EFFECTS OF LUTEINIZING HORMONE RELEASING HORMONE AND THYROTROPHIN RELEASING HORMONE ON RABBIT ADIPOSE TISSUE

1974 ◽  
Vol 62 (3) ◽  
pp. 639-643 ◽  
Author(s):  
G. G. MURTHY ◽  
R. R. MODESTO
Keyword(s):  
Adipose Tissue ◽  
Luteinizing Hormone ◽  
Glucose Oxidation ◽  
Lipolytic Activity ◽  
Acid Synthesis ◽  
Thyrotrophin Releasing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Glucose Incorporation ◽  
Lh Rh

SUMMARY The effects of luteinizing hormone releasing hormone (LH-RH) and thyrotrophin releasing hormone (TRH) on rabbit adipose tissue were studied. LH-RH increased [14C]glucose oxidation and incorporation into fatty acids and had lipolytic activity, at the same time decreasing [14C]glucose incorporation in glyceride—glycerol fractions. TRH had no significant effect on glucose oxidation or lipolysis but decreased [14C]fatty acid synthesis and [14C]glucose incorporation into glyceride—glycerol fractions.

Plasma cortisol response to thyrotrophin releasing hormone and luteinizing hormone releasing hormone in healthy kennel dogs and in dogs with pituitary-dependent hyperadrenocorticism

1982 ◽  
Vol 93 (3) ◽  
pp. 365-369 ◽  
Author(s):  
R. Stolp ◽  
R. J. M. Croughs ◽  
J. C. Meijer ◽  
A. Rijnberk
Keyword(s):  
Plasma Concentration ◽  
Luteinizing Hormone ◽  
Intravenous Injection ◽  
Plasma Cortisol ◽  
Cortisol Response ◽  
Thyrotrophin Releasing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh ◽  
Lh Releasing Hormone

The change in the plasma concentration of cortisol after the administration of thyrotrophin releasing hormone (TRH) and LH releasing hormone (LH-RH) was studied in normal dogs and in dogs with pituitary-dependent hyperadrenocorticism (PDH). The normal dogs showed a small but significant increase in the plasma concentration of cortisol 15 min after intravenous injection of TRH and LH-RH. In ten of the dogs with PDH the response to TRH was not significantly different from that in the normal dogs, but in 13 the response was significantly greater. In 15 of the dogs with PDH the response to LH-RH administration was within or below the range of responses in the normal dogs and in only one dog was the response to LH-RH greater than that in the normal dogs. These findings are discussed in relation to the pathogenesis of PDH.

VASOTOCIN RELEASE INTO THE CEREBROSPINAL FLUID OF CATS INDUCED BY LUTEINIZING HORMONE RELEASING HORMONE, THYROTROPHIN RELEASING HORMONE AND GROWTH HORMONE RELEASE-INHIBITING HORMONE

1977 ◽  
Vol 75 (1) ◽  
pp. 175-176 ◽  
Author(s):  
R. GOLDSTEIN ◽  
S. PAVEL
Keyword(s):  
Growth Hormone ◽  
Cerebrospinal Fluid ◽  
Luteinizing Hormone ◽  
Pineal Gland ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Thyrotrophin Releasing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh

Institute of Endocrinology, Bucharest, Rumania (Received 29 March 1977) The mammalian pineal gland contains (Pavel, 1965) and synthesizes (Pavel, Goldstein, Ghinea & Calb, 1977) the nonapeptide arginine-vasotocin (AVT). Since luteinizing hormone releasing hormone (LH–RH), thyrotrophin releasing hormone (TRH) and growth hormone release-inhibiting hormone (somatostatin, SRIF) have now been localized not only in the brain, but also in the pineal gland (White, Hedlund, Weber, Rippel, Johnston & Wilber, 1974; Pelletier, Le Clerc, Dube, Labrie, Puviani, Arimura & Schally, 1975), we investigated the effects of these peptides on the release of AVT into the cerebrospinal fluid (CSF) of cats. Intracarotid injections of 0·1 μg LH-RH, TRH (Hoechst, Frankfurt), SRIF (Serono, Rome) or oxytocin (Syntocinon, Sandoz Ltd, Basel) in 0·5 ml saline were given to urethane-anaesthetized male cats weighing 3–4 kg. Controls received an equal volume of saline only. The pineal glands were removed 60 min after the injections, quickly homogenized, and extracted

FAILURE OF LUTEINIZING HORMONE - RELEASING HORMONE AND INSULIN TO FURTHER AUGMENT THYROTROPHIN RELEASE IN PRIMARY HYPOTHYROIDISM

1977 ◽  
Vol 86 (3) ◽  
pp. 517-521
Author(s):  
A. D. B. Harrower ◽  
P. L. Yap ◽  
E. H. D. Cameron ◽  
G. P. Lidgard
Keyword(s):  
Luteinizing Hormone ◽  
Primary Hypothyroidism ◽  
Thyrotrophin Releasing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh ◽  
Tsh Levels

ABSTRACT The effect of luteinizing hormone - releasing hormone (LH-RH) and insulin-induced hypoglycaemia on the release of thyrotrophin (TSH) was studied in five patients with primary hypothyroidism. All five patients had elevated TSH levels with an exaggerated rise in response to thyrotrophin-releasing hormone (TRH). No rise over control values was found after LH-RH or insulin indicating that despite the augmentation of TSH release in primary hypothyroidism there is no alteration of the specificity of the thyrotroph response.

EFFECT OF CORTISOL OR ADRENOCORTICOTROPHIN ON RELEASE OF LUTEINIZING HORMONE INDUCED BY LUTEINIZING HORMONE RELEASING HORMONE IN THE DAIRY HEIFER

1982 ◽  
Vol 92 (1) ◽  
pp. 141-146 ◽  
Author(s):  
R. L. MATTERI ◽  
G. P. MOBERG
Keyword(s):  
Luteinizing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Dairy Heifers ◽  
Significant Difference ◽  
Significant Depression ◽  
Lh Rh ◽  
Lh Releasing Hormone ◽  
And Control ◽  
Slight Depression

During treatment with cortisol or ACTH, dairy heifers were given two doses of LH releasing hormone (LH-RH) spaced 1·5 h apart. Serum concentrations of cortisol and LH were monitored during each treatment. Treatment with both ACTH and cortisol raised plasma cortisol levels above the respective saline controls (P<0·001). Neither treatment affected basal LH concentrations. A slight depression in LH response was seen in the cortisol-treated animals after the first LH-RH injection, as shown by a statistically significant depression at three of the sample times. There was no significant difference between treated and control LH values after the second LH-RH administration. Treatment with ACTH resulted in significantly reduced LH values at all sample times after both injections of LH-RH.

Acidic Aqueous Extraction of Hypothalamic Luteinizing Hormone Releasing Hormone to Study Biological Effects

1974 ◽  
Vol 52 (3) ◽  
pp. 754-758 ◽  
Author(s):  
S. H. Shin ◽  
C. J. Howitt
Keyword(s):  
Luteinizing Hormone ◽  
Biological Effects ◽  
Extraction Procedure ◽  
Extraction Methods ◽  
Water Soluble ◽  
Acid Extraction ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Aqueous Solvent ◽  
Lh Rh

Several aqueous solvent systems were tested for their efficiency in extracting luteinizing hormone releasing hormone (LH-RH) from rat hypothalamus. Although LH-RH is a water-soluble decapeptide, neutral distilled water extracted only 10% of the LH-RH obtained using acid extraction methods. The efficiency of the acid extraction procedure suggests that in the hypothalamus the releasing hormone is bound to a relatively large molecular weight compound. Using the acidic extraction procedure, we found that hypothalamic LH-RH content is significantly lower in the castrated animal than in the normal rat.

PROLONGED RELEASE BY DIOESTROUS RATS OF FOLLICLE-STIMULATING HORMONE DURING THE PERIOD OF OVULATION INDUCED BY LUTEINIZING HORMONE RELEASING HORMONE

1979 ◽  
Vol 81 (1) ◽  
pp. 109-118 ◽  
Author(s):  
SHUJI SASAMOTO ◽  
SHIGEO HARADA ◽  
KAZUYOSHI TAYA
Keyword(s):  
Luteinizing Hormone ◽  
Plasma Concentrations ◽  
High Plasma ◽  
Oestrous Cycle ◽  
Prolonged Release ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Follicular Maturation ◽  
Lh Rh ◽  
Premature Ovulation

When 1·0 μg luteinizing hormone releasing hormone (LH-RH) was given i.v. three times at 1 h intervals from 17.00 to 19.00 h on the day of dioestrus (day 0) to regular 4 day cyclic rats, premature ovulation was induced the next morning (day 1) with the number of ova present comparable to normal spontaneous ovulation. The next spontaneous ovulation occurred on the morning of day 5, 4 days after premature ovulation induced by LH-RH. Plasma concentrations of FSH and LH showed transient rises and falls within 1 h of administration of LH-RH; concentrations of FSH in the plasma decreased from 20.00 h on day 0 but markedly increased again from 23.00 h on day 0 to 02.00 h on day 1 and these high levels persisted until 14.00 h on day 1, with only a small increase of plasma LH during this period. The duration of increased FSH release during premature ovulation induced by LH-RH treatment was 6 h longer than the FSH surge occurring after administration of HCG on day 0. Surges of gonadotrophin were absent on the afternoon of day 1 (the expected day of pro-oestrus) and the surges characteristic of pro-oestrus occurred on the afternoon of day 4 and ovulation followed the next morning. The pituitary content of FSH did not decrease despite persisting high plasma levels of FSH during premature ovulation induced by either LH-RH or HCG on day 0. The changes in uterine weight indicated that the pattern of oestrogen secretion from the day of premature ovulation induced by LH-RH to the day of the next spontaneous ovulation was similar to that of the normal 4 day oestrous cycle. When 10 i.u. HCG were given on day 0, an increase in oestrogen secretion occurred on day 2, 1 day earlier than in the group given LH-RH on day 0. This advancement of oestrogen secretion was assumed to be responsible for the gonadotrophin surges on day 3. Similar numbers of fully developed follicles were found by 17.00 h on day 2 after premature ovulation induced by either LH-RH or HCG, suggesting that the shorter surge of FSH during premature ovulation induced by HCG had no serious consequences on the initiation of follicular maturation for the succeeding oestrous cycle in these rats. Administration of LH-RH on day 0 had no direct effect on the FSH surge during premature ovulation. Secretory changes in the ovary during ovulation may be responsible for this prolonged selective release of FSH.

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