Abstract
Chronic food restriction (FR) of rats and mice results in moderate hyperadrenocorticism, which may play a role in activating cellular mechanisms that retard aging. Previously, we reported that the FR-induced hyperadrenocorticism is not due to an activated hypothalamo-pituitary unit. Therefore, we investigated in a series of experiments whether adrenal responsiveness to adrenocorticotropic hormone (ACTH), in vitro and in vivo, is enhanced by FR. Three mo-old male Fischer 344 rats were either given free access to food (AL rats) or restricted to 60% of food consumed by AL rats (FR rats) from 6 wk of age. They were killed by decapitation in the morning (AM) and afternoon (PM) when endogenously circulating corticosterone levels are at their nadir and peak, respectively. In vitro, adrenal glands from FR rats (1.5 mo FR) produced more corticosterone per mg at all doses of ACTH than those from AL rats in both the AM and PM (diet main effect, P < 0.001). FR (1.5 to 2.5 mo) also enhanced adrenal responsiveness to physiologic (diet main effect, P < 0.05) and superphysiologic (diet main effect, P < 0.001) levels of ACTH administered in vivo to dexamethasone-treated rats. ACTH- receptor (ACTH-R) mRNA, normalized to adrenal mass or to total RNA, was not influenced by FR (1.5 mo). However, adrenal ACTHR mRNA, as well as adrenal mass, per unit body weight was greater in FR than in AL rats (diet main effect, P 0.001). These results indicate that enhanced adrenocortical responsiveness to ACTH plays a major role in the hyperadrenocortical state of chronically FR rats.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1415-1420 |
| Number of pages | 6 |
| Journal | Journal of Nutrition |
| Volume | 128 |
| Issue number | 9 |
| State | Published - Sep 1998 |
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Keywords
- Adrenal sensitivity
- Corticosterone
- Male Fischer 344 rats food restriction
ASJC Scopus subject areas
- Medicine (miscellaneous)
- Food Science
Cite this
Adrenocortical responsiveness to adrenocorticotropic hormone is enhanced in chronically food-restricted rats. / Han, Eun Soo; Evans, Ted R.; Nelson, James F.
In: Journal of Nutrition, Vol. 128, No. 9, 09.1998, p. 1415-1420.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Adrenocortical responsiveness to adrenocorticotropic hormone is enhanced in chronically food-restricted rats
AU - Han, Eun Soo
AU - Evans, Ted R.
AU - Nelson, James F
PY - 1998/9
Y1 - 1998/9
N2 - Chronic food restriction (FR) of rats and mice results in moderate hyperadrenocorticism, which may play a role in activating cellular mechanisms that retard aging. Previously, we reported that the FR-induced hyperadrenocorticism is not due to an activated hypothalamo-pituitary unit. Therefore, we investigated in a series of experiments whether adrenal responsiveness to adrenocorticotropic hormone (ACTH), in vitro and in vivo, is enhanced by FR. Three mo-old male Fischer 344 rats were either given free access to food (AL rats) or restricted to 60% of food consumed by AL rats (FR rats) from 6 wk of age. They were killed by decapitation in the morning (AM) and afternoon (PM) when endogenously circulating corticosterone levels are at their nadir and peak, respectively. In vitro, adrenal glands from FR rats (1.5 mo FR) produced more corticosterone per mg at all doses of ACTH than those from AL rats in both the AM and PM (diet main effect, P < 0.001). FR (1.5 to 2.5 mo) also enhanced adrenal responsiveness to physiologic (diet main effect, P < 0.05) and superphysiologic (diet main effect, P < 0.001) levels of ACTH administered in vivo to dexamethasone-treated rats. ACTH- receptor (ACTH-R) mRNA, normalized to adrenal mass or to total RNA, was not influenced by FR (1.5 mo). However, adrenal ACTHR mRNA, as well as adrenal mass, per unit body weight was greater in FR than in AL rats (diet main effect, P 0.001). These results indicate that enhanced adrenocortical responsiveness to ACTH plays a major role in the hyperadrenocortical state of chronically FR rats.
AB - Chronic food restriction (FR) of rats and mice results in moderate hyperadrenocorticism, which may play a role in activating cellular mechanisms that retard aging. Previously, we reported that the FR-induced hyperadrenocorticism is not due to an activated hypothalamo-pituitary unit. Therefore, we investigated in a series of experiments whether adrenal responsiveness to adrenocorticotropic hormone (ACTH), in vitro and in vivo, is enhanced by FR. Three mo-old male Fischer 344 rats were either given free access to food (AL rats) or restricted to 60% of food consumed by AL rats (FR rats) from 6 wk of age. They were killed by decapitation in the morning (AM) and afternoon (PM) when endogenously circulating corticosterone levels are at their nadir and peak, respectively. In vitro, adrenal glands from FR rats (1.5 mo FR) produced more corticosterone per mg at all doses of ACTH than those from AL rats in both the AM and PM (diet main effect, P < 0.001). FR (1.5 to 2.5 mo) also enhanced adrenal responsiveness to physiologic (diet main effect, P < 0.05) and superphysiologic (diet main effect, P < 0.001) levels of ACTH administered in vivo to dexamethasone-treated rats. ACTH- receptor (ACTH-R) mRNA, normalized to adrenal mass or to total RNA, was not influenced by FR (1.5 mo). However, adrenal ACTHR mRNA, as well as adrenal mass, per unit body weight was greater in FR than in AL rats (diet main effect, P 0.001). These results indicate that enhanced adrenocortical responsiveness to ACTH plays a major role in the hyperadrenocortical state of chronically FR rats.
KW - Adrenal sensitivity
KW - Corticosterone
KW - Male Fischer 344 rats food restriction
UR - http://www.scopus.com/inward/record.url?scp=14444281987&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=14444281987&partnerID=8YFLogxK
M3 - Article
C2 - 9732299
AN - SCOPUS:14444281987
VL - 128
SP - 1415
EP - 1420
JO - Journal of Nutrition
JF - Journal of Nutrition
SN - 0022-3166
IS - 9
ER -