Decline In Growth Hormone Research Articles

Influence of Prepubertal Dietary Regimen on Mammary Growth of Holstein Heifers

One hundred-sixteen Holstein heifers (mean BW, 175kg) were randomly assigned to diets of alfalfa silage or corn silage and were fed to gain approximately 725 or 950 g/d in order to study the influence of prepubertal diet and rate of gain on mammary growth and milk production. Blood was collected before puberty for hormone determination, and 8 heifers per group were killed at puberty for evaluation of tissue variables. Serum growth hormone was reduced, and IGF-I was increased, in the group of heifers reared at a high rate of gain on the corn silage diet. Accompanying the decline in growth hormone, total mammary parenchymal DNA and RNA was reduced in heifers reared at a high rate of gain on the corn silage diet. Mammary parenchyma in heifers of the latter group contained a greater volume of adipocytes and a lower volume of epithelial cells than did mammary parenchyma in heifers of other groups. Data are consistent with previous investigations that showed a deleterious effect of prepubertal rapid weight gain on mammogenesis when accompanied by excess body fat deposition. However, this effect did not cause a decline in subsequent milk production.

Hormonal substitution in older men.

The biological bases of endocrine alterations in ageing men are now well identified: progressive impairment of testicular function, decline in growth hormone (GH) secretion with decreased insulin-like growth factor-I (IGF-I) levels, and reduced adrenal androgen secretion. Insulin resistance and glucose intolerance also accompany male ageing. The mechanisms of these age-related changes are still unknown. There are preliminary results on the effects of hormonal replacement therapy in older males with mild hypogonadism or decreased IGF-I levels. Controlled placebo studies will in the future define the risks and benefits of long-term administration of androgens, GH or GH-releasing hormone in these patients. In view of the severe potential side effects, the generalized use of hormonal substitution in elderly men cannot, for the moment, be recommended.

Somatostatin gene expression in hypothalamus and cortex of aging male rats

Somatostatin has been reported to decrease with age in many brain regions and these changes generally have been considered to have important implications for the regulation of both neural activity and neuroendocrine regulatory systems. The purpose of this study was to determine whether the age-related changes in somatostatin concentration in cortex and hypothalamus are attributable to alterations in the regulation of somatostatin gene expression. Hypothalamic and cortical tissue were dissected from young (3–4 month), middle-aged (12–14 month), and old (22 month) male Fischer 344 rats. Total RNA was extracted and dilutions blotted to nitrocellulose. Somatostatin cDNA in expression vector pSP65 was used to produce a 32P-labeled antisense probe for hybridization. After washing, blots were autoradiographed and analyzed by densitometry. Dilutions of total RNA were also probed with 32P-labeled oligo d(pT) 16 to determine poly A +RNA levels. Data were expressed as relative somatostatin gene expression (somatostatin mRNA/poly A +RNA). Results indicated that in cortex, relative somatostatin gene expression was similar in young, middle-aged, and old animals (0.54 ± 0.11, 0.60 ± 0.08, and 0.51 ± 0.04, respectively). However, somatostatin gene expression in the hypothalamus decreased consistently with age and ratios in old rats were approximately 50% of levels observed in young animals ( p < 0.05). Northern analysis of RNA revealed a single somatostatin transcript of approximately 0.65 kb in all age groups. In situ hybridization analysis of somatostatin mRNA in the hypothalamus indicated that the age-related decrease in somatostatin gene expression is a consequence of decreased expression within specific hypothalamic nuclei rather than a loss of somatostatin-containing neurons. Our results indicate that 1) somatostatin gene expression decreases in hypothalamus but not in cortex of aging rats, 2) the decrease in hypothalamic somatostatin mRNA is due to a decrease in gene expression per cell, and 3) there are no apparent changes in the size of the somatostatin transcript with age. We conclude that increases in steady-state levels of somatostatin mRNA are not a causative factor in the reduction in growth hormone with age. Therefore, relative somatostatin/GRF gene expression or alterations in somatostatin posttranslational processes may be responsible for the decline in growth hormone and these changes may be an early consequence of brain aging.

Growth Hormone Status and Growth Characteristics of Japanese Quail Divergently Selected for Four-Week Body Weights1

A randombred line of quail (R1) and two lines selected for either increased (HW) or decreased (LW) 4-wk body weight were used to examine the relationship of growth to circulating growth hormone (GH) levels during growth. Differences in GH between males and females were not detected. Growth hormone was low at hatching in all lines but then increased to relatively high levels by the first post-hatching sample (3 to 7 days). A decline in GH then occurred in all lines, with low adult levels detected earlier in lines HW and R1 than in LW. The patterns of GH secretion and growth characteristics of lines HW and R1 were similar while those of LW were unique.

Counteraction by morphine of stress-induced inhibition of growth hormone release in the rat.

The purpose of this study was to determine the effect of morphine (MOR) administration on pituitary growth hormone (GH) release during stress in the male rat. Circulating GH levels were significantly decreased following a brief (2 min) exposure to either, during repetitive etherization coupled with blood withdrawal, and during continuous immobilization. Under all three stress conditions, systemic administration of MOR resulted in a significant increase in plasma GH levels compared to the vehicle-treated group. These results indicate that the pathway for opiate-induced stimulation of GH release is functional during stress, and suggest that the suppressive effect of stress does not involve a blockade of opiate receptor stimulation of GH. Thus, the present findings, taken together with reports that the overall activity of central opioid neurons is enhanced during stress, support the view that the decline in GH is due to the overriding inhibitory influence of an independent nonopioid mechanism. However, MOR can apparently increase opiate receptor stimulation sufficiently to counteract this inhibitory signal, implying that stress and the opiates may influence GH release via separate mechanisms.

Lack of dissociation of prolactin responses to thyrotropin releasing hormone and metoclopramide in chronic alcoholic men.

Prolactin, growth hormone and thyroid stimulating hormone responses to thyrotropin releasing hormone (TRH) and metoclopramide were determined in 12 alcoholic men with biopsy proven liver disease and were compared to those of 8 age matched normal controls. All subjects were challenged with TRH (400 micrograms) and metoclopramide (10 mg) given as an intravenous bolus each on a separate day. Alcoholics had increased basal prolactin and growth hormone levels compared to controls. Alcoholics had a brisk and statistically significant (p less than 0.01) response for each of the 3 hormones studied in response to TRH. In contrast to the alcoholics, the controls did not demonstrate a growth hormone response to TRH. Moreover, the TSH response to TRH of the alcoholics was exaggerated (p less than 0.05) compared to that of the controls. In response to metoclopramide, alcoholics had a brisk prolactin response, failed to demonstrate a TSH response, and had a decline in growth hormone when compared to controls. These results for alcoholics with liver disease differ from those reported for individuals with renal failure while those for the controls are similar to previously reported normal responses. These data suggest that liver disease and renal disease must differ in terms of their patterns of hypothalamic-pituitary neuroregulation as documented by their differing pituitary hormone responses to TRH and metoclopramide.

Prostaglandin E 2 (PGE 2)-induced growth hormone (GH) release: Effect of intrahypothalamic and intrapituitary implants

Overiectomized rats were unilaterally implanted with a 23-gauge stainless steel cannula in different hypothalamic areas or in the pituitary gland and subsequently were treated with estrogen (sc, 10 μg estradiol benzoate, Eb). Two days after the estrogen injection, an inner cannula containing PGE 2 or PHF 2α at its tip was inserted into the cannula. Other animals were implanted with empty inner cannula. Plasma GH concentrations were measured by RIA in blood samples drawn from the jugular vein while the animals were lightly etherized before (−2) and at 20, 40, 60 and 120 min following the implantation. Plasma GH levels in control animals bearing an empty cannula in the body of the arcuate nucleus-median eminence region (BARH-ME) were signifantly depressed by the ether stress. The implantation of PGF 2α in this area was completely ineffective in preventing ether stress-induced decline in plasma GH. By contrast, PGE 2 implanted in BARH-ME or the post-chiasmatic region of the hypothalamus (HARH-ME) elevated plasma GH 20 min following its implantation and partially prevented the subsequent decrease in GH levels induced by ether stress. PGE 2 implants located in several other hypothalamic areas failed to induce GH release or to prevent the decline in GH levels induced by ether stress. However, PGE 2 implanted in the pituitary gland elicited a marked increase in plasma GH at 20 min and completely prevented the subsequent ether stress-induced decline in GH levels. The results suggest that PGE 2 can act at both hypothalamic (ARH-ME) and pituitary levels to stimulate GH release. At the hypothalamus, PGE 2 may inhibit GH-inhibiting factor (GIF) release or induce release of GH releasing factor (GHRF).

Age-related changes in growth hormone in non-diabetic women.

ABSTRACT: In non‐obese women with unimpaired glucose tolerance (1,185 oral glucose tolerance tests) the serum level of growth hormone (GH) in the fifth and sixth age decades was below that in the third and fourth decades. Although obesity was associated with serum GH levels below those characteristic of non‐obese women, there was no evidence of a further age‐related decrease of the type observed in the non‐obese subjects. The lower serum GH level in women of the later age decades may well be related to the menopause with its decrease in the serum level of estrogen. Since there is no further age‐related decline in GH in obesity, it would appear that in obese premenopausal females, estrogen does not exert its usual GH‐enhancing effects.