male rats were injected s.c. once a week for 3 weeks with DBCP, 20 mg/kg BW. Animals were sacrified 20 weeks after last injection. Body and testes weights were recorded and testes were taken for standard histological preparation and for in vitro experiments. The in vitro experiments were carried out on testes slices (90-110 mg) incubated for 3 h with or without the addition of hCG to the incubation medium. Cyclic AMP content of the tissue as well as testosterone released into the incubation medium were determined. Testes weights of DBCP treated animals were 68% lower than that of controls. All semiferous tubules were damaged and shrunken, thus, their number per microscope field was 2.6 times that of controls. Cyclic AMP levels in testes slices were similar in both DBCP treated and controls. The addition of hCG stimulated cyclic AMP accumulation to a much higher level in the DBCP treated than in controls. When calculated per one pair of testes the content in unstimulated pair was more than twice that of DBCP treated. Stimulation of hCG increased both DBCP treated and controls to similar levels. Testosterone release into the medium by slices was higher in DBCP treated than in controls and so was also the increment due to hCG stimulation. Similar results were obtained when testosterone release was calculated per one pair of testes. It is suggested that since the major testicular compartment damaged by DBCP is the tubular one, the proportion of the interstitium per testicular unit weight is larger than in controls, thus, cyclic AMP content increment due to hCG stimulation is much higher.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult male rats were injected s.c. once a week for 3 weeks with DBCP, 20 mg/kg B.W. Animals were sacrificed 5, 9, 13, 17, 25 and 50 weeks after last injection. Body weight was recorded once a week. Prior to sacrifice each male was presented with proestral females in order to determine the male's mating behaviour and fertility. Testes were removed, weighed and taken for standard histological examination. DBCP treatment caused a reduction of body weight which reverted back to control levels some 17 weeks post injection. Testes weights were reduced and remained low despite the recovery of body weight. Generally, all males showed normal mating behaviour but most of them were infertile. Testicular histology showed a correlation between decreasing testicular weight and increasing percentage of degenerated seminiferous tubules, which was on the other hand correlated with decreasing tubular diameter. Serum levels of FSH and LH were significantly increased in the infertile DBCP treated males while values for the fertile ones were similar to those of controls. There were no differences in serum testosterone levels between DBCP treated and control animals. It is concluded that in DBCP treated rats testicular degenerative damages are associated with increased circulating gonadotrophin levels and with normal testosterone levels. Although mating behaviour is unaffected fertility is depressed and does not recover for at least 50 weeks post injection. It is suggested that DBCP treatment affects mainly the activity of the Sertoli cells while the Leydig cells are affected to a much lesser degree.
Adult male rats were treated with a single, whole body exposure to a dose of 0.001, 0.01 or 0.1 Gy (1 Gy = 100 rad). The animals were sacrificed 1, 7, 30, 100 or 180 days following exposure. Serum testosterone, serum and hypophyseal LH, FSH and prolactin as well as hypothalamic LHRH were measured. In the 0.1 Gy irradiated rats, serum LH and FSH were 100% higher and serum prolactin was 30% lower as compared to controls, 30 days after irradiation. The concentrations of these hormones remained significantly different from control values even after 180 days after exposure. On the other hand, the hypophyseal content of LH, FSH and prolactin decreased in the 0.1 Gy treated rats, 100 days after irradiation. In the group of the 0.01 Gy irradiated rats, serum FSH increased by 70% and hypophyseal FSH decreased. No changes were observed in serum testosterone and hypothalamic LHRH in any of the irradiated groups and no changes were observed in the group exposed to 0.001 Gy. It may be concluded that a long term damage to the reproductive system of the male rat was induced by a single, whole body exposure to 0.1 Gy of gamma radiation.
Explore the source record for details and available documents.
Explore the source record for details and available documents.