Acute and chronic leptin effect upon in vivo and in vitro rat thyroid iodide uptake

Oliveira, Elaine de; Fagundes, A. T. S.; Bonomo, I; Curty, F. H.; Passos, M. C. F.; Moura, Egberto Gaspar de; Lisboa, Patrícia Cristina

doi:10.1016/j.lfs.2007.08.030

Cited by 17 publications

(24 citation statements)

References 35 publications

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“…As already discussed, we did not detect any food intake change; therefore, it is possible that these animals presented hypothalamic leptin resistance to its anorexigenic effect. These data corroborate previous studies carried out by our group concerning other programing models , Bonomo et al 2007, in which BW changes were not accompanied by food intake alterations. Leptin and leptin receptors are both found in skeletal muscle (Wang et al 1998, Steinberg & Dyck 2000, Maroni et al 2003.…”

Section: Discussionsupporting

confidence: 92%

“…Since thyroid dysfunction is associated with marked changes on both energy expenditure and BW (Pontikides & Krassas 2007), it is interesting to evaluate the thyroid status in the model of programing by maternal NIC exposure during lactation. In addition, it seems likely that thyroid hormones and leptin play mutual roles (Ahima et al 1996, Escobar-Morreale et al 1997, Ortiga-Carvalho et al 2002, Rosenbaum et al 2002, De Oliveira et al 2007.…”

Section: Introductionmentioning

confidence: 99%

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Short- and long-term effects of maternal nicotine exposure during lactation on body adiposity, lipid profile, and thyroid function of rat offspring

Oliveira

Moura²,

Santos-Silva³

et al. 2009

Journal of Endocrinology

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Epidemiological studies show a higher prevalence of obesity in children from smoking mothers and smoking may affect human thyroid function. To evaluate the mechanism of smoking as an imprinting factor for these dysfunctions, we evaluated the programing effects of maternal nicotine (NIC) exposure during lactation. Two days after birth, osmotic minipumps were implanted in lactating rats, divided into: NIC (6 mg/kg per day s.c.) for 14 days; Control -saline. All the significant data were P!0 . 05 or less. Body weight was increased from 165 days old onwards in NIC offspring. Both during exposure (at 15 days old) and in adulthood (180 days old), NIC group showed higher total fat (27 and 33%). In addition, NIC offspring presented increased visceral fat and total body protein. Lipid profile was not changed in adulthood. Leptinemia was higher at 15 and 180 days old (36 and 113%), with no changes in food intake. Concerning the thyroid status, the 15-days-old NIC offspring showed lower serum-free tri-iodothyronine (FT 3 ) and thyroxine (FT 4 ) with higher TSH. The 180-days-old NIC offspring exhibited lower TSH, FT 3 , and FT 4 ). In both periods, liver type 1 deiodinase was lower (26 and 55%). We evidenced that NIC imprints a neonatal thyroid dysfunction and programs for a higher adiposity, hyperleptinemia, and secondary hypothyroidism in adulthood. Our study identifies lactation as a critical period to NIC programing for obesity, with hypothyroidism being a possible contributing factor.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Short- and long-term effects of maternal nicotine exposure during lactation on body adiposity, lipid profile, and thyroid function of rat offspring

Oliveira

Moura²,

Santos-Silva³

et al. 2009

Journal of Endocrinology

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“…Fetal Lepr is expressed in the human endothelium of umbilical veins and arteries (Akerman et al 2002). Other studies have shown that administration of leptin induces a threefold increase in leptinemia in both fetuses and adult animals (de Oliveira et al 2007, Su et al 2012. We found that fetal leptin administration induced a downregulation of Lepra expression in both the placenta and fetal liver from the control rats.…”

Section: Discussionsupporting

confidence: 52%

“…The concentration was chosen based on previous in vitro studies that showed the effects of 20 ng/ml (1 nM) leptin on fetal and placental lipid metabolism in fetuses (White et al 2004(White et al , 2007. In addition, similar studies have shown that a single s.c. administration of 80 ng leptin/g to adult rats induces a threefold increase in their leptinemia (de Oliveira et al 2007). Although the clearance rates of adults and fetuses are not the same, we estimate that leptin levels in the fetal circulation after leptin administration could increase up to twofold.…”

Section: Experimental Designmentioning

confidence: 74%

Saturated fat-rich diet increases fetal lipids and modulates LPL and leptin receptor expression in rat placentas

Mazzucco

Higa

Capobianco

et al. 2013

Journal of Endocrinology

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Metabolic alterations in obese and overweight mothers impact the placenta and the fetus, leading to anomalies in fetal growth and lipid accretion. The primary aim of the study was to examine the effect of a saturated fat-rich diet (FD) on growth, lipid accretion, and lipases, leptin and leptin receptor (ObR) expression in the placenta and fetal liver. We also aimed to find a role for fetal leptin in the modulation of placental and fetal liver lipase and ObR expression. Six-week-old rats were fed with a standard rat chow (control) or a 25% FD for 7 weeks until mating and during pregnancy. Also, in a group of control rats, fetuses were injected with leptin on days 19, 20, and 21 of pregnancy. On day 21, we assessed lipidemia, insulinemia, and leptinemia in mothers and fetuses. In the placenta and fetal liver, lipid concentration was assessed by thin layer chromatography (TLC) and the gene expression of lipoprotein lipase (LPL), endothelial lipase, insulin receptor (Insr), leptin, and ObR by RT-PCR. The FD induced hypertriglyceridemia and hyperleptinemia (P!0.01) in mothers and fetuses, an increase in maternal (P!0.05) and fetal weight (P!0.01), overaccumulation of lipids in fetal liver (P!0.01), and enhanced leptin expression in the placenta and fetal liver (P!0.05). Placental expression of IR and LPL was increased (P!0.05), and ObR decreased (P!0.05) in the FD group. Fetal administration of leptin induced the placental and fetal liver downregulation of ObR (P!0.05) and upregulation of LPL expression (P!0.05). The FD led to increased fetal lipid levels, which may result from high maternal lipid availability and fetal leptin effects. Key Words" Saturated fat-rich diet

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“…A subsequent study showed that thyroid 125 I uptake was not changed in rats receiving a single dose of leptin whereas rats receiving chronic leptin administration had a higher uptake (22). In human thyroid cancer, we have observed that leptin and leptin receptors are overexpressed in some surgical specimens of thyroid tumors (Cheng et al, unpublished data).…”

Section: Discussionmentioning

confidence: 94%

Differential roles of leptin in regulating cell migration in thyroid cancer cells

Chi¹

2010

Oncol Rep

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Abstract. Excess body weight is associated with a moderately increased risk of thyroid cancer. Adipocyte-derived hormone, leptin, has been shown to enhance cell growth and migration in many cancer types. Limited evidence suggests that leptin has direct actions on the thyroid gland, but there are no data available on the effect of leptin on thyroid cancer cells. We evaluated the action of leptin on gene expression, cell growth, cell cycle, and cell migration in anaplastic (ARO), follicular (WRO) and papillary (CGTH-W3) thyroid carcinoma cell lines. Expression of long-form leptin receptors was observed in all thyroid cancer cell lines. Leptin stimulation did not alter the expression levels of leptin, leptin receptor and sodiumiodide symporter. Cell growth and cell cycle were not changed after leptin treatment. However, leptin was able to promote cell migration of papillary thyroid cancer cells, but inhibited migration of anaplastic and follicular cancer cells. In summary, our study suggests that leptin modulates cell migration of thyroid cancer cells in a cell type-specific manner.

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Acute and chronic leptin effect upon in vivo and in vitro rat thyroid iodide uptake

Cited by 17 publications

References 35 publications

Short- and long-term effects of maternal nicotine exposure during lactation on body adiposity, lipid profile, and thyroid function of rat offspring

Short- and long-term effects of maternal nicotine exposure during lactation on body adiposity, lipid profile, and thyroid function of rat offspring

Saturated fat-rich diet increases fetal lipids and modulates LPL and leptin receptor expression in rat placentas

Differential roles of leptin in regulating cell migration in thyroid cancer cells

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