Search Results
You are looking at 1 - 7 of 7 items for
- Author: Elaine de Oliveira x
- Refine by access: All content x
Search for other papers by Patricia C Lisboa in
Google Scholar
PubMed
Search for other papers by Ellen P S Conceição in
Google Scholar
PubMed
Search for other papers by Elaine de Oliveira in
Google Scholar
PubMed
Search for other papers by Egberto G Moura in
Google Scholar
PubMed
Early overnutrition (EO) during lactation leads to obesity, leptin resistance and lower thyroid hormone (TH) levels during adulthood. To better understand the biological significance of this thyroid hypofunction, we studied the long-term effects of postnatal EO on both the function of hypothalamic–pituitary–thyroid (HPT) axis and the metabolism and action of TH. To induce EO, the litter size was reduced to three pups per litter (small litter (SL) group) on the third day of lactation. In the controls (normal litter group), litter size was adjusted to 10 pups per litter. Rats were killed at PN180. TRH content and in vitro TSH were evaluated. Iodothyronine deiodinase (D1 and D2) activities were measured in different tissues. Mitochondrial α-glycerol-3-phosphate dehydrogenase (mGPD), uncoupling protein 1 (UCP1) and TH receptor (TRβ1) were evaluated to assess TH action. The SL group presented lower TRH, intra-pituitary and released TSH levels, despite unchanged plasma TSH. They presented lower D1 activity in thyroid, muscle and white adipose tissue (WAT) and higher D2 activity in the hypothalamus, pituitary, brown adipose tissue (BAT) and WAT, which confirmed the hypothyroidism. UCP1 in BAT and TRβ1 in WAT were decreased, which can contribute to a lower catabolic status. Despite the lower TH, the D2 activity in the thyroid, heart and testes was unchanged. Hepatic D1, mGPD and TRβ1 were also unchanged in SL rats, suggesting that the TH conversion and action were preserved in the liver, even with lower TH. Thus, this model indicates that postnatal EO changes thyroid function in adult life in a tissue-specific way, which can help in the understanding of obesogenesis.
Search for other papers by Rosemari Otton in
Google Scholar
PubMed
Search for other papers by Danielly Oliveira da Silva in
Google Scholar
PubMed
Search for other papers by Thais Regina Campoio in
Google Scholar
PubMed
Search for other papers by Leonardo R Silveira in
Google Scholar
PubMed
Search for other papers by Maria Oliveira de Souza in
Google Scholar
PubMed
Search for other papers by Elaine Hatanaka in
Google Scholar
PubMed
Search for other papers by Rui Curi in
Google Scholar
PubMed
Search for other papers by Rosemari Otton in
Google Scholar
PubMed
Search for other papers by Danielly Oliveira da Silva in
Google Scholar
PubMed
Search for other papers by Thais Regina Campoio in
Google Scholar
PubMed
Search for other papers by Leonardo R Silveira in
Google Scholar
PubMed
Search for other papers by Maria Oliveira de Souza in
Google Scholar
PubMed
Search for other papers by Elaine Hatanaka in
Google Scholar
PubMed
Search for other papers by Rui Curi in
Google Scholar
PubMed
Search for other papers by Rosemari Otton in
Google Scholar
PubMed
Search for other papers by Danielly Oliveira da Silva in
Google Scholar
PubMed
Search for other papers by Thais Regina Campoio in
Google Scholar
PubMed
Search for other papers by Leonardo R Silveira in
Google Scholar
PubMed
Search for other papers by Maria Oliveira de Souza in
Google Scholar
PubMed
Search for other papers by Elaine Hatanaka in
Google Scholar
PubMed
Search for other papers by Rui Curi in
Google Scholar
PubMed
Search for other papers by Rosemari Otton in
Google Scholar
PubMed
Search for other papers by Danielly Oliveira da Silva in
Google Scholar
PubMed
Search for other papers by Thais Regina Campoio in
Google Scholar
PubMed
Search for other papers by Leonardo R Silveira in
Google Scholar
PubMed
Search for other papers by Maria Oliveira de Souza in
Google Scholar
PubMed
Search for other papers by Elaine Hatanaka in
Google Scholar
PubMed
Search for other papers by Rui Curi in
Google Scholar
PubMed
Search for other papers by Elaine Cristina Lima de Souza in
Google Scholar
PubMed
Search for other papers by Álvaro Souto Padrón in
Google Scholar
PubMed
Search for other papers by William Miranda Oliveira Braga in
Google Scholar
PubMed
Search for other papers by Bruno Moulin de Andrade in
Google Scholar
PubMed
Search for other papers by Mário Vaisman in
Google Scholar
PubMed
Search for other papers by Luiz Eurico Nasciutti in
Google Scholar
PubMed
Search for other papers by Andrea Claudia Freitas Ferreira in
Google Scholar
PubMed
Search for other papers by Denise Pires de Carvalho in
Google Scholar
PubMed
Phosphoinositide-3-kinase (PI3K) inhibition increases functional sodium iodide symporter (NIS) expression in both FRTL-5 rat thyroid cell line and papillary thyroid cancer lineages. In several cell types, the stimulation of PI3K results in downstream activation of the mechanistic target of rapamycin (MTOR), a serine–threonine protein kinase that is a critical regulator of cellular metabolism, growth, and proliferation. MTOR activation is involved in the regulation of thyrocyte proliferation by TSH. Here, we show that MTOR inhibition by rapamycin increases iodide uptake in TSH-stimulated PCCL3 thyroid cell line, although the effect of rapamycin was less pronounced than PI3K inhibition. Thus, NIS inhibitory pathways stimulated by PI3K might also involve the activation of proteins other than MTOR. Insulin downregulates iodide uptake and NIS protein expression even in the presence of TSH, and both effects are counterbalanced by MTOR inhibition. NIS protein expression levels were correlated with iodide uptake ability, except in cells treated with TSH in the absence of insulin, in which rapamycin significantly increased iodide uptake, while NIS protein levels remained unchanged. Rapamycin avoids the activation of both p70 S6 and AKT kinases by TSH, suggesting the involvement of MTORC1 and MTORC2 in TSH effect. A synthetic analog of rapamycin (everolimus), which is clinically used as an anticancer agent, was able to increase rat thyroid iodide uptake in vivo. In conclusion, we show that MTOR kinase participates in the control of thyroid iodide uptake, demonstrating that MTOR not only regulates cell survival, but also normal thyroid cell function both in vitro and in vivo.
Search for other papers by Elaine de Oliveira in
Google Scholar
PubMed
Search for other papers by Egberto G Moura in
Google Scholar
PubMed
Search for other papers by Ana Paula Santos-Silva in
Google Scholar
PubMed
Search for other papers by Cíntia R Pinheiro in
Google Scholar
PubMed
Search for other papers by Natalia S Lima in
Google Scholar
PubMed
Search for other papers by José Firmino Nogueira-Neto in
Google Scholar
PubMed
Search for other papers by Andre L Nunes-Freitas in
Google Scholar
PubMed
Search for other papers by Yael Abreu-Villaça in
Google Scholar
PubMed
Search for other papers by Magna C F Passos in
Google Scholar
PubMed
Search for other papers by Patrícia C Lisboa in
Google Scholar
PubMed
Maternal nicotine (NIC) exposure during lactation leads to overweight, hyperleptinemia, and hypothyroidism in adult rat offspring. In this model, we analyzed adipocyte morphology, glucose homeostasis (serum insulin and adiponectin; liver and muscle glycogen), serum lipid, and the leptin signaling pathway. After birth, osmotic minipumps were implanted in lactating rats, which were divided into the groups NIC (6 mg/kg per day s.c. for 14 days) and control (C, saline). NIC and C offspring were killed at the age of 180 days. Adult NIC rats showed higher total body fat (+10%, P<0.05), visceral fat mass (+12%, P<0.05), and cross-sectional area of adipocytes (epididymal: +12% and inguinal: +43%, P<0.05). Serum lipid profile showed no alteration except for apolipoprotein AI, which was lower. We detected a lower adiponectin:fat mass ratio (−24%, P<0.05) and higher insulinemia (+56%, P<0.05), insulin resistance index (+43%, P<0.05), leptinemia (+113%, P<0.05), and leptin:adiponectin ratio (+98%, P<0.05) in the adult NIC group. These rats presented lower hypothalamic contents of the proteins of the leptin signaling pathway (leptin receptor (OB-R): −61%, janus tyrosine kinase 2: −41%, and p-signal transducer and activator of transcription 3: −56%, P<0.05), but higher suppressor of cytokine signaling 3 (+81%, P<0.05). Therefore, NIC exposure only during lactation programs rats for adipocyte hypertrophy in adult life, as well as for leptin and insulin resistance. Through the effects of NIC, perinatal maternal cigarette smoking may be responsible for the future development of some components of the metabolic syndrome in the offspring.
