Rat thyroid gland expresses the long form of leptin receptors, and leptin stimulates the function of the gland in euthyroid non-fasted animals

Nowak, Krzysztof W.; Kaczmarek, Przemysław; Maćkowiak, Paweł; Ziółkowska, Agnieszka; Albertin, Giovanna; Ginda, Waclaw J.; Trejter, Marcin; Nussdorfer, Gastone G.; Malendowicz, Ludwik K.

doi:10.3892/ijmm.9.1.31

Cited by 36 publications

(53 citation statements)

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“…Leptin may also alter thyroid function not only by affecting the thyroid axis but also by raising thyroid gland weight and the secretion of T3 and T4 through a direct mechanism involving the thyroid gland Ob-Rb (Nowak et al, 2002). In agreement with this, our obese hyperleptinemic phytoestrogen deprived rats showed higher circulating total T4 and slightly (but not significant) decreased TSH that may be a consequence of negative feedback from T4.…”

Section: Discussionsupporting

confidence: 86%

Withdrawal of dietary phytoestrogens in adult male rats affects hypothalamic regulation of food intake, induces obesity and alters glucose metabolism

Andreoli

Stoker

Rossetti

et al. 2015

Molecular and Cellular Endocrinology

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A B S T R A C TThe absence of phytoestrogens in the diet during pregnancy has been reported to result in obesity later in adulthood. We investigated whether phytoestrogen withdrawal in adult life could alter the hypothalamic signals that regulate food intake and affect body weight and glucose homeostasis.Male Wistar rats fed from conception to adulthood with a high phytoestrogen diet were submitted to phytoestrogen withdrawal by feeding a low phytoestrogen diet, or a high phytoestrogen-high fat diet. Withdrawal of dietary phytoestrogens increased body weight, adiposity and energy intake through an orexigenic hypothalamic response characterized by upregulation of AGRP and downregulation of POMC. This was associated with elevated leptin and T4, reduced TSH, testosterone and estradiol, and diminished hypothalamic ERα expression, concomitant with alterations in glucose tolerance.Removing dietary phytoestrogens caused manifestations of obesity and diabetes that were more pronounced than those induced by the high phytoestrogen-high fat diet intake.

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Section: Discussionsupporting

confidence: 86%

Withdrawal of dietary phytoestrogens in adult male rats affects hypothalamic regulation of food intake, induces obesity and alters glucose metabolism

Andreoli

Stoker

Rossetti

et al. 2015

Molecular and Cellular Endocrinology

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“…However, some studies have described an increase in T 3 and higher adiposity as an adaptive mechanism that occurs in obesity (Reinehr et al 2006, Alevizaki et al 2009, de Pergola et al 2010. The hyperthyroid status of the SE group can be partially explained by hyperleptinemia as leptin has a well-known stimulatory action on the thyroid axis (Casanueva & Dieguez 1999, Nowak et al 2002, Ortiga-Carvalho et al 2002, de Oliveira et al 2007. There is also an association between hyperthyroidism and hyperadiponectinemia (Yaturu et al 2004, Seifi et al 2012, which could help to explain the present findings in adult SE rats.…”

Section: Adulthood Alterationssupporting

confidence: 62%

Endocrine effects of tobacco smoke exposure during lactation in weaned and adult male offspring

Santos-Silva

Oliveira

Pinheiro

et al. 2013

Journal of Endocrinology

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Children from pregnant smokers show more susceptibility to develop obesity in adult life. Previously, we failed to demonstrate a program for obesity in rat offspring only when the mothers were exposed to tobacco smoke during lactation. Here, we studied the short-and long-term effects of smoke exposure (SE) to both dams and their pups during lactation on endocrine and metabolic parameters. For this, we designed an experimental model where nursing rats and their pups were divided into two groups: SE group, exposed to smoke in a cigarette smoking machine (four times/day, from the third to the 21st day of lactation), and group, exposed to filtered air. Pups were killed at 21 and 180 days. At weaning, SE pups showed lower body weight (7%), length (5%), retroperitoneal fat mass (59%), visceral adipocyte area (60%), and higher subcutaneous adipocyte area (95%) with hypoinsulinemia (K29%), hyperthyroxinemia (59%), hypercorticosteronemia (60%), and higher adrenal catecholamine content (C58%). In adulthood, SE offspring showed higher food intake (C10%), body total fat mass (C50%), visceral fat mass (retroperitoneal: 55%; mesenteric: 67%; and epididymal: 55%), and lower subcutaneous adipocyte area (24%) with higher serum glucose (11%), leptin (85%), adiponectin (1.4-fold increase), total triiodothyronine (71%), free thyroxine (57%), TSH (36%), triglycerides (65%), VLDL cholesterol (C66%), and HDL cholesterol (91%) levels and lower corticosteronemia (41%) and adrenal catecholamine content (57%). Our present findings suggest that tobacco SE to both dams and their pups during lactation causes malnutrition in early life that programs for obesity and hormonal and metabolic disturbances in adulthood, only if the pups are submitted to the same smoke environment as the mother.

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“…In rodents but not in humans, leptin receptors have been identified on thyroid follicular cells (7,12), and both in rodents and humans leptin receptors are widely expressed in the brain and peripherally in a variety of tissues (7,12,13). The function, if any, of leptin in many of these tissues has yet to be determined, but recently it was suggested that systematically administered leptin in rats stimulated growth and secretion of the thyroid gland through a direct mechanism involving OB-R (14).…”

Section: Introductionmentioning

confidence: 99%

Circulating leptin and thyroid dysfunction

Zimmermann-Belsing

Brabant²,

Holst³

et al. 2003

Eur J Endocrinol

153

111

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The identification and sequencing of the ob gene and its product, leptin, in 1994 opened new insights in the study of the mechanisms controlling body weight and led to a surge of research activity. Since its discovery, leptin has been the subject of an enormous amount of work especially within the fields of nutrition, metabolism and endocrinology. Leptin is accepted as an adipose signal, and even though the underlying mechanisms are not fully clarified, leptin, in addition to the thyroid hormones, is believed to be involved in regulation during the switch from the fed to the starved state. It is not clear whether leptin and the melanocortin pathways interact with the thyroid axis under physiological conditions other than during starvation or in response to severe illness, both states in which the hypothalamo -pituitary -thyroid axis may be severely suppressed. In addition to the suggested central relationship between leptin and thyroid hormones, there might also be a peripheral relationship although this effect is not clear. Both thyroid hormones and leptin might be involved in the adaptive thermogenesis through mitochondrial uncoupling proteins and heat production because both thyroxine and triiodothyronine are involved in the starvation-induced decrease in thermogenesis. Both rodent and human studies of leptin have failed to show any consistent relationship between thyroid function and serum leptin concentrations. However, leptin might have an important role in thyroid pathophysiology due to thyroid hormone involvement in thermogenesis and regulation of uncoupling proteins. In this review, we have focused on leptin in relation to thyroid pathophysiology.

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Rat thyroid gland expresses the long form of leptin receptors, and leptin stimulates the function of the gland in euthyroid non-fasted animals

Cited by 36 publications

References 0 publications

Withdrawal of dietary phytoestrogens in adult male rats affects hypothalamic regulation of food intake, induces obesity and alters glucose metabolism

Withdrawal of dietary phytoestrogens in adult male rats affects hypothalamic regulation of food intake, induces obesity and alters glucose metabolism

Endocrine effects of tobacco smoke exposure during lactation in weaned and adult male offspring

Circulating leptin and thyroid dysfunction

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