Sexually Dimorphic Effects of Aging on Rat Somatotropes and Lactotropes

Rossi, G. L.; Ge, Bao-Feng; Galbiati, Enrico; Müller, Eugenio E.

doi:10.1093/geronj/46.4.b152

Cited by 14 publications

(8 citation statements)

References 30 publications

(29 reference statements)

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“…Our finding in male F344 rats, however, is inconsistent with that reported in male Sprague-Dawley rats [19], The cell density of immuno stained somatotropes was reported to increase in old (20-22 months) male rats as compared with that in young (4 months) rats. The cause of this disparity cannot as yet be sufficiently explained.…”

Section: Discussioncontrasting

confidence: 99%

The Growth Hormone-Releasing Hormone-Cyclic Adenosine-3’,5’-Monophosphate Signal Pathway in Somatotropes Is Practically Intact during Aging

et al. 1994

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To elucidate the mechanisms of the impaired pituitary response to growth hormone-releasing hormone (GHRH) in aged animals on a cellular basis, a reverse hemolytic plaque assay was performed on dispersed pituitary cells from young (8-month-old) and old (26-month-old) male F344 rats. The proportion of growth hormone (GH)-plaque forming somatotropes, i.e., actually functioning somatotropes, was reduced in old rats to 50-60% of that in young rats under both unstimulated and GHRH-stimulated conditions. The response of dispersed cells to GHRH, however, seemed to remain unchanged with age when expressed as a percent increase of plaque-forming cells from the basal value. The mean diameter of plaques, which reflects the average amount of GH secreted from a single cell, was not smaller in old rats under either the unstimulated or stimulated conditions. There was also no difference between the two age groups in the frequency distribution of the plaque size of functioning somatotropes. The stimulation by forskolin, a compound that directly activates membrane-bound adenylate cyclase and consequently provokes the cyclic adenosine-3,5’-monophosphate (cAMP) pathway for GH secretion in somatotropes, produced almost the same results as those by GHRH stimulation. It was concluded, therefore, that the impaired response of the pituitary gland to GHRH could be due mostly to a reduction in the density of functioning somatotropes rather than to impairments in steps of the GHRH-cAMP signal pathway in somatotropes.

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Section: Discussioncontrasting

confidence: 99%

The Growth Hormone-Releasing Hormone-Cyclic Adenosine-3’,5’-Monophosphate Signal Pathway in Somatotropes Is Practically Intact during Aging

et al. 1994

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“…diminution of pituitary GH content in both humans [27] and rats [1], decreased number of somatotrophs [13] and high-affinity GHRH-binding sites [28], and decreased GH responsive ness to GHRH in vitro [10,13,14] and in vivo [2,6,29], Nevertheless, it seems unlikely that these alterations may account for the defective GH secretion present in old mammals. In a previous study we showed that acute ad ministration of CLO strikingly potentiated in old dogs the GH response to GHRH, which was similar to that elicited by CLO + GHRH in young dogs [11].…”

Section: Discussionmentioning

confidence: 99%

“…The mechanism(s) underlying these changes are presently poorly understood. The existence of an age-related pituitary impairment can be envisaged, since pituitaries from old rats secrete less GH in vitro, both under basal conditions [12,13] and in response to GHRH [10,13,14]. However, accumulating evidence suggests that major alterations in ageing may be located at the hypothalamic and/or suprahypothalamic level.…”

mentioning

confidence: 99%

Combined Administration of Growth-Hormone-Releasing Hormone and Clonidine Restores Defective Growth Hormone Secretion in Old Dogs

et al. 1993

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We have studied in old dogs the effects of short-term administration of growth hormone (GH)-releasing hormone (GHRH) alone or co-administered with clonidine (CLO), an ct2-adrenergic agonist, on the GH secretory pattern (cluster analysis), and GH responsiveness to an acute GHRH or GHRH + CLO challenge and plasma somatomedin C (SMC) levels. Dogs were given either GHRH alone twice daily for 10 days (treatment 1) or combined GHRH + CLO both given twice daily (treatment 2) or GHRH + CLO given once daily (treatment 3). Animals were sampled from 09.00 to 15.00 h, at 10-min intervals, both before and 14 h after treatments. At the end of the 6-hour sampling period, dogs were challenged with simultaneous administration of GHRH and CLO, while they were tested with GHRH alone on the morning of the following day. In dogs undergoing treatment 1, acute administration of GHRH or GHRH + CLO elicited mean GH peak responses higher than before treatment, but none of the GH secretory indices were modified during the 6-hour sampling period, except for the increase in mean GH peak amplitude. In dogs undergoing treatment 2, acute administration of GHRH elicited a mean GH peak response higher than that before treatment, whereas administration of GHRH + CLO induced a mean GH peak response not different from that elicited by GHRH + CLO before treatment or by GHRH alone after treatment. However, this treatment significantly augmented the frequency of spontaneous bursts of GH secretion, the mean GH peak amplitude and the total peak area. In dogs undergoing treatment 3, acute administration of GHRH alone or GHRH + CLO elicited a mean GH peak response higher than that elicited by the same drugs before treatment. Moreover, there was an increase of GH peak frequency, mean GH peak amplitude and total peak area, even higher than after treatment 2. Plasma SMC levels rose significantly after all treatments, treatment 3 being the most effective in this instance. These data demonstrate that: (1) both a hypothalamic and a pituitary component play a role in the defective GH secretion in old dogs; (2) GH hypofunction is not an irreversible event, since GH secretion may be restored by pharmacological means acting at both the pituitary and the hypothalamic level, and (3) CLO given only once daily was more effective than CLO given twice daily, perhaps due to the property of this drug to down-regulate at high doses hypothalamic α₂-adrenoceptors.

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“…Although quantitative immunohistochemical studies have been reported for the somatotrophs of old rats (Rossi et at, 1991;Takahashi, 1992), few attempts have been made to estimate the progressive ultrastructural changes that occur in these cells along with the aging in general and after pinealectomy in particular. The demonstrated atrophic changes will be reflected on the decreased secretory capacity of the somatotrophs in aged rats.…”

Section: Grup III (Aged Pinealectmize D Rats)mentioning

confidence: 99%

Augmentation of Age·related Changes of Somatotrophs of Life-Long Melatonin Deficient Rats

EI-Sokkary

Abdel-Maksoud

Abu-Die

2003

The Egyptian Journal of Anatomy

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Sexually Dimorphic Effects of Aging on Rat Somatotropes and Lactotropes

Cited by 14 publications

References 30 publications

The Growth Hormone-Releasing Hormone-Cyclic Adenosine-3’,5’-Monophosphate Signal Pathway in Somatotropes Is Practically Intact during Aging

The Growth Hormone-Releasing Hormone-Cyclic Adenosine-3’,5’-Monophosphate Signal Pathway in Somatotropes Is Practically Intact during Aging

Combined Administration of Growth-Hormone-Releasing Hormone and Clonidine Restores Defective Growth Hormone Secretion in Old Dogs

Augmentation of Age·related Changes of Somatotrophs of Life-Long Melatonin Deficient Rats

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