Interdependence of the peripheral metabolism of glucocorticoids and thyroid hormones under calorie deficit in rats at different ages

• Autorzy: Stachon M. , Gromadzka-Ostrowska J. , Lachowicz K. , Furstenberg E. , Palkowska E. , Gajewska D. , Myszkowska-Ryciak J. , Kozlowska L. , Rosolowska-Huszcz D.
• Języki publikacji: EN

Abstrakty

EN

The joint effects of energy restriction and age on adrenal glucocorticoid synthesis, liver signalling and liver thyroid hormone metabolism were examined. Adrenal type 1 11β-hydroxylase expression was chosen as a marker of adrenal steroidogenesis, liver 11β-hydroxysteroid dehydrogenase 1 and glucocorticoid receptor proteins as measures of glucocorticoid signalling, and liver type 1 and 3 deiodinase proteins as determinants of thyroid hormone metabolism. A nine-week study covered two groups (n = 21 each) of 17- and 45-week-old Sprague-Dawley male rats fed ad libitum and on diets with 20% or 40% energy deficit. Adrenal type 1 11β-hydroxylase mRNA and protein, hepatic type 1 11β-hydroxysteroid dehydrogenase level, glucocorticoid receptor and type 1 and 3 deiodinase protein levels, as well as plasma adrenocorticotropic hormone (ACTH) and corticosterone concentrations. Calorie restriction increased ACTH plasma concentrations and type 1 11β-hydroxylase protein levels were determined. Plasma ACTH and type 1 11β-hydroxylase protein were higher in older rats, while in the younger group, type 1 deiodinase protein exceeded the enzyme level in older rats. Calorie restriction decreased plasma corticosterone and type 1 11β-hydroxysteroid dehydrogenase only in older rats. Direct relationships between glucocorticoid receptors and type 1 and 3 deiodinases, as well as between type 3 deiodinase and type 1 11β-hydroxysteroid dehydrogenase, were observed. Taken together, the results indicate that responses of the rat pituitary-adrenal axis to calorie deficit are age-dependent. Moreover, the observed correlations suggest a mechanism linking an increase in glucocorticoid receptors with a reduction in peripheral thyroid hormone action resulting from a rise in the level of type 3 deiodinase.

• Wydawca: -
• Czasopismo: Journal of Animal and Feed Sciences
• Rocznik: 2014
• Tom: 23
• Numer: 2
• Opis fizyczny: p.167-176,fig.,ref.

Twórcy

autor

Stachon M.

• Department of Dietetics, Faculty of Human Nutrition and Consumer Sciences, Warsaw University of Life Sciences - SGGW, Nowoursynowska 159c, 02-776 Warsaw, Poland

autor

Gromadzka-Ostrowska J.

• Department of Dietetics, Faculty of Human Nutrition and Consumer Sciences, Warsaw University of Life Sciences - SGGW, Nowoursynowska 159c, 02-776 Warsaw, Poland

autor

Lachowicz K.

• Department of Dietetics, Faculty of Human Nutrition and Consumer Sciences, Warsaw University of Life Sciences - SGGW, Nowoursynowska 159c, 02-776 Warsaw, Poland

autor

Furstenberg E.

• Department of Dietetics, Faculty of Human Nutrition and Consumer Sciences, Warsaw University of Life Sciences - SGGW, Nowoursynowska 159c, 02-776 Warsaw, Poland

autor

Palkowska E.

• Department of Dietetics, Faculty of Human Nutrition and Consumer Sciences, Warsaw University of Life Sciences - SGGW, Nowoursynowska 159c, 02-776 Warsaw, Poland

autor

Gajewska D.

• Department of Dietetics, Faculty of Human Nutrition and Consumer Sciences, Warsaw University of Life Sciences - SGGW, Nowoursynowska 159c, 02-776 Warsaw, Poland

autor

Myszkowska-Ryciak J.

• Department of Dietetics, Faculty of Human Nutrition and Consumer Sciences, Warsaw University of Life Sciences - SGGW, Nowoursynowska 159c, 02-776 Warsaw, Poland

autor

Kozlowska L.

• Department of Dietetics, Faculty of Human Nutrition and Consumer Sciences, Warsaw University of Life Sciences - SGGW, Nowoursynowska 159c, 02-776 Warsaw, Poland

autor

Rosolowska-Huszcz D.

• Department of Dietetics, Faculty of Human Nutrition and Consumer Sciences, Warsaw University of Life Sciences - SGGW, Nowoursynowska 159c, 02-776 Warsaw, Poland

Bibliografia

• Aceves C., Escobar C., Rojas-Huidobro R., Vázquez-Martínez O., Martínez-Merlos T., Aguilar-Roblero R., Díaz-Muñoz M., 2003. Liver 5’-deiodinase activity is modified in rats under restricted feeding schedules: evidence for post-translational regulation. J. Endocrinol. 179, 91–96
• Adcock I.M., Caramori G., Ito K., 2006. New insights into the molecular mechanisms of corticosteroids actions. Curr. Drug Targets 7, 649–660
• Aguilera G., 2011. HPA axis responsiveness to stress: implications for healthy aging. Exp. Gerontol. 46, 90–95
• Arai K., Soga T., Ohata H., Otagiri A., Shibasaki T., 2004. Effects of food restriction on peroxisome proliferator-associated receptor-γ and glucocorticoid receptor signaling in adipose tissues of normal rats. Metabolism 53, 28–36
• Araujo R.L., Andrade B.M., Figueiredo A.S., da Silva M.L., Marassi M.P., Pereira Vdos S., Bouskela E., Carvalho D.P., 2008. Low replacement doses of thyroxine during food restriction restores type I deiodinase activity in rats and promotes body protein loss. J. Endocrinol. 198, 119–125
• Araujo R.L., Andrade B.M., da Silva M.L., Ferreira A.C., Carvalho D.P., 2009. Tissue-specific deiodinase regulation during food restriction and low replacement dose of leptin in rats. Amer. J. Physiol.-Endocrinol. Met. 296, E1157–E1163
• Auvinen H.E., Romijn J.A., Biermasz N.R., Pijl H., Havekes L.M., Smit J.W.A., Rensen P.C.N., Pereira A.M., 2012. The effects of high fat diet on the basal activity of the hypothalamus-pituitary-adrenal axis in mice. J. Endocrinol. 214, 191–197
• Belda X., Ons S., Carrasco J., Armario A., 2005. The effects of chronic food restriction on hypothalamic-pituitary-adrenal activity depend on morning versus evening availability of food. Pharmacol. Biochem. Behav. 81, 41–46
• Bianco A.C., Salvatore D., Gereben B., Berry M.J., Larsen P.R., 2002. Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases. Endocrine Rev. 23, 38–89
• Boelen A., van Beeren M., Vos X., Surovtseva O., Belegri E., Saaltink D.J., Vreugdenhil E., Kalsbeek A., Kwakkel J., Fliers E., 2012. Leptin administration restores the fasting-induced increase of hepatic type 3 deiodinase expression in mice. Thyroid 22, 192–199
• Cheng B., Horst I.A., Mader S.L., Kowal J., 1990. Diminished adrenal steroidogenic activity in aging rats: new evidence from adrenal cells culterued from young and aged normal and hypoxic animals. Mol. Cell. Endocrinol. 73, R7–R12
• Chopra I.J., Williams D.E., Orgiazzi J., Solomon D., 1975. Opposite effects of dexamethasone on serum concentrations of 3,3’,5’-triiodothyronine (reverse T3) and 3,3’,5-triiodothyronine (T3). J. Clin. Endocrinol. Metab. 41, 911–920
• Cooper M.S., Walker E.A., Bland R., Fraser W.D., Hewison M., Stewart P.M., 2000. Expression and functional consequences of 11beta-hydroxysteroid dehydrogenase activity in human bone. Bone 27, 375–381
• Darras V.M., Kotanen S.P., Geris K.L., Bergham L.R., Kϋhn E.R., 1996. Plasma thyroid hormone levels and iodothyronine deiodinase activity following an acute glucocorticoid challenge in embryonic compared with posthatch chickens. Gen. Comp. Endocrinol. 104, 203–212
• Davies P.H., Sheppard M.C., Franklyn J.A., 1996. Regulation of type I 5’-deiodinase by thyroid hormone and dexamethasone in rat liver and kidney cells. Thyroid 6, 221–228
• Degroot L.J., Hoye K., 1976. Dexamethasone suppression of serum T3 and T4. J. Clin. Endocrinol. Metab. 42, 976–978
• Dellwo M., Beauchene R.E., 1990. The effects of exercise, diet restriction, and aging on the pituitary-adrenal axis in the rat. Exp. Gerontol. 25, 553–562
• Dutta D., Sharma R., 2003. Regulation of hepatic glucocorticoid receptors in mice during dietary restriction. Hormone Metab. Res. 35, 415–420
• Fernando H.A., Chin H.-F., Ton S.H., Kadir K.A., 2013. Stress and its effects on glucose metabolism and 11β-HSD activities in rats fed on a combination of high-fat and high-sucrose diet with glycyrrhizic acid. J. Diabetes Res. http://dx.doi.org/10.1155/2013/190395
• Forhead A.J., Jellyman J.K., Gardner D.S., Giussani D.A., Kaptein E., Visser T.J., Fowden A.L., 2007. Differential effects of maternal dexamethasone treatment on circulating thyroid hormone concentrations and tissue deiodinase activity in the pregnant ewe and fetus. Endocrinology 148, 800–805
• Gottschalk J., Einspanier A., Ungemach F.R., Abraham G., 2011. Influence of topical dexamethasone applications on insulin, glucose, thyroid hormone and cortisol levels in dogs. Res. Vet. Sci. 90, 491–497
• Guarnieri D.J., Brayton C.E., Richards S.M., Maldonado-Aviles J., Trinko J.R., Nelson J., Taylor J.R., Gourley S.L., DiLeone R.J., 2012. Gene profiling reveals a role for stress hormones in the molecular and behavioral response to food restriction. Biol. Psychol. 71, 358–365
• Hernandez A., St. Germain L., 2002. Dexamethasone inhibits growth factor-induced type 3 deiodinase activity and mRNA expression in a cultured cell line derived from rat neonatal brown fat vascular-stromal cells. Endocrinology 143, 2652–2658
• Holmes M.C., Carter R.N., Noble J., Chitnis S., Dutia A., Paterson J.M., Mullins J.J., Seckl J.R., Yau J.L.W., 2010. 11β-Hydroxysteroid dehydrogenase type 1 expression is increased in the aged mouse hippocampus and parietal cortex and causes memory impairments. J. Neurosci. 30, 6916–6920
• Johnstone A.M., Faber P., Andrew R., Gibney E.R., Elia M., Lobley G., Stubbs R.J., Walker B.R., 2004. Influence of short-term dietary weight loss on cortisol secretion and metabolism in obese men. Eur. J. Endocrinol. 150, 185–194
• Kharwanlang B., Sharma R., 2011. Molecular interaction between the glucocorticoid receptor and MAPK signalling pathway: a novel link in modulating the anti-inflammatory role of glucocorticoids. Indian J. Biochem. Biophys. 48, 236–242
• Lachowicz K., Fürstenberg E, Pałkowska E., Stachoń M., Gajewska D., Myszkowska-Ryciak J., Kozłowska L., Ciecierska A., Rosołowska-Huszcz D., 2014. Effect of caloric restriction and age on thyroid hormone signalling in the heart. J. Food Anim. Sci. 23, 97–104
• Lee J., Herman J.P., Mattson M.P., 2000. Dietary restriction selectively decreases glucocorticoid receptor expression in the hippocampus and cerebral cortex of rats. Exp. Neurol. 166, 435–441
• London E., Castonguay T.W., 2009. Diet and the role of 11β-hydroxysteroid dehydrogenase-1 on obesity. J. Nutr. Biochem. 20, 485–493
• London E., Castonguay T.W., 2011. High fructose diets increase 11β-hydroxysteroid dehydrogenase type 1 in liver and visceral adipose in rats within 24-h exposure. Obesity 19, 925–932
• LoPresti J.S., Eigen A., Kaptein E., Anderson K.P., Spencer C.A., Nicoloff J.T., 1989. Alterations in 3,3’,5’-triiodothyronine metabolism in response to propylthiouracyl, dexamethasone, and thyroxine administration in man. J. Clin. Invest. 84, 1650–1656 Maes M., Vandewoude M., Schotte C., Martin M., Blockx P., 1990. Suppressive effects of dexamethasone on hypothalamicpituitary-thyroid axis function in depressed patients. J. Affect. Disorders 20, 55–61
• Maia A.L., Harney J.W., Larsen P.R., 1995. Pituitary cells respond to thyroid hormone by discrete, gene-specific pathways. Endocrinology 136, 1488–1494
• Menjo M., Murata Y., Fujii T., Nimura Y., Seo H., 1993. Effects of thyroid and glucocorticoid hormones on the level of messenger ribonucleic acid for iodothyronine type I 5’-deiodinase in rat primary hepatocytes grown as spheroids. Endocrinology 133, 2984–2990
• Milošević V.L.J., Ajdžanović V.Z., Bogojević D.B., Medigović I.M., Ivanović-Matić S.K., Martinović V.I., Grigorov I.I., 2011. The effect of chronic food restriction on immunopositive ACTH cells in peripubertal female rats. Gen. Physiol. Biophys. 30, 321–324
• Morton N.M., Ramage L., Seckl J.R., 2004. Down-regulation od adipose 11β-hydroxysteroid dehydrogenase type 1 by high-fat feeding in mice: a potential adaptive mechanism counteracting metabolic disease. Endocrinology 145, 2707–2712
• Phuc Le P., Friedman J.R., Schug J., Brestelli J.E., Parker J.B., Bochkis I.M., Kaestner K.H., 2005. Glucocorticoid receptor-dependent gene regulatory networks. PLoS Genet. 1, e16
• Ranhotra H.S., Sharma R., 2001. Modulation of hepatic and renal glucocorticoid receptors during aging of mice. Biogerontology 2, 245–251
• Rask E., Simonyte L., Axelson M., 2013. Cortisol metabolism after weight loss: associations with 11β-HSD type 1 and markers of obesity in women. Clin. Endocrinol. 78, 700–705
• Seckl J.R., 2004. 11β-hydroxysteroid dehydrogenases: changing glucocorticoid action. Curr. Opin. Pharmacol. 4, 597–602
• Sewer M.B., Dammer E.B., Jagarlapudi S., 2007. Transcriptional regulation of adrenocortical steroidogenic gene expression. Drug Metab. Rev. 39, 371–388
• Sharma R., Dutta D., 2006. Age-dependent decrease in renal glucocorticoid receptor function is reversed by dietary restriction in mice. Ann. NY Acad. Sci. 1067, 129–141
• Simonyte K., Olsson T., Näslund I., Angelhed J.E., Lönn L., Mattsson C., Rask E., 2010. Weight loss after gastric bypass surgery in women is followed by a metabolically favorable decrease in 11beta-hydroxysteroid dehydrogenase 1 expression in subcutaneous adipose tissue. J. Clin. Endocrinol. Metab. 95, 3527–3531
• Spindler S.R., Grizzle J.M., Walford R.L., Mote P.L., 1991. Aging and restriction of dietary calories increases insulin receptor mRNA, and aging increases glucocorticoid receptor mRNA in the liver of female C3B10RF1 mice. J. Gerontol. 46, B233–237
• Tiganescu A., Walker E.A., Hardy R.S., Mayes A.E., Stewart P.M., 2011. Localization, age- and site-dependent expression, and regulation of 11β-hydroxysteroid dehydrogenase type 1 in skin. J. Invest. Dermatol. 131, 30–36
• Tomiyama A.J., Mann T., Vinas D., Hunger J.M., Dejager J., Taylor S.E., 2010. Low calorie dieting increases cortisol. Psychosom. Med. 72, 357–364
• Tomlinson J.W.., Walker E.A., Bujalska I.J., Draper N., Lavery G.G., Cooper M.S., Hewison M., Stewart P.M., 2004. 11β-hydroxysteroid dehydrogenase type 1: a tissue-specific regulator of glucocorticoid response. Endocrine Rev. 25, 831–866
• Van der Geyten S., Darras V.M., 2005. Developmentally defined regulation of thyroid hormone metabolism by glucocorticoids in the rat. J. Endocrinol. 185, 127–1376
• Williams D.E., Chopra I.J., Orgiazzi J., Solomon D.H., 1975. Acute effects of corticosteroids on thyroid activity in Graves’ disease. J. Clin. Endocrinol. Metab. 45, 354–361