Glucocorticoid Effects on the Diurnal Rhythm of Circulating Leptin Levels

Nishiyama, Mitsuru; Makino, Shinya; Suemaru, Shuso; Nanamiya, Wakako; Asaba, Koichi; Kaneda, Tadafumi; Mimoto, Tomoko; Nishioka, Tatsuya; Takao, Toshihiro; Hashimoto, Kozo

doi:10.1159/000053234

Cited by 25 publications

(13 citation statements)

References 27 publications

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“…In view of the developing damage of the ARC as the leptin target, it is not clear whether or not the observed disinhibition of phasically reduced BAT thermogenesis by the MSG treatment in the suckling-age rats is due to their relative hyperleptinemia. Hypercorticosteronism as a direct stress response to MSG treatment in suckling-age rats (14) may account for their disproportionately higher plasma leptin, when it is considered that glucocorticoids are potent stimulators of leptin secretion (24).…”

Section: Discussionmentioning

confidence: 99%

MSG lesions decrease body mass of suckling-age rats by attenuating circadian decreases of energy expenditure

Schoelch

Hübschle

Schmidt

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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Schoelch, Corinna, Thomas Hü bschle, Ingrid Schmidt, and Barbara Nuesslein-Hildesheim. MSG lesions decrease body mass of suckling-age rats by attenuating circadian decreases of energy expenditure. Am J Physiol Endocrinol Metab 283: E604-E611, 2002. First published April 23, 2002 10.1152/ajpendo.00439.2001.-Suckling-age rats display endogenous circadian rhythmicity of metabolic rate (MR) with energy-saving, torpor-like decreases, which are sympathetically controlled and suppressed by leptin treatment. We investigated whether neonatal monosodium glutamate (MSG) treatment, known to cause arcuate nucleus damage and adult-age obesity, alters energy balance in the first two postnatal weeks. Continuously recorded MR and core temperatures (Tc) show that MSG treatment disinhibits the periodic, sympathetically controlled, energy-saving drops of Tc and MR. Increased energy expenditure thus explains reduced body fat at normal lean body mass found in MSGtreated pups artificially nourished identically to controls. In MSG-treated mother-reared pups, lean body mass is additionally reduced, suggesting that MSG also reduces suckling. Plasma leptin levels are similar in controls and MSG-treated pups but higher per unit of fat mass in the latter. We conclude that the postweaning development of MSG obesity and depressed thermogenesis are preceded by an early phase of increased energy expenditure with decreased fat deposition during suckling age and hypothesize cell damage in the arcuate nucleus to be involved in both. monosodium glutamate; juvenile rat; arcuate nucleus; obesity; leptin; torpor RODENTS TREATED POSTNATALLY with monosodium glutamate (MSG) develop into obese, stunted adults (4, 29, 37) and have been studied frequently as models for obesity. Postnatal MSG treatment produces central nervous (CNS) neurotoxic cell destruction, with the arcuate nucleus (ARC) as the most sensitive structure (35). With MSG doses sufficient to induce adult-age obesity but low enough to avoid extensive destruction such as retinal lesioning and tail automutilation (3,22,29), the CNS damage is seen in the ventromedial hypothalamus (VMH) and especially the ARC, two brain regions involved in the control of food intake. ARC damage is associated with impaired secretion of the releasing hormones for growth hormone (GHRH) and luteinizing hormone (LHRH) (2, 32), and the resulting changes in adenohypophysial growth hormone (GH) and gonadotropin secretion would explain retarded lean body mass growth and aberrations of gonadal development (19,36). Moreover, in the ARC, neuropeptide Y (NPY) production is almost completely, and proopiomelanocortin (POMC) production distinctly, reduced (1, 16). With these alterations of two peptide systems contributing importantly to the control of food intake and energy expenditure, mice (29, 37) and rats (22) are more or less hypophagic but ultimately become obese. MSG-induced damage of the ARC as the origin of these peptidergic pathways further implies impairment of the neuronal targets for circulating leptin as a hormone ...

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Section: Discussionmentioning

confidence: 99%

MSG lesions decrease body mass of suckling-age rats by attenuating circadian decreases of energy expenditure

Schoelch

Hübschle

Schmidt

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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“…Serum leptin, which is usually anorexic, is increased at night (Pickavance et al 1998, Xu et al 1999, Ahren 2000, Mastronardi et al 2000, Nishiyama et al 2000, Pu et al 2000, Ziotopoulou et al 2000, Kalsbeek et al 2001, Denis et al 2003a, probably due to the increase in food intake around the onset of night (Ahima et al 1998, Xu et al 1999. Whether the elevated leptin levels act to constrain nocturnal eating (that is, rats would eat even more if leptin concentration did not increase) or whether the hypothalamus becomes refractory to leptin at night is not known.…”

Section: Diurnal Changes In Hypothalamic Gene Expression: Relationshimentioning

confidence: 99%

Diurnal changes in hypothalamic neuropeptide and SOCS-3 expression: effects of lactation and relationship with serum leptin and food intake

Denis¹,

Chen²,

Brocklehurst³

et al. 2004

Journal of Endocrinology

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Rats normally eat about 85% of their food at night. Lactation increases food intake 3-to 4-fold, but the diurnal pattern of food intake persists. The mechanisms responsible for the diurnal and lactation-induced changes in food intake are still unresolved, hence we have further investigated the possible roles of serum leptin and hypothalamic expression of neuropeptide Y (NPY), agouti-related peptide (AgRP) and pro-opiomelanocortin (POMC) in rats. Suppressor of cytokine signalling-3 (SOCS-3) acts as a feedback inhibitor of leptin signalling in the hypothalamus, hence changes in expression of SOCS-3 were also investigated.Changes in expression of NPY, AgRP or POMC alone could not account for the diurnal changes in intake and their alteration by lactation. However, there were increased AgRP mRNA:POMC mRNA ratios at night and also during lactation, which were very similar to estimated changes in food intake. Such changes in expression may result in dominance of the orexigenic AgRP peptide over the appetite-suppressing POMC-derived peptides, and so could contribute to the hyperphagia in these states. Diurnal and lactation-related changes in the AgRP mRNA:POMC mRNA ratio and food intake are not due to changes in leptin alone. However, hypoleptinaemia, possibly through increased expression of NPY, may contribute to the hyperphagia of lactation.In the dark, expression of SOCS-3 was decreased in non-lactating rats; lactation decreased SOCS-3 expression in both light and dark phases. However, such changes are likely to enhance the ability of leptin-responsive neurones to transmit the leptin signal, and so are unlikely to contribute to either the nocturnal increase in appetite or the hyperphagia of lactation.

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“…Rats, however, normally consume 80% or more of their food at night (Kimura et al 1970, Bruckdorfer et al 1974) and this pattern of eating is retained during lactation (Strubbe & Gorissen 1980, Munday & Williamson 1983, Pickavance et al 1996. Both adipose tissue leptin mRNA expression (Saladin et al 1995, Pickavance et al 1998, Xu et al 1999 and serum leptin concentration (Pickavance et al 1998, Xu et al 1999, Nagatani et al 2000, Nishiyama et al 2000, Mastronadi et al 2000, Pu et al 2000, Johnstone & Higuchi 2001, Kalsbeek et al 2001 show a diurnal rhythm in fed rats, increasing at night. The nocturnal increase in leptin is dependent on food intake, as the rise in leptin mRNA in adipocytes was not observed in fasted rats (Saladin et al 1995).…”

Section: Introductionmentioning

confidence: 99%

Regulation of serum leptin and its role in the hyperphagia of lactation in the rat

Denis¹,

Williams²,

Vernon³

2003

Journal of Endocrinology

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The factors regulating serum leptin concentration and its relationship to the hyperphagia of lactation have been investigated in rats. Lactation results in hypoleptinaemia and loss, or at least marked attenuation, of the nocturnal rise in serum leptin. Litter removal resulted in a fall in food intake and restoration of the nocturnal rise in serum leptin. Returning the litter to the mother after a 48-h absence increased food intake and began to reinitiate milk production, but the nocturnal serum leptin levels were still increased at 48 h after litter restoration. Adjusting litter size to four, eight, ten or fourteen pups at parturition resulted in different rates of litter growth and food intake during the subsequent lactation, but had no effect on the degree of hypoleptinaemia. Reducing litter size from ten to four pups at mid-lactation resulted in a transient increase in both serum leptin and pup growth rate, while food intake fell to a level found in rats suckling four pups throughout lactation. Reducing milk production by injection of bromocriptine increased serum leptin, but did not restore the nocturnal rise in serum leptin; food intake decreased, but remained much higher than in nonlactating rats. Feeding a varied, high-energy diet resulted in a decrease in the weight of food ingested, but no change in calorie intake, and had no effect on the hypoleptinaemia. These studies suggested that the hypoleptinaemia of lactating rats is due to negative energy balance, but the loss of the nocturnal rise in serum leptin is due to the suckling stimulus. The negative energy balance of lactation does not appear to be caused by a physical constraint on food intake. While the hypoleptinaemia should facilitate the hyperphagia of lactation, other orexigenic signals must also be involved.

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Glucocorticoid Effects on the Diurnal Rhythm of Circulating Leptin Levels

Cited by 25 publications

References 27 publications

MSG lesions decrease body mass of suckling-age rats by attenuating circadian decreases of energy expenditure

MSG lesions decrease body mass of suckling-age rats by attenuating circadian decreases of energy expenditure

Diurnal changes in hypothalamic neuropeptide and SOCS-3 expression: effects of lactation and relationship with serum leptin and food intake

Regulation of serum leptin and its role in the hyperphagia of lactation in the rat

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