Abstract
The hypothalamic damage induced by neonatal treatment with monosodium l-glutamate (MSG) induces several metabolic abnormalities, resulting in a rat hyperleptinemic–hyperadipose phenotype. This study was conducted to explore the impact of the neonatal MSG treatment, in the adult (120 days old) female rat on: (a) the in vivo and in vitro mineralocorticoid responses to ACTH and angiotensin II (AII); (b) the effect of leptin on ACTH- and AII-stimulated mineralocorticoid secretions by isolated corticoadrenal cells; and (c) abdominal adiposity characteristics. Our data indicate that, compared with age-matched controls, MSG rats displayed: (1) enhanced and reduced mineralocorticoid responses to ACTH and AII treatments, respectively, effects observed in both in vivo and in vitro conditions; (2) adrenal refractoriness to the inhibitory effect of exogenous leptin on ACTH-stimulated aldosterone output by isolated adrenocortical cells; and (3) distorted omental adiposity morphology and function. This study supports that the adult hyperleptinemic MSG female rat is characterized by enhanced ACTH-driven mineralocorticoid function, impaired adrenal leptin sensitivity, and disrupted abdominal adiposity function. MSG rats could counteract undesirable effects of glucocorticoid excess, by developing a reduced AII-driven mineralocorticoid function. Thus, chronic hyperleptinemia could play a protective role against ACTH-mediated allostatic loads in the adrenal leptin resistant, MSG female rat phenotype.
Similar content being viewed by others
References
C.B. Nemeroff, L.D. Grant, G. Bissette et al., Psychoneuroendocrinology 2, 179–196 (1997)
M.A. Holzwarth-McBride, J.R. Sladek Jr., K.M. Knigge, Anat. Rec. 186, 197–205 (1976)
D.T. Krieger, A.S. Liotta, G. Nicholsen, J.S. Kizer, Nature 278, 562–563 (1979)
J.W. Olney, L.G. Sharpe, Science 166, 386–388 (1969)
R.M. Burde, B. Schainker, J. Kayes, Nature 233, 58–60 (1971)
T.W. Redding, A.V. Schally, A. Arimura, I. Wakabayashi, Neuroendocrinology 8, 245–255 (1971)
P.J. Larsen, J.D. Mikkelsen, D. Jessop, S.L. Lightman, H.S. Chowdrey, J. Endocrinol. 141, 497–503 (1994)
I. Skultetyova, A. Kiss, D. Jezova, Neuroendocrinology 67, 412–420 (1998)
L. Macho, D. Jezova, S. Zorad, M. Fickova, Endocr. Regul. 33, 61–67 (1999)
M.S. Dolnikoff, C.E. Kater, M. Egami, I.S. de Andrade, M.R. Marmo, Neuroendocrinology 48, 645–649 (1988)
M. Perelló, G. Moreno, G. Camihort et al., Endocrine 24, 167–175 (2004)
M. Perelló, G. Moreno, R.C. Gaillard, E. Spinedi, Neurendocrinol. Lett. 25, 119–126 (2004)
M. Perelló, R.C. Gaillard, A. Chisari, E. Spinedi, Neuroendocrinology 78, 176–184 (2003)
G. Moreno, M. Perelló, G. Camihort et al., Int. J. Obes. (Lond.) 30, 73–82 (2006)
E. Spinedi, R.C. Gaillard, Endocrinology 139, 4016–4020 (1998)
F.P. Pralong, R. Roduit, G. Waeber et al., Endocrinology 139, 4264–4268 (1998)
M. Tena-Sempere, L. Pinilla, L.C. Gonzalez, F.F. Casanueva, C. Dieguez, E. Aguilar, J. Endocrinol. 167, 479–486 (2000)
M. Perello, D. Castrogiovanni, A. Giovambattista, R.C. Gaillard, E. Spinedi, Neuroendocrinology 89, 276–287 (2009)
N. Cherradi, A.M. Capponi, R.C. Gaillard, F.P. Pralong, Endocrinology 142, 3302–3308 (2001)
D. Tokarev, V. Kristova, M. Kriska, D. Jezova, Physiol. Res. 46, 165–171 (1997)
B. Peters, S. Clausmeyer, N. Obermuller et al., J. Histochem. Cytochem. 46, 1215–1221 (1998)
A. Glasow, A. Haidan, U. Hilbers et al., J. Clin. Endocrinol. Metab. 83, 4459–4466 (1998)
C. Salzmann, M. Otis, H. Long, C. Roberge, N. Gallo-Payet, C.D. Walker, Endocrinology 145, 1810–1822 (2004)
G.M. Reaven, H. Lithell, L. Landsberg, N. Engl. J. Med. 334, 374–381 (1996)
T.C. Friedman, G. Mastorakos, T.D. Newman et al., Endocr. J. 43, 645–655 (1996)
W.G. Haynes, W.I. Sivitz, D.A. Morgan, S.A. Walsh, A.L. Mark, Hypertension 30, 619–623 (1997)
E.W. Shek, M.W. Brands, J.E. Hall, Hypertension 31, 409–414 (1998)
M. Iwase, K. Ichikawa, K. Tashiro et al., Hypertens. Res. 23, 503–510 (2000)
F.A. Caputo, A.C. Scallet, Physiol. Behav. 58, 25–29 (1995)
L. Pinterova, B. Zelezna, M. Fickova et al., Horm. Metab. Res. 33, 708–712 (2001)
I. Rogulja, J.W. Harding, S. Ritter, Brain Res. 419, 333–335 (1987)
I. Kojima, K. Kojima, D. Kreutter, H. Rasmussen, J. Biol. Chem. 259, 14448–14457 (1984)
R. Muzumdar, D.B. Allison, D.M. Huffman et al., Aging Cell. 7, 438–440 (2008)
C.C. Coimbra, R.H. Migliorini, Am. J. Physiol. 251, E703–E706 (1997)
M. Buyse, S. Viengchareun, A. Bado, M. Lombès, FASEB J. 15, 1357–1366 (2001)
E. Spinedi, C.A. Johnston, A. Negro-Vilar, Endocrinology 115, 267–272 (1984)
M. Kaneko, T. Hiroshige, J. Shinsako, M.F. Dallman, Am. J. Physiol. 39, R309–R316 (1980)
E. Spinedi, A. Negro-Vilar, Neuroendocrinology 37, 446–453 (1983)
E. Spinedi, L. Aguado, G. Basilotta, D. Carrizo, J. Endocrinol. Invest. 12, 321–327 (1989)
G. Camihort, C. Gomez Dumm, G. Luna et al., Cells Tissues Organs 179, 192–201 (2005)
E. Spinedi, M. Giacomini, M.C. Jacquier, R.C. Gaillard, Neuroendocrinology 53, 160–170 (1991)
J. Piermaría, G. Console, M. Perelló, G. Moreno, R.C. Gaillard, E. Spinedi, Endocrine 20, 239–246 (2003)
E. Spinedi, A. Negro-Vilar, Endocrinology 114, 2247–2251 (1984)
W.D. McElroy, C.P. Swanson (eds.), Biostatistical Analysis (Prentice-Hall-Englewood Cliffs, New Jersey, 1974)
Acknowledgments
Authors are indebted to Mr. O Vercellini and Mrs. C Ferese for animal care and histological preparations, respectively. The editorial assistance of Mrs. G. Vigo is recognized. This work was supported by grants from FONCyT (PICT 1051-2007) and CONICET (PIP 0704), Argentina, and FPRE (07-09), Switzerland.
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Perelló, M., Cónsole, G., Gaillard, R.C. et al. Analysis of angiotensin II- and ACTH-driven mineralocorticoid functions and omental adiposity in a non-genetic, hyperadipose female rat phenotype. Endocr 37, 497–506 (2010). https://doi.org/10.1007/s12020-010-9335-3
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s12020-010-9335-3