scholarly journals Biosynthesis and release of thyrotropin-releasing hormone immunoreactivity in rat pancreatic islets in organ culture. Effects of age, glucose, and streptozotocin.

1983 ◽  
Vol 72 (6) ◽  
pp. 1867-1873 ◽  
Author(s):  
L O Dolva ◽  
J H Nielsen ◽  
B S Welinder ◽  
K F Hanssen
Keyword(s):  
Organ Culture ◽  
Pancreatic Islets ◽  
Thyrotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Rat Pancreatic Islets ◽  
Culture Effects

Four-week ethanol drinking increases both thyrotropin-releasing hormone (TRH) release and content in rat pancreatic islets

Life Sciences ◽  
2000 ◽  
Vol 66 (7) ◽  
pp. 629-639 ◽  
Author(s):  
J. Benický ◽  
M. Nikodémová ◽  
S. Scsuková ◽  
Š. Zórad ◽  
V. Štrbák
Keyword(s):  
Pancreatic Islets ◽  
Thyrotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Rat Pancreatic Islets ◽  
Ethanol Drinking

scholarly journals Pancreatic Thyrotropin Releasing Hormone and Mechanism of Insulin Secretion

2018 ◽  
Vol 50 (1) ◽  
pp. 378-384 ◽  
Author(s):  
Vladimír  Štrbák
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Basal Insulin ◽  
Thyrotropin Releasing Hormone ◽  
Insulin Content ◽  
Β Cells ◽  
Releasing Hormone ◽  
Rat Pancreatic Islets ◽  
Basal Insulin Secretion

Thyrotropin releasing hormone (TRH; pGlu-His-ProNH2) is expressed also in pancreatic β cells where it is colocalized in secretory granules with insulin. High perinatal changes of the TRH gene expression and TRH concentrations in rat pancreatic islets coincide with the perinatal maturation of the adequate insulin secretory responsiveness to glucose and other nutrient secretagogues. TRH secretion from pancreatic islets is stimulated by glucose and inhibited by insulin. Disruption of the TRH gene in knockout mice results in hyperglycemia accompanied by impaired insulin secretory response to glucose. Progress in understanding TRH - insulin relations may be substantial for improving knowledge of pathophysiological mechanisms included in changes of insulin secretion with possible clinical impact. Block of the last step of biosynthesis of α-amidated peptides, including TRH by disulfiram (DS) treatment of adult male rats subcutaneously with 200 mg/kg for five days in our experiments resulted in barely detectable levels of peptidyl-glycine α-amidating monooxygenase (PAM) in their pancreatic islets. TRH in physiological concentration (1 nM) does not affect basal insulin secretion from intact rat pancreatic islets. In contrast, basal insulin secretion from islets of DS-treated rats is four times higher compared to controls and could not be further stimulated by high-glucose. The addition of 1 nM TRH into medium decreased immediately basal insulin secretion in DS (TRH lacking) islets to control level and normalized also their response to glucose. Interestingly, absence of the secretory response to glucose in islets from TRH depleted rats was connected with their increase of insulin content during stimulation. Glucose stimulation together with 1 nM TRH normalized also insulin content in DS islets. Apparently, high insulin content in islets from TRH depleted animals is a result of block of regulatory secretion pathway redirected to constitutional secretion which was corrected by the addition of TRH. Type 2 diabetes mellitus is a disease characterized by various range from predominant insulin resistance with relative insulin deficiency to a predominant secretory defect with insulin resistance. These symptoms suggest a possible role of TRH dysregulation. In conclusion, presence of TRH in β cells ensures appropriate low basal (constitutive) insulin secretion. Release of TRH induced by glucose and possibly by other secretagogues has autocrine effect resulting in directing insulin secretion to regulatory pathway reacting to stimulation. If some defects of insulin secretion could be treated by TRH, various ways of applications (also oral and nasal) could be utilized. Moreover, positive side effects shown in animal experiments may accompany the treatment: TRH has the potential to prevent apoptosis and promotes insulin-producing cell proliferation and has also aging-reversing properties.

A role of thyrotropin-releasing hormone in insulin secretion by isolated rat pancreatic islets

2004 ◽  
Vol 449 (6) ◽  
pp. 547-552 ◽  
Author(s):  
Miroslava Najvirtová ◽  
Zuzana Bačová ◽  
Adela Mátéffyová ◽  
Vladimír Štrbák
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Thyrotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Rat Pancreatic Islets ◽  
Isolated Rat

scholarly journals High concentration of thyrotropin-releasing hormone in pancreatic islets.

1978 ◽  
Vol 75 (9) ◽  
pp. 4265-4267 ◽  
Author(s):  
E. Martino ◽  
A. Lernmark ◽  
H. Seo ◽  
D. F. Steiner ◽  
S. Refetoff
Keyword(s):  
Pancreatic Islets ◽  
Thyrotropin Releasing Hormone ◽  
High Concentration ◽  
Releasing Hormone

Expression of Thyrotropin-Releasing Hormone (TRH) receptor subtype 1 in mouse pancreatic islets and HIT-T15, an insulin-secreting clonal β cell line

Life Sciences ◽  
2000 ◽  
Vol 66 (12) ◽  
pp. 1119-1125 ◽  
Author(s):  
Masanobu Yamada ◽  
Nobuyuki Shibusawa ◽  
Tetsu Hashida ◽  
Atsushi Ozawa ◽  
Tsuyoshi Monden ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Cell Line ◽  
Thyrotropin Releasing Hormone ◽  
Receptor Subtype ◽  
Β Cell ◽  
Releasing Hormone ◽  
Mouse Pancreatic Islets ◽  
Trh Receptor

Effect of thyrotropin-releasing hormone on development of the pituitary-thyroid system in fetal rats in organ culture

1987 ◽  
Vol 218 (4) ◽  
pp. 441-445 ◽  
Author(s):  
Tatsuya Takizawa ◽  
Masako Yamamoto ◽  
Kazuyoshi Arishima ◽  
Yasunobu Eguchi
Keyword(s):  
Organ Culture ◽  
Thyrotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Fetal Rats

Effects of repetitive intravenous administration of thyrotropin-releasing hormone in normal subjects

1987 ◽  
Vol 116 (3_Suppl) ◽  
pp. S68-S69
Author(s):  
M. LOSA ◽  
J. ALBA-LOPEZ ◽  
S. SOBIESCZCZYK ◽  
A. KÖNIG ◽  
C. R. PICKARDT ◽  
...  
Keyword(s):  
Intravenous Administration ◽  
Normal Subjects ◽  
Thyrotropin Releasing Hormone ◽  
Releasing Hormone
Sign in / Sign up

Export Citation Format

Share Document