Effect of Growth Hormone (GH) on the Promotion of Body Weight Gain in the Spontaneous Dwarf Rat: A Novel Experimental Model for Isolated GH Deficiency

1992 ◽  
Vol 24 (06) ◽  
pp. 300-301 ◽  
Author(s):  
H. Nogami ◽  
T. Watanabe ◽  
T. Takeuchi
1993 ◽  
Vol 264 (6) ◽  
pp. E986-E992 ◽  
Author(s):  
J. C. Byatt ◽  
N. R. Staten ◽  
W. J. Salsgiver ◽  
J. G. Kostelc ◽  
R. J. Collier

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.


2000 ◽  
pp. 535-541 ◽  
Author(s):  
Y Furuhata ◽  
R Kagaya ◽  
K Hirabayashi ◽  
A Ikeda ◽  
KT Chang ◽  
...  

BACKGROUND: Human growth hormone (hGH) transgenic (TG) rats have been produced in our laboratory. These TG rats are characterized by low circulating hGH levels, virtually no endogenous rGH secretion, and massive obesity. OBJECTIVE: To elucidate how energy balance and leptin sensitivity contributed to the establishment of this obesity. DESIGN AND METHODS: Food intake, locomotor activity and leptin concentrations in serum and cerebrospinal fluid were measured in TG rats and their non-transgenic littermates (control). The effect of intraperitoneal and intracerebroventricular injection of leptin on food intake and body weight gain was also examined. RESULTS: An increase in food intake and a decrease in locomotor activity were observed from 4 and 7 weeks of age, respectively, in the transgenic rats compared with control. Serum leptin concentrations of the transgenic rats were more than twice as high as those of control rats and were associated with an increased white adipose tissue mass and ob gene expression. Intraperitoneal injection of leptin significantly decreased food intake and body weight gain in control rats, but not in transgenic rats. Leptin concentration in the cerebrospinal fluid of transgenic rats was not different from that of control rats, and intracerebroventricular injection of leptin was similarly effective in reducing food intake and body weight gain as it was in control rats. CONCLUSIONS: These results suggest that the transgenic rats, whose GH secretion is suppressed, develop obesity due to early onset of an increase in food intake and a decrease in locomotor activity with leptin resistance resulting from deteriorating leptin transport from peripheral blood to cerebrospinal fluid.


1963 ◽  
Vol 41 (1) ◽  
pp. 1449-1453
Author(s):  
John R. Beaton ◽  
T. Orme ◽  
J. Laufer ◽  
A. Turner

Male, growing rats were injected daily with anterior pituitary growth hormone (3 mg/100 g body weight) and fed ad libitum for 7 days at environmental temperatures of 22 °C and 2–3 °C. Body weight gain, nitrogen retention, and four liver enzyme activities were measured. As observed previously, cold exposure retarded body weight gain and decreased nitrogen retention despite an increased food intake. These effects of cold were not eliminated by administration of growth hormone. The increased activities of liver arginase, alanine-glutamic transminase, and phosphate-activated glutaminase consequent upon cold exposure were not significantly affected by growth hormone although, at 22 °C, growth hormone decreased the activities of liver arginase and alanine-glutamic transaminase. Cold exposure eliminated the lowering effect of growth hormone on liver glutamic acid dehydrogenase activity observed at 22 °C. It is concluded that, under these conditions, growth hormone does not overcome the protein catabolic effects of cold exposure but rather, cold exposure eliminates the protein anabolic effects of the hormone.


2002 ◽  
Vol 15 (2) ◽  
pp. 231-244 ◽  
Author(s):  
Yasufumi Furuhata ◽  
Masugi Nishihara ◽  
Michio Takahashi

AbstractGrowth hormone (GH) is an endocrine regulator of glucose and lipid metabolism as well as body growth. GH levels are decreased and a unique pulsatile secretory pattern becomes obvious after puberty particularly in males. Coincidentally with this, males tend to deposit body fat. Experimental and clinical evidence has accumulated that obesity is associated with a decrease in GH levels. A strain of transgenic rats has been generated with severe obesity but normal nose-to-tail length, which has low circulating GH levels without pulsatility (human growth hormone (hGH) transgenic rats). The present review mainly focuses on recent and current work analysing the relationship between the occurrence of obesity and low GH levels and/or the absence of GH pulsatility in this transgenic animal model. This model has elevated blood glucose, non-esterified fatty acid, insulin and leptin levels associated with hyperphagia, suggesting that these rats also carry insulin- and leptin-resistant characteristics. hGH transgenic rats were subjected to a pair-feeding treatment to normalize food intake and chronic GH replacement to normalize GH levels. While the pair-feeding for 8 weeks successfully suppressed body-weight gain, the fat pad : body weight ratio remained very similar to freely-eating control hGH transgenic rats, which indicates the hyperphagia is not the sole contributor to the excess fat accumulation in this model. However, continuous elevation of peripheral hGH levels (approximately 2-fold) for 8 weeks by means of a slow-release vehicle resulted in a significant decrease in the fat mass : body weight ratios by 30 %. This GH treatment altered neither food intake nor body-weight gain. Thus, two characteristic phenotypes observed in the hGH transgenic rats, hyperphagia and obesity, seem to be closely related to GH levels and GH secretory pattern. This relationship might be working in the regulation of changes in seasonal body composition in wild animals.


1963 ◽  
Vol 41 (6) ◽  
pp. 1449-1453 ◽  
Author(s):  
John R. Beaton ◽  
T. Orme ◽  
J. Laufer ◽  
A. Turner

Male, growing rats were injected daily with anterior pituitary growth hormone (3 mg/100 g body weight) and fed ad libitum for 7 days at environmental temperatures of 22 °C and 2–3 °C. Body weight gain, nitrogen retention, and four liver enzyme activities were measured. As observed previously, cold exposure retarded body weight gain and decreased nitrogen retention despite an increased food intake. These effects of cold were not eliminated by administration of growth hormone. The increased activities of liver arginase, alanine-glutamic transminase, and phosphate-activated glutaminase consequent upon cold exposure were not significantly affected by growth hormone although, at 22 °C, growth hormone decreased the activities of liver arginase and alanine-glutamic transaminase. Cold exposure eliminated the lowering effect of growth hormone on liver glutamic acid dehydrogenase activity observed at 22 °C. It is concluded that, under these conditions, growth hormone does not overcome the protein catabolic effects of cold exposure but rather, cold exposure eliminates the protein anabolic effects of the hormone.


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