GH is the most important protein anabolic agent in the body, and is essential for protein synthesis throughout the lifespan. We have shown that pulsatile GH secretion is reduced in old rats, and other have reported a GH decline in elderly human subjects. A decrease in protein synthesis in many aging body organs and tissues also has been demonstrated and may be associated with the decreases in function of these organs and tissues. Our objectives are to determine why GH secretion declines during aging, and the relation of this decline to reduced protein synthesis. The causes for the aging-related decrease in GH secretion will be studied by determining (a) the effects of GRF and somatostatin on GH release in vivo and in vitro in old (18-28 months), middle-aged (10-15 months) and young (2-4 months) rats (b) hypothalamic release in vitro of somatostatin?14? and?28? (and of GRF if antiserum can be obtained) in the 3 age groups (c) whether there are differences in size and biological activity of the GH release by the 3 age groups (d) the effects of GH on in vitro somatomedin-C release by liver fragments from the 3 age groups. The relation of GH secretion to protein synthesis will be studied by measuring amino acid in corporation into protein in diaphragm muscle, liver, and possibly other tissues in the 3 age groups. Attempts will be made to increase protein synthesis in these tissues of old rats by administering GH, GRF, and CNS active drugs that stimulate GH secretion (L-Dopa, clonidine, opiates, etc.) These studies will be performed both in male and female rats, since males continue to show a slow degree of body growth (in length as well as in weight) even late in life, whereas females show growth stasis beginning in middle age but respond readily to GH administration by weight and length increases. Our preliminary results show that the objectives and methods are feasible, and that solutions to the problems proposed are attainable.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Research Project (R01)
Project #
2R01AG000416-10A1
Application #
3114056
Study Section
Reproductive Biology Study Section (REB)
Project Start
1980-05-01
Project End
1987-11-30
Budget Start
1984-12-01
Budget End
1985-11-30
Support Year
10
Fiscal Year
1985
Total Cost
Indirect Cost
Name
Michigan State University
Department
Type
Schools of Veterinary Medicine
DUNS #
193247145
City
East Lansing
State
MI
Country
United States
Zip Code
48824
Goya, R G; Castro, M G; Meites, J (1991) Differential effect of aging on serum levels of prolactin and alpha-melanotropin in rats. Proc Soc Exp Biol Med 196:218-21
Goya, R G; Lu, J K; Meites, J (1990) Gonadal function in aging rats and its relation to pituitary and mammary pathology. Mech Ageing Dev 56:77-88
Goya, R G; Quigley, K L; Takahashi, S et al. (1990) Changes in somatotropin and thyrotropin secretory patterns in aging rats. Neurobiol Aging 11:625-30
Goya, R G; Sosa, Y E; Quigley, K L et al. (1990) Homeostatic thymus hormone stimulates corticosterone secretion in a dose- and age-dependent manner in rats. Neuroendocrinology 51:59-63
Goya, R G; Naylor, P H; Goldstein, A L et al. (1990) Changes in circulating levels of neuroendocrine and thymic hormones during aging in rats: a correlation study. Exp Gerontol 25:149-57
Goya, R G; Quigley, K L; Takahashi, S et al. (1989) Differential effect of homeostatic thymus hormone on plasma thyrotropin and growth hormone in young and old rats. Mech Ageing Dev 49:119-28
Goya, R G; Sosa, Y E; Quigley, K L et al. (1988) Differential activity of thymosin peptides (thymosin fraction 5) on plasma thyrotropin in female rats of different ages. Neuroendocrinology 47:379-83
Meites, J (1988) Neuroendocrine biomarkers of aging in the rat. Exp Gerontol 23:349-58
Gottschall, P E; Meites, J (1987) Bromocryptine prevents the decline in tuberoinfundibular neuronal release of dopamine after removal of chronic estrogen treatment. Proc Soc Exp Biol Med 186:150-6
Goya, R G; Takahashi, S; Quigley, K L et al. (1987) Immune-neuroendocrine interactions during aging: age-dependent thyrotropin-inhibiting activity of thymosin peptides. Mech Ageing Dev 41:219-27

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