Starvation-induced changes in rat brain corticotropin-releasing factor (CRF) and putuitary-adrenocortical response

Suemaru, Shuso; Hashimoto, Kozo; Hattori, Teruhiko; Inoué, Hiroshi; Kageyama, Jingo; Ota, Zensuke

doi:10.1016/0024-3205(86)90347-4

Cited by 71 publications

(32 citation statements)

References 21 publications

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“…Examples drawn from several digestive enzymes such as sucrase-isomaltase or aminopeptidase also suggested that glucocorticoids might play an important role in the expression of these enzymes [35, 36]. In our study, we also considered the effects of endogenous glucocorticoids on the expression of PepT1 mRNA, because the serum corticosterone levels are markedly elevated in starved rats [37]. However, the PepT1 mRNA levels were not altered significantly after the first and second day of treatment with hydrocortisone (100 mg/kg) (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Regulation of PepT1 Peptide Transporter Expression in the Rat Small Intestine under Malnourished Conditions

Ihara

Tsujikawa²,

Fujiyama³

et al. 2000

Digestion

119

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Background and Aims: Many investigations suggested that peptide nutrition had a clinical advantage for nitrogen absorption. Recently, the cDNA encoding the H⁺/peptide cotransporter PepT1 was cloned. However, the regulatory mechanism of PepT1 expression under malnourished conditions has not been elucidated. The aim of this study was to clarify regulatory mechanisms of PepT1 expression. Methods: Sprague-Dawley rats were starved for 4 days, semistarved (50% amount of control) for 10 days, or given total parenteral nutrition (TPN) for 10 days. Rats with free feeding were used as control. Among those groups, the changes of PepT1 mRNA level in the jejunal mucosa and PepT1 protein density at the brush-border membranes were examined by Northern blot and by Western blot analysis, respectively. Results: Both starvation and TPN treatment caused a significant decrease in mucosal weight by 41 and 50% respectively. PepT1 mRNA level increased to 179% in the starved group and also to 161 and 164% in the TPN and semistarved groups, respectively. In contrast, sodium-dependent glucose transporter 1 mRNA expression showed no significant change. PepT1 protein density showed similar changes with the mRNA. Conclusions: PepT1 gene expression was significantly enhanced under the malnourished conditions in spite of atrophic changes of intestinal mucosa.

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Section: Discussionmentioning

confidence: 99%

Regulation of PepT1 Peptide Transporter Expression in the Rat Small Intestine under Malnourished Conditions

Ihara

Tsujikawa²,

Fujiyama³

et al. 2000

Digestion

119

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“…On the other hand, increased synthesis of CRF-41 has been observed in many regions of the brain, including the hypothalamus during many kinds of stress (Suemaru, Hashimoto, Hattori, Inoue, Kageyama & Ota, 1986;Haas & George, 1988;Murakami, Akana, Dallman & Ganong, 1989). In addition, central administration of CRF-41 has been shown to cause several responses accompanying activation of the sympathetic nervous system, which are usually observed during stress Fisher, 1989).…”

Section: Introductionmentioning

confidence: 99%

The central role of corticotrophin‐releasing factor (CRF‐41) in psychological stress in rats.

Morimoto¹,

Nakamori²,

Morimoto³

et al. 1993

The Journal of Physiology

106

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SUMMARY1. We investigated the central role of corticotrophin-releasing factor (CRF-41) in psychological stress-induced responses, including cardiovascular, thermoregulatory and locomotive activity in free-moving rats.2. Psychological stress was induced by cage-switch stress. After rats were placed in the novel environment, blood pressure, heart rate, body temperature and locomotive activity significantly increased. The intracerebroventricular (i.c.v.) injection of a-helical CRF(9-41), a CRF-41 receptor antagonist, significantly attenuated the stress-induced hypertension, tachycardia, hyperthermia and increase in locomotive activity. However, in unstressed rats, the i.c.v. injection of a-helical CRF(9-41) had no effect on physiological parameters measured in this study.3. In unstressed rats, the i.c.V. injection of CRF-41 (1 ,ug and 10 ,ug) increased blood pressure, heart rate, body temperature and locomotive activity in a dosedependent manner. The changes in these responses were quite similar to those observed during cage-switch stress.4. The results suggest that central CRF-41 plays an important role in psychological stress-induced hypertension, hyperthermia, tachycardia and increase in locomotive activity. However, it is likely that central CRF-41 does not contribute to normal cardiovascular and body temperature regulation when rats are free from stress.

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“…Starvation is one of the persistent forms of stress with prominent hypercortisolemia, but unlike during other kinds of chronic stress, decreased CRH content in the hypothalamus [13]and decreased CRH mRNA in the PVN [14]have been reported during starvation. This decrease in PVN CRH is thought to be mediated by the glucocorticoid feedback inhibition.…”

Section: Introductionmentioning

confidence: 99%

Lack of Decrease in Hypothalamic and Hippocampal Glucocorticoid Receptor mRNA during Starvation

Makino

Kaneda²,

Nishiyama³

et al. 2001

Neuroendocrinology

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We have shown in a previous study that high corticosterone levels during repeated immobilization stress result in a reduction of glucocorticoid receptor (GR) mRNA in the hypothalamic paraventricular nucleus (PVN) and the hippocampus. The reduction of GR presumably accounts for loss of or decrease in glucocorticoid-negative feedback, and thus hyperfunction of the hypothalamic-pituitary-adrenocortical (HPA) axis persists during chronic stress. Starvation is a stress state in which the counterregulatory responses against the loss of food occur in the central nervous system. We explored the impact of starvation on the HPA axis, GR and mineralocorticoid receptor (MR) mRNAs in the hippocampus, the PVN, and the anterior pituitary (AP) of rats. Rats were starved for 4 days and sacrificed in the morning. Starved rats showed high levels of plasma corticosterone, whereas neither plasma corticotropin (ACTH), AP proopiomelanocortin (POMC) mRNA nor AP type-1 corticotropin-releasing hormone (CRH) receptor mRNA was altered in the starved rats. In the presence of high corticosterone, starvation resulted in a decrease in both CRH mRNA and type-1 CRH receptor mRNA in the PVN. Consistently, the starved rats did not show any changes in GR mRNA in the hippocampus (CA1-2, CA3, and dentate gyrus), the PVN or the AP despite the elevation of plasma corticosterone. A significant decrease in MR mRNA was seen in the dentate gyrus and the AP, but not in CA1–2, CA3 or PVN. The lack of reduction of GR may be one of the organism’s counterregulatory responses during starvation, which allows an intact glucocorticoid negative feedback, thereby resulting in decreased anorectic neuropeptide levels, namely CRH, in the PVN. The results also indicate that GR mRNA in the hippocampus and other brain regions is not solely regulated by circulating glucocorticoids. The mechanism underlying the regulation of GR mRNA in the central nervous system remains to be clarified.

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Starvation-induced changes in rat brain corticotropin-releasing factor (CRF) and putuitary-adrenocortical response

Cited by 71 publications

References 21 publications

Regulation of PepT1 Peptide Transporter Expression in the Rat Small Intestine under Malnourished Conditions

Regulation of PepT1 Peptide Transporter Expression in the Rat Small Intestine under Malnourished Conditions

The central role of corticotrophin‐releasing factor (CRF‐41) in psychological stress in rats.

Lack of Decrease in Hypothalamic and Hippocampal Glucocorticoid Receptor mRNA during Starvation

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