Restraint-Induced Glucocorticoid Receptor Downregulation is Dysregulated in High Fat Diet-Fed Rats Likely from Impairment of miR-142-3p Expression in the Hypothalamus and Hippocampus

Takahiro Nemoto; Yoshihiko Kakinuma; Tamotsu Sibasaki

doi:doi:10.11648/j.ajls.s.2015030302.15

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Restraint-Induced Glucocorticoid Receptor Downregulation is Dysregulated in High Fat Diet-Fed Rats Likely from Impairment of miR-142-3p Expression in the Hypothalamus and Hippocampus

Takahiro Nemoto, Yoshihiko Kakinuma, Tamotsu Sibasaki

Published in American Journal of Life Sciences (Volume 3, Issue 3-2)

Received: 25 February 2015 Accepted: 25 March 2015 Published: 6 May 2015

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Abstract

High fat diet (HFD) induces dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis function. The HPA axis is controlled by the feedback of glucocortioids on the hypothalamus, hippocampus and pituitary. At least three miRNAs (miR-101a, miR-124, miR-142-3p) have been reported to suppress glucocorticoid receptor (GR) translation. Because their relation to stress-induced downregulation of GR expression and dysregulation of its expression in HFD feeding are unclear, we studied to identify which miRNAs are involved in restraint-induced downregulation of GR expression in the hypothalamus and hippocampus, and to compare the basal and restraint-modified miRNA expressions in these tissues in HFD-fed rats. Rats exposed to HFD were divided into two groups, HFD-induced obese (HFD-ob) and obesity resistant (HFD-obR) rats. Basal plasma corticosterone concentrations were higher in HFD-ob than in standard chow-fed (SC) rats and in HFD-obR. Restraint-induced elevation of plasma corticosterone was higher in HFD-obR than in the other groups. Restraint decreased GR expressions and increased miR-142-3p expression in the hypothalamus and hippocampus without affecting others expressions. miR-142-3p expressions in both areas were increased by dexamethasone and restraint-induced miR-142-3p expression was blocked in adrenalectomy. The basal expression of GR or miR-142-3p expression in both areas of HFD-fed rats did not differ from those of SC, and restraint induced no changes in GR or miR-142-3p expression in both areas in HFD-ob and HFD-obR. These results suggest that impairment of glucocorticoid-induced increase in miR-142-3p may be involved in dysregulation of stress-induced downregulation of GR expression in the hypothalamus and hippocampus of HFD-fed rats.

Published in	American Journal of Life Sciences (Volume 3, Issue 3-2) This article belongs to the Special Issue Biology and Medicine of Peptide and Steroid Hormones
DOI	10.11648/j.ajls.s.2015030302.15
Page(s)	24-30
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2015. Published by Science Publishing Group

Keywords

Stress, High Fat Diet, Hypothalamus, Hippocampus, microRNA

References

[1]	C. Dong, L. E. Sanchez, R. A. Price, "Relationship of obesity to depression: a family-based study," Int J Obesity Relat Metab Disorders, vol. 28, pp. 790-795, 2004.
[2]	R. G. Kathol, "Circannual rhythm and peak frequency of corticosteroid excretion: relationship to affective disorder," Psychiatric Med., vol. 3, pp. 53-63, 1985.
[3]	B. J. Carroll, A. Iranmanesh, D. M. Keenan, F. Cassidy, W. H. Wilson, J. D. Veldhuis, "Pathophysiology of hypercortisolism in depression: pituitary and adrenal responses to low glucocorticoid feedback," Acta Psychiatr Scand., vol. 125, pp. 478-491, 2012.
[4]	B. Claustrat, G. Chazot, J. Brun, D. Jordan, G. Sassolas, "A chronobiological study of melatonin and cortisol secretion in depressed subjects: plasma melatonin, a biochemical marker in major depression," Biol Psychiatry., vol. 19, pp. 1215-1228, 1984.
[5]	C. Anacker, P. A. Zunszain, L. A. Carvalho, C. M. Pariante, "The glucocorticoid receptor: pivot of depression and of antidepressant treatment?," Psychoneuroendocrinol., vol. 36, pp. 415-425, 2011.
[6]	P. Cano, V. Jimenez-Ortega, A. Larrad, C. F. Reyes Toso, D. P. Cardinali, A. I. Esquifino, "Effect of a high-fat diet on 24-h pattern of circulating levels of prolactin, luteinizing hormone, testosterone, corticosterone, thyroid-stimulating hormone and glucose, and pineal melatonin content, in rats," Endocrine, vol. 33, pp. 118-125, 2008.
[7]	B. M. Tannenbaum, D. N. Brindley, G. S. Tannenbaum, M. F. Dallman, M. D. McArthur, M. J. Meaney, "High-fat feeding alters both basal and stress-induced hypothalamic-pituitary-adrenal activity in the rat," Am J Physiol., vol. 273, pp. E1168-1177, 1997.
[8]	B. L. Roland, Z. S. Krozowski, J. W. Funder, "Glucocorticoid receptor, mineralocorticoid receptors, 11 beta-hydroxysteroid dehydrogenase-1 and -2 expression in rat brain and kidney: in situ studies," Mol Cell Endocrinol., vol. 111, pp. R1-7, 1995.
[9]	M. Morimoto, N. Morita, H. Ozawa, K. Yokoyama, M. Kawata, "Distribution of glucocorticoid receptor immunoreactivity and mRNA in the rat brain: an immunohistochemical and in situ hybridization study," Neurosci Res., vol. 26, pp. 235-269, 1996.
[10]	F. Han, H. Ozawa, K. Matsuda, M. Nishi, M. Kawata, "Colocalization of mineralocorticoid receptor and glucocorticoid receptor in the hippocampus and hypothalamus," Neurosci Res., vol. 51, pp. 371-381, 2005.
[11]	S. Makino, T. Kaneda, M. Nishiyama, K. Asaba, K. Hashimoto, "Lack of decrease in hypothalamic and hippocampal glucocorticoid receptor mRNA during starvation," Neuroendocrinol., vol. 74, pp. 120-128, 2001.
[12]	R. W. Carthew, E. J. Sontheimer, "Origins and Mechanisms of miRNAs and siRNAs," Cell, vol. 136, pp. 642-655, 2009.
[13]	A. Riester, O, Issler, A. Spyroglou, S. H. Rodrig, A. Chen, F. Beuschlein, "ACTH-dependent regulation of microRNA as endogenous modulators of glucocorticoid receptor expression in the adrenal gland," Endocrinol., vol. 153, pp. 212-222, 2012.
[14]	C. Ledderose, P. Mohnle, E. Limbeck, S. Schutz, F. Weis, J. Rink, J. Briegel, S. Kreth, "Corticosteroid resistance in sepsis is influenced by microRNA-124--induced downregulation of glucocorticoid receptor-alpha," Critical Care Med., vol. 40, pp. 2745-2753, 2012.
[15]	B. E. Levin, A. C. Sullivan, "Glucose-induced sympathetic activation in obesity-prone and resistant rats," Int J Obesity, vol. 13, pp. 235-246, 1989.
[16]	T. Nemoto, A. Iwasaki-Sekino, N. Yamauchi, T. Shibasaki, "Role of urocortin 2 secreted by the pituitary in the stress-induced suppression of luteinizing hormone secretion in rats," Am J Physiol Endocrinol Metab., vol. 299, pp. E567-575, 2010.
[17]	S. Makino, K. Hashimoto, P. W. Gold, PW "Multiple feedback mechanisms activating corticotropin-releasing hormone system in the brain during stress," Pharmacol Biochem Behav., vol. 73, pp. 147-158, 2002.
[18]	R. M. Sapolsky, S. Zola-Morgan, L. R. Squire, "Inhibition of glucocorticoid secretion by the hippocampal formation in the primate," J. Neurosci., vol. 11, pp. 3695-3704, 1991.
[19]	L. Jacobson, R. Sapolsky, "The role of the hippocampus in feedback regulation of the hypothalamic-pituitary- adrenocortical axis," Endocrine Reviews, vol. 12, pp. 118-134, 1991.
[20]	E. Kitraki, D. Karandrea, C. Kittas, "Long-lasting effects of stress on glucocorticoid receptor gene expression in the rat brain," Neuroendocrinol., vol. 69, pp. 331-338, 1999.
[21]	J. P. Herman, M. M. Ostrander, N. K. Mueller, H. Figueiredo, Limbic system mechanisms of stress regulation: hypothalamo-pituitary-adrenocortical axis," Prog Neuropsychopharmacol Biol Psychiatry, vol. 29, pp. 1201-1213, 2005.
[22]	M. W. Schwartz, D. G. Baskin, T. R. Bukowski, J. L. Kuijper, D. Foster, G. Lasser, D. E. Prunkard, D. Jr., Porte, S. C. Woods, R. J. Seeley, D. S. Weigle, "Specificity of leptin action on elevated blood glucose levels and hypothalamic neuropeptide Y gene expression in ob/ob mice," Diabetes, vol. 45, pp. 531-535, 1996.
[23]	B. Beck, R. Kozak, A. Stricker-Krongrad, C. Burlet, "Neuropeptide Y release in the paraventricular nucleus of Long-Evans rats treated with leptin," Biochem Biophys Res Commun, vol. 242, pp. 636-639, 1998.
[24]	M. Jang, A. Mistry, A. G. Swick, D. R. Romsos, "Leptin rapidly inhibits hypothalamic neuropeptide Y secretion and stimulates corticotropin-releasing hormone secretion in adrenalectomized mice," J. Nutrition, vol. 130, pp. 2813-2820, 2000.
[25]	A. Stricker-Krongrad, F. Cumin, C. Burlet, B. Beck, "Hypothalamic neuropeptide Y and plasma leptin after long-term high-fat feeding in the rat," Neurosci Lett . vol. 254, pp. 157-160, 1998.
[26]	A. Stofkova, M. Skurlova, A. Kiss, B. Zelezna, S. Zorad, J. Jurcovicova, "Activation of hypothalamic NPY, AgRP, MC4R, AND IL-6 mRNA levels in young Lewis rats with early-life diet-induced obesity," Endocrine Regulations, vol. 43, pp. 99-106, 2009.
[27]	J. P. Herman JP, "Regulation of adrenocorticosteroid receptor mRNA expression in the central nervous system," Cell. Mol. Neurobiol., vol. 13, pp. 349-372, 1993.
[28]	N. Tritos, E. Kitraki, H. Philippidis, F. Stylianopoulou, "Neurotransmitter modulation of glucocorticoid receptor mRNA levels in the rat hippocampus," Neuroendocrinol., vol. 69, pp. 324-330, 1999.
[29]	S. Okret, L. Poellinger, Y. Dong, J. A. Gustafsson, "Down-regulation of glucocorticoid receptor mRNA by glucocorticoid hormones and recognition by the receptor of a specific binding sequence within a receptor cDNA clone," Proc Natl Acad Sci U S A, vol. 83, pp. 5899-5903, 1986.
[30]	Y. Dong, L. Poellinger, J. A. Gustafsson, S. Okret S, "Regulation of glucocorticoid receptor expression: evidence for transcriptional and posttranslational mechanisms," Mol. Endocrinol., vol. 2, pp. 1256-1264, 1988.
[31]	W. V. Vedeckis, M. Ali, H. R. Allen, "Regulation of glucocorticoid receptor protein and mRNA levels," Cancer Res, vol. 49, pp. 2295s-2302s, 1989.
[32]	J. Li, Y. Tang, D. Cai, "IKKbeta/NF-kappaB disrupts adult hypothalamic neural stem cells to mediate a neurodegenerative mechanism of dietary obesity and pre-diabetes," Nature cell biology, vol. 14, pp. 999-1012, 2012.
[33]	Y. Shpilberg, J. L. Beaudry, A. D'Souza, J. E. Campbell, A. Peckett, M. C. Riddell, "A rodent model of rapid-onset diabetes induced by glucocorticoids and high-fat feeding," Disease models & mechanisms, vol. 5, pp. 671-680, 2012.

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Takahiro Nemoto, Yoshihiko Kakinuma, Tamotsu Sibasaki. (2015). Restraint-Induced Glucocorticoid Receptor Downregulation is Dysregulated in High Fat Diet-Fed Rats Likely from Impairment of miR-142-3p Expression in the Hypothalamus and Hippocampus. American Journal of Life Sciences, 3(3-2), 24-30. https://doi.org/10.11648/j.ajls.s.2015030302.15

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Takahiro Nemoto; Yoshihiko Kakinuma; Tamotsu Sibasaki. Restraint-Induced Glucocorticoid Receptor Downregulation is Dysregulated in High Fat Diet-Fed Rats Likely from Impairment of miR-142-3p Expression in the Hypothalamus and Hippocampus. Am. J. Life Sci. 2015, 3(3-2), 24-30. doi: 10.11648/j.ajls.s.2015030302.15

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AMA Style

Takahiro Nemoto, Yoshihiko Kakinuma, Tamotsu Sibasaki. Restraint-Induced Glucocorticoid Receptor Downregulation is Dysregulated in High Fat Diet-Fed Rats Likely from Impairment of miR-142-3p Expression in the Hypothalamus and Hippocampus. Am J Life Sci. 2015;3(3-2):24-30. doi: 10.11648/j.ajls.s.2015030302.15

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@article{10.11648/j.ajls.s.2015030302.15,
  author = {Takahiro Nemoto and Yoshihiko Kakinuma and Tamotsu Sibasaki},
  title = {Restraint-Induced Glucocorticoid Receptor Downregulation is Dysregulated in High Fat Diet-Fed Rats Likely from Impairment of miR-142-3p Expression in the Hypothalamus and Hippocampus},
  journal = {American Journal of Life Sciences},
  volume = {3},
  number = {3-2},
  pages = {24-30},
  doi = {10.11648/j.ajls.s.2015030302.15},
  url = {https://doi.org/10.11648/j.ajls.s.2015030302.15},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajls.s.2015030302.15},
  abstract = {High fat diet (HFD) induces dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis function. The HPA axis is controlled by the feedback of glucocortioids on the hypothalamus, hippocampus and pituitary. At least three miRNAs (miR-101a, miR-124, miR-142-3p) have been reported to suppress glucocorticoid receptor (GR) translation. Because their relation to stress-induced downregulation of GR expression and dysregulation of its expression in HFD feeding are unclear, we studied to identify which miRNAs are involved in restraint-induced downregulation of GR expression in the hypothalamus and hippocampus, and to compare the basal and restraint-modified miRNA expressions in these tissues in HFD-fed rats. Rats exposed to HFD were divided into two groups, HFD-induced obese (HFD-ob) and obesity resistant (HFD-obR) rats. Basal plasma corticosterone concentrations were higher in HFD-ob than in standard chow-fed (SC) rats and in HFD-obR. Restraint-induced elevation of plasma corticosterone was higher in HFD-obR than in the other groups. Restraint decreased GR expressions and increased miR-142-3p expression in the hypothalamus and hippocampus without affecting others expressions. miR-142-3p expressions in both areas were increased by dexamethasone and restraint-induced miR-142-3p expression was blocked in adrenalectomy. The basal expression of GR or miR-142-3p expression in both areas of HFD-fed rats did not differ from those of SC, and restraint induced no changes in GR or miR-142-3p expression in both areas in HFD-ob and HFD-obR. These results suggest that impairment of glucocorticoid-induced increase in miR-142-3p may be involved in dysregulation of stress-induced downregulation of GR expression in the hypothalamus and hippocampus of HFD-fed rats.},
 year = {2015}
}

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TY  - JOUR
T1  - Restraint-Induced Glucocorticoid Receptor Downregulation is Dysregulated in High Fat Diet-Fed Rats Likely from Impairment of miR-142-3p Expression in the Hypothalamus and Hippocampus
AU  - Takahiro Nemoto
AU  - Yoshihiko Kakinuma
AU  - Tamotsu Sibasaki
Y1  - 2015/05/06
PY  - 2015
N1  - https://doi.org/10.11648/j.ajls.s.2015030302.15
DO  - 10.11648/j.ajls.s.2015030302.15
T2  - American Journal of Life Sciences
JF  - American Journal of Life Sciences
JO  - American Journal of Life Sciences
SP  - 24
EP  - 30
PB  - Science Publishing Group
SN  - 2328-5737
UR  - https://doi.org/10.11648/j.ajls.s.2015030302.15
AB  - High fat diet (HFD) induces dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis function. The HPA axis is controlled by the feedback of glucocortioids on the hypothalamus, hippocampus and pituitary. At least three miRNAs (miR-101a, miR-124, miR-142-3p) have been reported to suppress glucocorticoid receptor (GR) translation. Because their relation to stress-induced downregulation of GR expression and dysregulation of its expression in HFD feeding are unclear, we studied to identify which miRNAs are involved in restraint-induced downregulation of GR expression in the hypothalamus and hippocampus, and to compare the basal and restraint-modified miRNA expressions in these tissues in HFD-fed rats. Rats exposed to HFD were divided into two groups, HFD-induced obese (HFD-ob) and obesity resistant (HFD-obR) rats. Basal plasma corticosterone concentrations were higher in HFD-ob than in standard chow-fed (SC) rats and in HFD-obR. Restraint-induced elevation of plasma corticosterone was higher in HFD-obR than in the other groups. Restraint decreased GR expressions and increased miR-142-3p expression in the hypothalamus and hippocampus without affecting others expressions. miR-142-3p expressions in both areas were increased by dexamethasone and restraint-induced miR-142-3p expression was blocked in adrenalectomy. The basal expression of GR or miR-142-3p expression in both areas of HFD-fed rats did not differ from those of SC, and restraint induced no changes in GR or miR-142-3p expression in both areas in HFD-ob and HFD-obR. These results suggest that impairment of glucocorticoid-induced increase in miR-142-3p may be involved in dysregulation of stress-induced downregulation of GR expression in the hypothalamus and hippocampus of HFD-fed rats.
VL  - 3
IS  - 3-2
ER  -

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Author Information

Takahiro Nemoto

Dept. Physiology, Nippon Medical School, Tokyo, Japan
Yoshihiko Kakinuma

Dept. Physiology, Nippon Medical School, Tokyo, Japan
Tamotsu Sibasaki

Dept. Physiology, Nippon Medical School, Tokyo, Japan

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Takahiro Nemoto, Yoshihiko Kakinuma, Tamotsu Sibasaki. (2015). Restraint-Induced Glucocorticoid Receptor Downregulation is Dysregulated in High Fat Diet-Fed Rats Likely from Impairment of miR-142-3p Expression in the Hypothalamus and Hippocampus. American Journal of Life Sciences, 3(3-2), 24-30. https://doi.org/10.11648/j.ajls.s.2015030302.15

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ACS Style

Takahiro Nemoto; Yoshihiko Kakinuma; Tamotsu Sibasaki. Restraint-Induced Glucocorticoid Receptor Downregulation is Dysregulated in High Fat Diet-Fed Rats Likely from Impairment of miR-142-3p Expression in the Hypothalamus and Hippocampus. Am. J. Life Sci. 2015, 3(3-2), 24-30. doi: 10.11648/j.ajls.s.2015030302.15

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AMA Style

Takahiro Nemoto, Yoshihiko Kakinuma, Tamotsu Sibasaki. Restraint-Induced Glucocorticoid Receptor Downregulation is Dysregulated in High Fat Diet-Fed Rats Likely from Impairment of miR-142-3p Expression in the Hypothalamus and Hippocampus. Am J Life Sci. 2015;3(3-2):24-30. doi: 10.11648/j.ajls.s.2015030302.15

Copy | Download

@article{10.11648/j.ajls.s.2015030302.15,
  author = {Takahiro Nemoto and Yoshihiko Kakinuma and Tamotsu Sibasaki},
  title = {Restraint-Induced Glucocorticoid Receptor Downregulation is Dysregulated in High Fat Diet-Fed Rats Likely from Impairment of miR-142-3p Expression in the Hypothalamus and Hippocampus},
  journal = {American Journal of Life Sciences},
  volume = {3},
  number = {3-2},
  pages = {24-30},
  doi = {10.11648/j.ajls.s.2015030302.15},
  url = {https://doi.org/10.11648/j.ajls.s.2015030302.15},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajls.s.2015030302.15},
  abstract = {High fat diet (HFD) induces dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis function. The HPA axis is controlled by the feedback of glucocortioids on the hypothalamus, hippocampus and pituitary. At least three miRNAs (miR-101a, miR-124, miR-142-3p) have been reported to suppress glucocorticoid receptor (GR) translation. Because their relation to stress-induced downregulation of GR expression and dysregulation of its expression in HFD feeding are unclear, we studied to identify which miRNAs are involved in restraint-induced downregulation of GR expression in the hypothalamus and hippocampus, and to compare the basal and restraint-modified miRNA expressions in these tissues in HFD-fed rats. Rats exposed to HFD were divided into two groups, HFD-induced obese (HFD-ob) and obesity resistant (HFD-obR) rats. Basal plasma corticosterone concentrations were higher in HFD-ob than in standard chow-fed (SC) rats and in HFD-obR. Restraint-induced elevation of plasma corticosterone was higher in HFD-obR than in the other groups. Restraint decreased GR expressions and increased miR-142-3p expression in the hypothalamus and hippocampus without affecting others expressions. miR-142-3p expressions in both areas were increased by dexamethasone and restraint-induced miR-142-3p expression was blocked in adrenalectomy. The basal expression of GR or miR-142-3p expression in both areas of HFD-fed rats did not differ from those of SC, and restraint induced no changes in GR or miR-142-3p expression in both areas in HFD-ob and HFD-obR. These results suggest that impairment of glucocorticoid-induced increase in miR-142-3p may be involved in dysregulation of stress-induced downregulation of GR expression in the hypothalamus and hippocampus of HFD-fed rats.},
 year = {2015}
}

Copy | Download

TY  - JOUR
T1  - Restraint-Induced Glucocorticoid Receptor Downregulation is Dysregulated in High Fat Diet-Fed Rats Likely from Impairment of miR-142-3p Expression in the Hypothalamus and Hippocampus
AU  - Takahiro Nemoto
AU  - Yoshihiko Kakinuma
AU  - Tamotsu Sibasaki
Y1  - 2015/05/06
PY  - 2015
N1  - https://doi.org/10.11648/j.ajls.s.2015030302.15
DO  - 10.11648/j.ajls.s.2015030302.15
T2  - American Journal of Life Sciences
JF  - American Journal of Life Sciences
JO  - American Journal of Life Sciences
SP  - 24
EP  - 30
PB  - Science Publishing Group
SN  - 2328-5737
UR  - https://doi.org/10.11648/j.ajls.s.2015030302.15
AB  - High fat diet (HFD) induces dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis function. The HPA axis is controlled by the feedback of glucocortioids on the hypothalamus, hippocampus and pituitary. At least three miRNAs (miR-101a, miR-124, miR-142-3p) have been reported to suppress glucocorticoid receptor (GR) translation. Because their relation to stress-induced downregulation of GR expression and dysregulation of its expression in HFD feeding are unclear, we studied to identify which miRNAs are involved in restraint-induced downregulation of GR expression in the hypothalamus and hippocampus, and to compare the basal and restraint-modified miRNA expressions in these tissues in HFD-fed rats. Rats exposed to HFD were divided into two groups, HFD-induced obese (HFD-ob) and obesity resistant (HFD-obR) rats. Basal plasma corticosterone concentrations were higher in HFD-ob than in standard chow-fed (SC) rats and in HFD-obR. Restraint-induced elevation of plasma corticosterone was higher in HFD-obR than in the other groups. Restraint decreased GR expressions and increased miR-142-3p expression in the hypothalamus and hippocampus without affecting others expressions. miR-142-3p expressions in both areas were increased by dexamethasone and restraint-induced miR-142-3p expression was blocked in adrenalectomy. The basal expression of GR or miR-142-3p expression in both areas of HFD-fed rats did not differ from those of SC, and restraint induced no changes in GR or miR-142-3p expression in both areas in HFD-ob and HFD-obR. These results suggest that impairment of glucocorticoid-induced increase in miR-142-3p may be involved in dysregulation of stress-induced downregulation of GR expression in the hypothalamus and hippocampus of HFD-fed rats.
VL  - 3
IS  - 3-2
ER  -

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