Induction of growth hormone (GH) mRNA by pulsatile GH-releasing hormone in rats is pattern specific

2000 ◽  
Vol 278 (5) ◽  
pp. E885-E891 ◽  
Author(s):  
Russell J. Borski ◽  
Wellington Tsai ◽  
Roberta Demott-Friberg ◽  
Ariel L. Barkan
Keyword(s):  
Growth Hormone ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Somatic Growth ◽  
Pulse Amplitude ◽  
Female Rats ◽  
Mrna Levels ◽  
Female Rat ◽  
Constant Frequency ◽  
Releasing Hormone

Growth hormone-releasing hormone (GHRH) is a main inducer of growth hormone (GH) pulses in most species studied to date. There is no information regarding the pattern of GHRH secretion as a regulator of GH gene expression. We investigated the roles of the parameters of exogenous GHRH administration (frequency, amplitude, and total amount) upon induction of pituitary GH mRNA, GH content, and somatic growth in the female rat. Continuous GHRH infusions were ineffective in altering GH mRNA levels, GH stores, or weight gain. Changing GHRH pulse amplitude between 4, 8, and 16 μg/kg at a constant frequency (Q3.0 h) was only moderately effective in augmenting GH mRNA levels, whereas the 8 μg/kg and 16 μg/kg dosages stimulated weight gain by as much as 60%. When given at a 1.5-h frequency, GHRH doubled the amount of GH mRNA, elevated pituitary GH stores, and stimulated body weight gain. In the rat model, pulsatile but not continuous GHRH administration is effective in inducing pituitary GH mRNA and GH content as well as somatic growth. These studies suggest that the greater growth rate, pituitary mRNA levels, and GH stores seen in male compared with female rats are likely mediated, in part, by the endogenous episodic GHRH secretory pattern present in males.

Stimulation of food intake and weight gain in mature female rats by bovine prolactin and bovine growth hormone

1993 ◽  
Vol 264 (6) ◽  
pp. E986-E992 ◽  
Author(s):  
J. C. Byatt ◽  
N. R. Staten ◽  
W. J. Salsgiver ◽  
J. G. Kostelc ◽  
R. J. Collier
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Mature Female ◽  
Female Rats ◽  
Bovine Growth Hormone ◽  
Female Rat ◽  
Moisture Percentage

Recombinant bovine prolactin (rbPRL) or bovine growth hormone (rbGH) was administered to mature female rats (10/treatment group) by daily subcutaneous injection for 10 days. Doses ranged from 7 to 5,000 micrograms/day (0.03-24 mg/kg body wt). Both rbPRL and rbGH increased body weight gain and food intake, but these parameters were increased at lower doses of rbPRL (7-63 micrograms/day) than rbGH (> 190 micrograms/day). Weight gain and food intake were maximally stimulated by 190 micrograms/day rbPRL, whereas maximal increased weight gain was obtained with the highest dose of rbGH (5,000 micrograms/day). Total carcass protein was increased by both hormones; however, protein as a percentage of body weight was unchanged. Similarly, neither rbPRL nor rbGH changed the percentage of carcass moisture. Percentage of body fat was increased by rbPRL but was decreased by rbGH. Weight of the gastrointestinal tract and kidneys was increased by both hormones, but increases were in proportion to body weight gain. These data confirm that ungulate prolactin is a hyperphagic agent in the female rat. In addition, they suggest that, while prolactin stimulates growth in mature female rats, this growth is probably not via a somatogenic mechanism.

BODY WEIGHT REGULATION IN FEMALE RATS FOLLOWING NEONATAL TESTOSTERONE

1976 ◽  
Vol 81 (1) ◽  
pp. 215-224 ◽  
Author(s):  
Paul U. Dubuc
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Ovarian Function ◽  
Body Weight Gain ◽  
Somatic Growth ◽  
Experimental Period ◽  
Skeletal Growth ◽  
Female Rats ◽  
Testosterone Treatment ◽  
Body Weights

ABSTRACT Neonatal testosterone treatment of female rats led to an increase in body weight and skeletal growth and produced evidence of altered ovarian function over a 76 day period following treatment. Bilateral ovariectomy performed eleven weeks after neonatal treatment increased the rate of body weight gain of both testosterone propionate- and oil-treated groups, but no differences in the increased rates of weight gain were evident between groups over a five week post-ovex observation period. Subsequently, long-term oestrogen replacement therapy, via subcutaneous Silastic implants, produced equal reductions in the rates of body weight gain and somatic growth of both early testosterone- and oil-treated ovariectomized groups. In spite of the marked effects of these manipulations on body weight and skeletal growth, no significant differences were noted in the Lee Index of obesity between androgenized and the appropriate non-androgenized control rats at any interval of the experimental period. These results indicate that neither ovarian hormones nor an altered sensitivity to oestrogen of body weight regulatory mechanisms are important in the increased body weight that follows perinatal testosterone treatment. Additionally, the present data add support to previous work which has suggested that a general increase of somatic growth rather than 'obesity' provides the major contribution to the elevated body weights of androgenized female rats.

scholarly journals Maternal obesity and fetal programming: effects of a high-carbohydrate nutritional modification in the immediate postnatal life of female rats

2008 ◽  
Vol 295 (4) ◽  
pp. E895-E903 ◽  
Author(s):  
Malathi Srinivasan ◽  
Catherine Dodds ◽  
Husam Ghanim ◽  
Tao Gao ◽  
Peter J. Ross ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Plasma Levels ◽  
Body Weight Gain ◽  
The Body ◽  
Female Rats ◽  
Milk Formula ◽  
Postnatal Life ◽  
Mrna Levels ◽  
High Carbohydrate

Our earlier studies have shown that the artificial rearing of newborn rat pups [first generation high carbohydrate (1-HC)] on an HC milk formula resulted in chronic hyperinsulinemia and adult-onset obesity (HC phenotype). Offspring [second-generation HC (2-HC)] of 1-HC female rats spontaneously acquired the HC phenotype in the postweaning period. In this study, we have characterized the development of the abnormal intrauterine environment in the 1-HC female rats and the effects on fetal development under such pregnancy conditions for the offspring. 1-HC female rats demonstrated hyperphagia on laboratory chow and increased body weight gain beginning from the immediate postweaning period along with hyperinsulinemia and hyperleptinemia. During pregnancy, 1-HC female rats showed several metabolic alterations including increased body weight gain and increased plasma levels of insulin, leptin, proinflammatory markers, and lipid peroxidation products. Although there were no significant changes in the body weights or litter size of term 2-HC fetuses, the plasma levels of insulin and leptin were significantly higher compared with those of control term fetuses. Quantitation of mRNA levels by real-time RT-PCR indicated significant increases in the mRNA levels of orexigenic neuropeptides in the hypothalamus of 2-HC term fetuses. Collectively, these results indicate that the HC diet in infancy results in an adverse pregnancy condition in female rats with deleterious consequences for the offspring.

Purified Chicken Growth Hormone (GH) and a Human Pancreatic GH-Releasing Hormone Increase Body Weight Gain in Chickens

Endocrinology ◽  
1986 ◽  
Vol 118 (5) ◽  
pp. 1961-1965 ◽  
Author(s):  
F. C. LEUNG ◽  
J. E. TAYLOR ◽  
S. WIEN ◽  
A. VAN IDERSTINE
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Increase Body Weight ◽  
Releasing Hormone

scholarly journals Persistent changes in somatostatin and neuropeptide Y mRNA levels but not in growth hormone-releasing hormone mRNA levels in adult rats after intrauterine growth retardation

2001 ◽  
Vol 168 (2) ◽  
pp. 273-281 ◽  
Author(s):  
CT Huizinga ◽  
CB Oudejans ◽  
HA Delemarre-van de Waal
Keyword(s):  
Growth Hormone ◽  
Neuropeptide Y ◽  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Growth Failure ◽  
Female Rats ◽  
Mrna Levels ◽  
Adult Rats ◽  
Releasing Hormone ◽  
Intrauterine Growth

A reduction in the availability of oxygen and nutrients across the placenta in the last trimester of pregnancy may lead to intrauterine growth retardation (IUGR) which, in turn, may cause a persistent postnatal growth failure. However, it is unknown whether this persistent growth retardation is centrally mediated through alterations in the components of the growth hormone (GH)-axis. We tested the hypothesis that alterations in the development of the central components of the GH-axis contribute to the persistent growth failure observed after experimentally induced IUGR or early postnatal food restriction (FR) in the rat. Using semi-quantitative in situ hybridization, we compared somatostatin (SS), GH-releasing hormone (GHRH) and neuropeptide Y (NPY) mRNA levels in adult rats experimentally subjected to IUGR or FR. We report that IUGR increased the expression of SS mRNA in the periventricular nucleus (PeN) of adult male and female rats by 128% and 153% respectively, did not alter the expression of GHRH mRNA in the arcuate nucleus (ARC) and decreased the NPY mRNA expression in the ARC by 73% in males and 61% in females, whereas in the FR group no changes in the expression of these mRNAs were observed. These data show that the timing of malnutrition or the presence of the placenta is important for the long-term alterations since the effects only occurred in the prenatally induced growth retardation and not in the early postnatally induced growth retardation group.

Stimulation of body weight gain of the mature female rat by bovine GH and bovine placental lactogen

1991 ◽  
Vol 130 (1) ◽  
pp. 11-19 ◽  
Author(s):  
J. C. Byatt ◽  
N. R. Staten ◽  
J. J. Schmuke ◽  
F. C. Buonomo ◽  
S. S. Galosy ◽  
...  
Keyword(s):  
Weight Gain ◽  
Body Weight Gain ◽  
Mature Female ◽  
Female Rats ◽  
Placental Lactogen ◽  
Feed Consumption ◽  
Female Rat ◽  
Binding Studies ◽  
Response Curves ◽  
Igf I

ABSTRACT Mature female rats (200 g) were treated for 10 days with either recombinant bovine GH (bGH) or recombinant bovine placental lactogen (bPL) to compare the somatogenic responses elicited by these hormones. The treatments were administered by daily s.c. injection at four dose levels (0·19, 0·56, 1·67 and 5·0 mg/day). Both bGH and bPL stimulated significant increases in weight gain, but the slopes of the dose–response curves were different (P<0·05). Bovine PL was more potent than bGH (P<0·01) at the lowest dose, although there were no differences between treatment groups at the three higher doses. Feed consumption was stimulated more by bPL than bGH at all doses (P<0·001). The concentration of insulin-like growth factor-I (IGF-I) in blood plasma was increased by bGH in a dose-responsive manner and was higher than control at doses of 1·67 and 5 mg/day (P<0·05). Low doses of bPL stimulated increases in IGF-I similar to those with bGH. At the highest dose of bPL, however, there was no concomitant increase in plasma IGF-I. Nevertheless, the growth rate of the animals in this group matched that of the group given the highest dose of bGH. Receptor binding studies indicated that bPL bound to both GH and prolactin receptors. This is consistent with the growth data which suggest that bPL stimulated weight gain through a somatogenic mechanism as well as by another route, possibly mediated by lactogenic receptors. Journal of Endocrinology (1991) 130, 11–19

IN-VITRO STUDIES OF THE EFFECTS OF OESTROGEN PRETREATMENT ON THE SENSITIVITY OF THE IMMATURE FEMALE RAT PITUITARY GLAND TO STIMULATION WITH GONADOTROPHIN RELEASING HORMONE

1977 ◽  
Vol 74 (1) ◽  
pp. 11-21 ◽  
Author(s):  
M. WILKINSON ◽  
D. DE ZIEGLER ◽  
DANIELLE CASSARD ◽  
K. B. RUF
Keyword(s):  
Pituitary Gland ◽  
Brain Lesion ◽  
Culture Technique ◽  
Female Rats ◽  
Female Rat ◽  
Immature Female ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Unilateral Brain Lesion

The effects of oestrogen priming on the sensitivity of the anterior pituitary gland to stimulation with gonadotrophin releasing hormone (GnRH) was investigated in immature female rats using a new organ culture technique. Hemipituitary glands obtained from animals primed with a single dose of oestradiol benzoate (OB; 20 μg/100 g body weight) released significantly more LH when pulsed with GnRH (4 nmol/l) than did control hemipituitary glands. This potentiating effect was detectable as early as 5 days after birth. After a second stimulation, LH secretion remained high. These results were compared with those obtained from animals treated to induce increased levels of endogenous oestrogen on day 26 of life. Thus, hemipituitary glands were obtained from animals given two injections of OB, an injection of pregnant mare serum gonadotrophin (PMSG) or a unilateral brain lesion placed in the basal hypothalamus. Pituitary tissue was stimulated as before with a pulse of GnRH. Two injections of OB enhanced the sensitivity to stimulation. Conversely, both PMSG and lesion treatment severely reduced the sensitivity to GnRH, although PMSG-treated and lesioned animals have been used as models for the study of ovulation.

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