Hypothalamic Control of Pituitary Thyrotrophic Hormone, of Cows and Buffaloes During the Estrous Cycle

2010 ◽  
Vol 18 (2) ◽  
pp. 124-130 ◽  
Author(s):  
F. A. Soliman ◽  
M. S. Abdo
1976 ◽  
Vol 81 (2) ◽  
pp. 495-506 ◽  
Author(s):  
A. Radvila ◽  
R. Roost ◽  
H. Bürgi ◽  
H. Kohler ◽  
H. Studer

ABSTRACT Lithium and excess iodide inhibit the release of thyroid hormone from preformed stores. We thus tested the hypothesis that this was due to an inhibition of thyroglobulin breakdown. Rats were pre-treated with propylthiouracil (PTU) for 3 weeks in order to deplete their thyroids of thyroglobulin. While the PTU was continued, lithium chloride (0.25 mEq./100 g weight) or potassium iodide (3 mg per rat) were injected every 12 h for 3 days. Thereafter the thyroglobulin content in thyroid gland homogenates was measured. PTU pre-treatment lowered the thyroglobulin content from 4.21 to 0.22 mg/100 mg gland. Lithium caused a marked re-accumulation of thyroglobulin to 0.60 mg/100 mg within 3 days. While iodide alone had only a borderline effect, it markedly potentiated the action of lithium and a combination of the two drugs increased the thyroglobulin content to 1.04 mg/100 mg. Thyroxine was injected into similarly pre-treated animals to suppress secretion of thyrotrophic hormone. This markedly inhibited the proteolysis of thyroglobulin and 1.3 mg/100 mg gland accumulated after 3 days. Excess iodide, given in addition to thyroxine, decreased the amount of thyroglobulin accumulated to 0.75 mg/100 mg gland. To study whether this could be explained by an inhibitory action of iodide on thyroglobulin biosynthesis, thyroid glands from animals treated with excess iodide were incubated in vitro in the presence of 0.2 mm iodide for 3 h. Iodide decreased the incorporation of radioactive leucine into total thyroidal protein and into thyroglobulin by 25 and 35 % respectively. Iodide did not inhibit protein synthesis in the kidney, liver or muscle tissue. Thus, large doses of iodide selectively inhibit thyroglobulin biosynthesis.


Endocrinology ◽  
1988 ◽  
Vol 123 (5) ◽  
pp. 2331-2340 ◽  
Author(s):  
RANDY B. HOWARD ◽  
ANTHONY G. PUCELL ◽  
F. MERLIN BUMPUS ◽  
AHSAN HUSAIN
Keyword(s):  

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 112-113
Author(s):  
Marcelo Siqueira El Azzi ◽  
Everardo Anta Galvan ◽  
Teresita Valdes Arciniega ◽  
Iago Leão ◽  
Rodrigo Sala ◽  
...  
Keyword(s):  

Abstract The objective was to determine the effect of hCG (3,300 IU) administered on days 0 and/or 5 of the estrous cycle on total luteal area (TLA) and circulating concentrations of progesterone (P4) in recipient heifers. All heifers (n = 232; BCS = 3.3 ± 0.2) were synchronized with a 5d CIDR-Synch protocol (d-8: used CIDR inserted; d-3: CIDR removed and PGF2α treatment; d0: 100µg GnRH or hCG). Heifers were randomly assigned to four treatments: control, hCGd0, hCGd5, and hCGd0&5. Controls were treated with GnRH on d0, while hCGd0 received hCG on d0. hCGd5 heifers were treated with GnRH on d0 and hCG on d5, while hCGd0&5 received hCG on d0 and 5. Ovaries were scanned by ultrasound on d0, 5, and 12. Blood was collected on d0, 5, 7, and 12. Synchronization rate (94%) did not differ (P = 0.94) by treatment. Treatment differences were only tested in synchronized heifers (n = 218). Proportion of heifers with 1 or 2+ CL on d5 did not differ (P = 0.10) for hCG d0 treatments (hCGd0 + hCGd0&5) vs. GnRH d0 treatments (controls + hCGd5). However, heifers treated with hCG on d0 had greater (P < 0.01) TLA and P4 on d5 vs. treatments with GnRH on d0 (311 ± 13 vs. 257 ± 9 mm2; and 2.39 ± 0.15 vs. 1.90 ± 0.09 ng/mL). Ovulation rate for d5 hCG did not differ (P = 0.63) for hCGd5 vs. hCGd0&5 (93 vs. 84%). Controls had the lowest serum P4 on d7 and 12. In contrast, hCGd0&5 had the highest serum P4 on d7 (Table 1). Serum P4 on d7 did not differ for hCGd0 vs. hCGd5. On d12, serum P4 and TLA were not different for hCGd5 vs. hCGd0&5. These data indicate that hCG can be used on d0 to induce an increase in serum P4 on d5 compared to GnRH. However, only heifers treated with hCG on d5 achieved mean serum P4 > 8ng/mL.


Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 832
Author(s):  
Damian Tanski ◽  
Agnieszka Skowronska ◽  
Malgorzata Tanska ◽  
Ewa Lepiarczyk ◽  
Mariusz T. Skowronski

Aquaporins (AQPs) are integral membrane proteins, which play an important role in water homeostasis in the uterus. According to the literature, the expression of aquaporins in reproductive structures depends on the local hormonal milieu. The current study investigated the effect of selected PKA kinase inhibitor H89 and MAPK kinase inhibitor PD98059, on the expression of AQP1, 2, 5, and 7, and steroid hormones (E2), progesterone (P4), and arachidonic acid (AA) in the porcine endometrium on days 18–20 and 2–4 of the estrous cycle (the follicular phase where estrogen and follicle-stimulating hormone (FSH) are secreted increasingly in preparation for estrus and the luteal phase where the ovarian follicles begin the process of luteinization with the formation of the corpus luteum and progesterone secretion, respectively). The luminal epithelial cells were incubated in vitro in the presence of the aforementioned factors. The expression of mRNA was determined by the quantitative real-time PCR technique. In general, in Experiment 1, steroid hormones significantly increased expression of AQP1, 2, and 5 while arachidonic acid increased expression of AQP2 and AQP7. On the other hand, MAPK kinase inhibitor significantly decreased the expression of AQP1 and 5. In Experiment 2, E2, P4, or AA combined with kinase inhibitors differentially affected on AQPs expression. E2 in combination with PKA inhibitor significantly decreased expression of AQP1 but E2 or P4 combined with this inhibitor increased the expression of AQP5 and 7. On the contrary, E2 with PD98059 significantly increased AQP5 and AQP7 expression. Progesterone in combination with MAPK kinase inhibitor significantly downregulated the expression of AQP5 and upregulated AQP7. Arachidonic acid mixed with H89 or PD98059 caused a decrease in the expression of AQP5 and an increase of AQP7. The obtained results indicate that estradiol, progesterone, and arachidonic acid through PKA and MAPK signaling pathways regulate the expression of AQP1 and AQP5 in the porcine luminal epithelial cells in the periovulatory period.


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