Thesis (Ph. D.)--University of Wisconsin--Madison, 1959. / Typescript. Abstracted in Dissertation abstracts, v. 19 (1959) no. 11, p. 2745-2746. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Orientador: Célia Regina Nogueira / Coorientador: Maria Teresa De Sibio / Banca: Patrícia Pinto Saraiva / Banca: Maria Isabel Chiamolera / Resumo: Na literatura é demonstrado que altos níveis de expressão de HIF-1α no CM humano estão relacionados à carcinogênese mamária e modificações moleculares decorrentes do processo de vascularização tumoral. Em trabalhos prévios do nosso grupo, demonstramos que a expressão de TGFα encontra-se aumentada nos tratamentos com T3, no entanto essa expressão não ocorre em modelos celulares que não apresentem o receptor de estrógeno ou quando as células são concomitantemente tratadas com antiestrogênio Tamoxifen. O objetivo do presente estudo é determinar a ação do hormônio T3 via extra-nuclear para a expressão dos genes HIF-1α e TGFα em linhagem celular de adenocarcinoma de mama MCF-7. A linhagem celular foi submetida ao tratamento com 10-8M de T3 nos tempos de 10', 30', 1h e 4h, na presença ou ausência dos inibidores Fulvestrant - inibidor de ER, Actinomicina D - inibidor da expressão gênica, Ciclohexamida - inibidor da síntese protéica, e LY294002 - inibidor da via PI3K. O mRNA de HIF-1α e TGFα foi analisado pela técnica de RT-PCR. Para a análise dos dados foi utilizado ANOVA complementado com teste de Tukey e adotado significância mínima de 5%. O presente trabalho confirma que a expressão gênica de HIF-1α e TGFα estão aumentadas na presença T3 nas células MCF-7 e em todos os tempos estudados. Ocorreu uma diminuição na expressão gênica de HIF-1α quando T3 está associado ao inibidor da transcrição gênica, no entanto para o gene TGFα a expressão gênica foi diminuída no tempo de 10', porém, o contrário foi observado a partir de 30' onde não houve diferença estatística com a inibição da transcrição gênica. Além disso, podemos sugerir que a ação de T3 sobre a expressão desses genes ocorre de forma indireta. A ativação da via PI3K pelo T3 é necessária para a modulação desses genes na linhagem estudada / Abstract: In the literature it has been demonstrated that high levels of expression of HIF-1α in human BC are related to mammary carcinogenesis and molecular changes resulting from the tumor vascularization process. In previous work from our group, we showed that the TGFα expression is increased upon treatments with T3, but this increase does not occur in cellular models devoid of the estrogen receptor or when the cells are concomitantly treated with the antiestrogen compound Tamoxifen. The objective of this study is to determine the extranuclear action of T3 hormone on HIF-1α and TGFα expression in MCF7 breast adenocarcinoma cell line. The cells were subjected to treatment with 10-8M T3 for 10', 30', 1h and 4h in the presence or absence of inhibitors Fulvestrant- ER inhibitor-, Actinomycin D - gene expression inhibitor -, cyclohexamide - protein synthesis inhibitor-, and LY294002 - PI3K inhibitor. The HIF-1α and TGFα mRNA expressions were analyzed by RT-PCR. For data analysis we used ANOVA complemented with Tukey test and adopted minimum 5% significance. The present study confirms that the gene expressions of HIF-1α and TGFα are increased in the presence of T3 in MCF-7 cells at all times studied. T3 represses HIF-1α at all time points assessed after inhibition of transcription, though for TGFα this effect was observed only at 10', after what no significant difference in its expression was detected, with inhibition of transcription. Furthermore, we suggest that the action of T3 on the expression of these genes occurs indirectly and occurs through activation of PI3K pathway, in the cell line studied / Mestre

Made available in DSpace on 2015-12-10T14:22:16Z (GMT). No. of bitstreams: 0 Previous issue date: 2015-02-27. Added 1 bitstream(s) on 2015-12-10T14:28:19Z : No. of bitstreams: 1 000849609_20160301.pdf: 669909 bytes, checksum: bd1857e74b2358391e3be46d5ba709b8 (MD5) Bitstreams deleted on 2016-03-02T17:37:25Z: 000849609_20160301.pdf,. Added 1 bitstream(s) on 2016-03-02T17:38:10Z : No. of bitstreams: 1 000849609.pdf: 2511879 bytes, checksum: 1123636262547a1ad0241984aa7ee9f4 (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / Na literatura é demonstrado que altos níveis de expressão de HIF-1α no CM humano estão relacionados à carcinogênese mamária e modificações moleculares decorrentes do processo de vascularização tumoral. Em trabalhos prévios do nosso grupo, demonstramos que a expressão de TGFα encontra-se aumentada nos tratamentos com T3, no entanto essa expressão não ocorre em modelos celulares que não apresentem o receptor de estrógeno ou quando as células são concomitantemente tratadas com antiestrogênio Tamoxifen. O objetivo do presente estudo é determinar a ação do hormônio T3 via extra-nuclear para a expressão dos genes HIF-1α e TGFα em linhagem celular de adenocarcinoma de mama MCF-7. A linhagem celular foi submetida ao tratamento com 10-8M de T3 nos tempos de 10', 30', 1h e 4h, na presença ou ausência dos inibidores Fulvestrant - inibidor de ER, Actinomicina D - inibidor da expressão gênica, Ciclohexamida - inibidor da síntese protéica, e LY294002 - inibidor da via PI3K. O mRNA de HIF-1α e TGFα foi analisado pela técnica de RT-PCR. Para a análise dos dados foi utilizado ANOVA complementado com teste de Tukey e adotado significância mínima de 5%. O presente trabalho confirma que a expressão gênica de HIF-1α e TGFα estão aumentadas na presença T3 nas células MCF-7 e em todos os tempos estudados. Ocorreu uma diminuição na expressão gênica de HIF-1α quando T3 está associado ao inibidor da transcrição gênica, no entanto para o gene TGFα a expressão gênica foi diminuída no tempo de 10', porém, o contrário foi observado a partir de 30' onde não houve diferença estatística com a inibição da transcrição gênica. Além disso, podemos sugerir que a ação de T3 sobre a expressão desses genes ocorre de forma indireta. A ativação da via PI3K pelo T3 é necessária para a modulação desses genes na linhagem estudada / In the literature it has been demonstrated that high levels of expression of HIF-1α in human BC are related to mammary carcinogenesis and molecular changes resulting from the tumor vascularization process. In previous work from our group, we showed that the TGFα expression is increased upon treatments with T3, but this increase does not occur in cellular models devoid of the estrogen receptor or when the cells are concomitantly treated with the antiestrogen compound Tamoxifen. The objective of this study is to determine the extranuclear action of T3 hormone on HIF-1α and TGFα expression in MCF7 breast adenocarcinoma cell line. The cells were subjected to treatment with 10-8M T3 for 10', 30', 1h and 4h in the presence or absence of inhibitors Fulvestrant- ER inhibitor-, Actinomycin D - gene expression inhibitor -, cyclohexamide - protein synthesis inhibitor-, and LY294002 - PI3K inhibitor. The HIF-1α and TGFα mRNA expressions were analyzed by RT-PCR. For data analysis we used ANOVA complemented with Tukey test and adopted minimum 5% significance. The present study confirms that the gene expressions of HIF-1α and TGFα are increased in the presence of T3 in MCF-7 cells at all times studied. T3 represses HIF-1α at all time points assessed after inhibition of transcription, though for TGFα this effect was observed only at 10', after what no significant difference in its expression was detected, with inhibition of transcription. Furthermore, we suggest that the action of T3 on the expression of these genes occurs indirectly and occurs through activation of PI3K pathway, in the cell line studied

Orientador: Célia Regina Nogueira / Banca: Maria Tereza Nunes / Resumo: A obesidade é uma doença crônica, multifatorial que leva ao aumento do risco de desenvolver outras doenças. É freqüentemente considerada como uma doença do estilo de vida, causada pela escolha errônea dos alimentos e pela diminuição da atividade física, sendo a restrição calórica a prática mais comum para tratar a obesidade. Em humanos, a perda de peso está associada com redução de fatores de risco para doenças cardiovasculares, diminuição da taxa de incidência de Diabetes Mellitus tipo 2 e aumento da qualidade de vida. O peso corporal é regulado por uma interação complexa entre hormônios e neuropeptídeos. A leptina e os hormônios tireoidianos (HT) estão envolvidos na regulação do balanço energético. Objetivo: Analisar, em ratos, a inter-relação entre leptina e hormônios tireoidianos na obesidade e na perda de peso. Metodologia: Foram utilizados ratos Wistar machos, com 30 dias de idade, separados em dois grupos, Controle (C) e Obeso (OB). Os animais C receberam ração comercial Labina e os do grupo OB um ciclo de dietas hipercalóricas por 15 semanas. Após o período de indução de obesidade, os animais OB foram novamente separados em outros 3 grupos, OB; animais com restrição alimentar (RIA); e animais com restrição mais administração de Hormônio Tireoidiano (RHT) na dose de 5 mg/100g de peso do animal. Os animais OB receberam as dietas hipercalóricas até o final do experimento, enquanto os animais RIA e RHT receberam 75% do total consumido pelo grupo C de dieta comercial, por 28 dias. Após este período, os animais RIA continuaram, somente, com a restrição alimentar e os RHT receberam além da restrição... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: Obesity is a chronic multifactor disease which brings increased risk of developing other diseases. It is frequently considered as a lifestyle disease, caused by choosing the wrong foods and reducing physical activity, with calorie restriction being the commonest way of treating it. Weight loss in humans is associated with reduced risk factors for cardiovascular disease, reduced incidence of type II Diabetes Mellitus, and increased quality of life. Bodyweight is regulated by a complex interaction between hormones and neopeptides. Leptin and the thyroid hormones (TH) are involved in regulating the energy balance. Objective: To analyze the interrelation in rats between leptin and thyroid hormones in obesity and weight loss. Methodology: Male 30-day-old Wistar rats were separated into two groups, Control (C) and Obese (OB). Control animals received commercial Labina rat food and the OB group a cycle of hypercaloric diets for 15 weeks. After the induced obesity period, the OB animals were separated into three subgroups; OB hypercaloric diet; RIA food restriction; RHT food restriction plus 5mg/100g body weight thyroid hormone. OB animals received the hypercaloric diets until the end of the experiment, where the RIA and RHT animals received 75% the total commercial food consumed by the control group for 28 days. After this period, the RIA animals continued with food restriction only, and the RHT animals received food restriction plus a dose of TH for 28 days. At each phase of the experiment, five animals from each group were sacrificed to analyze gene expression of leptin and TRb in adipose tissue using semiquantitative RT-PCR. Results: The OB animals showed increased weight and adipose tissue, lipid and glycemia profile changes, and increased plasmatic... (Complete abstract click electronic access below) / Mestre

Made available in DSpace on 2014-06-11T19:27:19Z (GMT). No. of bitstreams: 0 Previous issue date: 2007-02-27Bitstream added on 2014-06-13T19:55:47Z : No. of bitstreams: 1 luvizotto_ram_me_botfm.pdf: 645233 bytes, checksum: 378d843fc5ed20226d88f821c33714a2 (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / A obesidade é uma doença crônica, multifatorial que leva ao aumento do risco de desenvolver outras doenças. É freqüentemente considerada como uma doença do estilo de vida, causada pela escolha errônea dos alimentos e pela diminuição da atividade física, sendo a restrição calórica a prática mais comum para tratar a obesidade. Em humanos, a perda de peso está associada com redução de fatores de risco para doenças cardiovasculares, diminuição da taxa de incidência de Diabetes Mellitus tipo 2 e aumento da qualidade de vida. O peso corporal é regulado por uma interação complexa entre hormônios e neuropeptídeos. A leptina e os hormônios tireoidianos (HT) estão envolvidos na regulação do balanço energético. Objetivo: Analisar, em ratos, a inter-relação entre leptina e hormônios tireoidianos na obesidade e na perda de peso. Metodologia: Foram utilizados ratos Wistar machos, com 30 dias de idade, separados em dois grupos, Controle (C) e Obeso (OB). Os animais C receberam ração comercial Labina e os do grupo OB um ciclo de dietas hipercalóricas por 15 semanas. Após o período de indução de obesidade, os animais OB foram novamente separados em outros 3 grupos, OB; animais com restrição alimentar (RIA); e animais com restrição mais administração de Hormônio Tireoidiano (RHT) na dose de 5 mg/100g de peso do animal. Os animais OB receberam as dietas hipercalóricas até o final do experimento, enquanto os animais RIA e RHT receberam 75% do total consumido pelo grupo C de dieta comercial, por 28 dias. Após este período, os animais RIA continuaram, somente, com a restrição alimentar e os RHT receberam além da restrição... / Obesity is a chronic multifactor disease which brings increased risk of developing other diseases. It is frequently considered as a lifestyle disease, caused by choosing the wrong foods and reducing physical activity, with calorie restriction being the commonest way of treating it. Weight loss in humans is associated with reduced risk factors for cardiovascular disease, reduced incidence of type II Diabetes Mellitus, and increased quality of life. Bodyweight is regulated by a complex interaction between hormones and neopeptides. Leptin and the thyroid hormones (TH) are involved in regulating the energy balance. Objective: To analyze the interrelation in rats between leptin and thyroid hormones in obesity and weight loss. Methodology: Male 30-day-old Wistar rats were separated into two groups, Control (C) and Obese (OB). Control animals received commercial Labina rat food and the OB group a cycle of hypercaloric diets for 15 weeks. After the induced obesity period, the OB animals were separated into three subgroups; OB hypercaloric diet; RIA food restriction; RHT food restriction plus 5mg/100g body weight thyroid hormone. OB animals received the hypercaloric diets until the end of the experiment, where the RIA and RHT animals received 75% the total commercial food consumed by the control group for 28 days. After this period, the RIA animals continued with food restriction only, and the RHT animals received food restriction plus a dose of TH for 28 days. At each phase of the experiment, five animals from each group were sacrificed to analyze gene expression of leptin and TRb in adipose tissue using semiquantitative RT-PCR. Results: The OB animals showed increased weight and adipose tissue, lipid and glycemia profile changes, and increased plasmatic... (Complete abstract click electronic access below)

Orientador : Lucy Marie Ribeiro Muniz / Resumo: O hipertiroidismo é caracterizado pelo aumento das concentrações dos hormônios tiroideos, podendo levar a alterações cardiovasculares, hepáticas, renais, hematológicas, além de alterações de comportamento tanto em humanos quanto em animais. Neste estudo procurou-se investigar as alterações ultrasonográficas hepáticas produzidas pelo hipertiroidismo e correlacioná-las com os níveis séricos das enzimas hepáticas e achados citológicos e histológicos do fígado. Para tanto 20 gatos foram induzidos ao estado hipertiroideo pela administração de levotiroxina sódica, por via oral, na dose de 150 mg/kg, a cada 24 horas, durante 42 dias. Foram feitas avaliações ultra-sonográficas do fígado e colheitas de sangue semanais (M0 a M6), para dosagem das enzimas hepáticas e dos hormônios tiroideos, além de colheita de material para os exames citológicos e histológicos em M0, imediatamente antes do início da indução à tirotoxicose, e em M6, ao final do período experimental. Os resultados mostraram haver elevação das concentrações séricas de T4, livre e total, a partir da primeira semana experimental, no entanto os níveis de T3 total não sofreram alterações significativas. As enzimas hepáticas séricas também se apresentaram discretamente elevadas, porém sem significância estatística. Ocorreu correlação positiva entre os níveis séricos de TT4 e FT4, FT4 e FA, e ALT e AST... (Resumo completo, clicar acesso eletrônico abaixo). / Abstract: Hyperthyroidism is characterized by high concentrations of thyroid hormones, what may lead to cardiovascular, hepatic, renal and haematological alterations and behavioral changes in humans as well in animals. This study aimed to investigate ultrasonographic changes of liver parenchyma produced by hyperthyroidism and correlate them with serum hepatic enzymes levels and cytological and histological findings. Twenty cats were induced into hyperthyroid state by the administration, per oral, of 150 mg/kg dose of sodium L-thyroxine, each 24 hour, during 42 days. Sonographic evaluation of liver parenchyma and collection of blood samples were made weekly (M0-6), the last one to dose hepatic enzymes and thyroid hormones, besides collection of hepatic cells and tissue samples for cytological and histological analysis at M0, immediately before the beginning of the thyrotoxicosis induction, and M6, at the end of the experimental period. Results showed an increase on serum concentrations of total T4 and free T4 since the first week, however values for total T3 did not suffer significant variations. Serum hepatic enzymes also showed slight increase but not enough to be statistically significative. There was positive correlation between TT4 and FT4, FT4 and alkaline phosphatase (FA), and ALT and AST. Hyperthyroid state produced an hipoechoic liver pattern with progressive emergence of hyperecogenic periportal infiltration following TT4 curve. Cytological and histological findings although non specific at M6 suggested hepatitis. We could observe that changes on liver sonographic image preceded elevations on serum hepatic enzymes and occurred concomitant with alterations on TT4 and FT4 levels / Mestre

Orientador: Anderson Marliere Navarro / Banca: Vivian Marques Miguel Suen / Banca: Telma Maria Braga Costa / Banca: Thais Borges César / Banca: Maria Rita Marques de Oliveira / Resumo: A ingestão adequada de iodo durante a gestação é essencial para a síntese dos hormônios tireoidianos, que são importantes para as funções fisiológicas da mãe e para uma adequada maturação do sistema nervoso central do feto. Os efeitos da deficiência e/ou excesso de iodo são evidentes em todas as idades e se manifestam desde a fase fetal. O presente estudo teve como objetivo avaliar a excreção urinária de iodo, a função tireoidiana, e concentração séricas de antioxidantes e marcadores do estresse oxidativo em gestantes. Participaram do estudo 191 gestantes e 62 mulheres não gestantes que foram avaliadas segundo o estado nutricional e foram realizadas análises de iodo na urina, marcadores de estresse oxidativo e função tireoidiana. A partir das análises realizadas, foi observada insuficiência de iodo em 81 gestantes. Não houve alteração nas concentrações de TSH para 89% das gestantes. Os valores de anti-TPO foram superiores para o grupo controle em comparação com o grupo gestante (64,5% e 12,6%, respectivamente). Para o anti-TG, o grupo controle também apresentou valores maiores (11,6%). Não houve alteração significativa nos anticorpos quanto à sua classificação em relação aos valores de TSH e iodúria. A avaliação do estresse oxidativo revelou níveis de AOPP superiores para as gestantes e maiores níveis dos antioxidantes CAT e SOD. A classificação de iodúria com relação aos marcadores de estresse oxidativo revelou menores níveis de α-tocoferol para as gestantes com insuficiência de iodo. Sendo assim, os resultados sugerem que a insuficiência de iodo não foi capaz de induzir alterações nos níveis de TSH e anticorpos e que mulheres grávidas com excreção urinária de iodo adequada apresentaram melhor perfil do antioxidante α-tocoferol, indicando que o iodo pode desempenhar um papel significativo na capacidade antioxidante durante a gestação. / Abstract: Adequate intake of iodine during pregnancy is essential for synthesis of thyroid hormones, which are important for the physiological functions of the mother and proper maturation of the central nervous system of the fetus. The effects of disability and/or over are evident in all ages and manifest in the fetal stage. This study aimed to evaluate the urinary excretion levels of iodine, thyroid function and markers of oxidative stress in pregnant women. The study enrolled 191 pregnant women and 62 non-pregnant women who were evaluated according to the nutritional status and were held iodine analysis in urine, thyroid function and oxidative stress markers. From the analyzes, iodine deficiency was observed in 81 pregnant women. There was no change in TSH concentrations to 89% of pregnant women. The anti-TPO levels were higher in the control group compared to the pregnant group (64,5% and 12,6%, respectively). For anti-TG, the control group also showed higher values (11,6%). There was no significant change in antibodies and their classification about TSH levels and urinary iodine. Evaluation of oxidative stress revealed AOPP levels greater for pregnant women and higher levels of antioxidants SOD and CAT. Urinary iodine classification with respect to oxidative stress markers showed lower levels of α-tocopherol for pregnant women with iodine insufficiency. Thus, the results suggest that iodine deficiency was not able to induce altered levels of TSH and antibodies and pregnant women with urinary excretion of appropriate iodine showed a better profile of the α-tocopherol antioxidant, indicating that the iodine may play a role significant antioxidant capacity during pregnancy. / Doutor

As chickens hatch, there is a rapid change in their physiology and metabolism associated with attaining endothermy. It is thought that thyroid hormones (TH) play a major role in regulating developmental changes at hatching. In birds, TH regulates skeletal muscle growth, which has a direct impact on the chick's ability to thermoregulate via shivering thermogenesis. To better understand the role of TH in the timing of hatching, development of thermogenic capacity, and metabolic rate, we manipulated plasma TH levels in chicken embryos beginning at 85% development (day 17 of a 21 day incubation) with either thyroperoxidase inhibitor methimazole (MMI) or supplemental triiodothyronine (T3). After TH manipulation, we characterized O2 consumption and body temperature in the thermal neutral zone and during gradual cooling. Externally pipped embryos and 1 day post hatch (dph) chicks were cooled from 35 to 15°C. Manipulation of TH altered the timing of hatching, accelerating hatching under hyperthyroid conditions and decelerating hatching with hypothyroid conditions. Cohen's d revealed a large effect size on body temperature (Tb) of EP embryos of hypothyroid animals when compared to euthyroid animals in environmental temperatures of 32°C to 15°C, which was not seen in 1dph animals. Hyperthyroid EP animals were able to maintain metabolic rate over a wider range of ambient temperatures compared to control and hypothyroid animals, but these differences disappeared in 1dph animals. Here, we find that elevating TH levels prior to hatching accelerated hatching and the animal's thermogeneic ability to respond to cooling, but these differences disappear with age.

Thyroid hormones (THs) play a fundamental role in brain function during development and adulthood. THs are essential regulators of neurogenesis, cell maturation and migration as well myelination and synaptogenesis. Neuroglial cells, including astrocytes and microglia are targets of TH and implicated in TH regulation; however, the regulation is not properly understood at the cellular level. In this study, TH regulation was investigated in vitro using human brain cell lines of astrocytes (Svg-P12) and microglia (HMC3). The cells were exposed to TH receptor agonist (triiodothyronine; T3) and inhibitors (amiodarone/1-850), of different concentrations, followed by RNA extraction and quantitative PCR. The gene expression of known TH regulated genes was studied for a better understanding of TH signaling in astrocytes and microglia. All target genes were successfully measured in both cell types. Interestingly, the regulatory effects of TH in astrocytes and microglia exhibited differences. In astrocytes, T3 exposure resulted in an upregulation in gene expression of DDX54 (DEAD-Box Helicase 54) and KLF9 (Krüppel-like factor 9) but did not affect other genes. Also, THR inhibitor exposure resulted in n upregulation in gene expression of DDX54 (DEAD-Box Helicase 54) and KLF9 (Krüppel-like factor 9) but did not affect other genes. Also, THR inhibitor exposure resulted in downregulation in gene expression of KLF9, NES (Nestin), PTGDS (Prostaglandin D2 Synthase) and MAPT (Microtubule Associated Protein Tau). In contrast, none of the TH regulated genes demonstrated a statistical significance in T3-treated microglia compared to control cells. However, THR inhibitor exposure resulted in a downregulation in gene expression of KLF9 and DDX54 and an upregulation of NES, PTGDS and MAPT. The observed differences indicate that TH signaling and regulation is different in microglia and astrocytes. The The differential signaling suggests that T3 does not regulate all of its target genes directly; rather, the regulatory effects of T3 may be exerted through complex mechanisms with other key factors involved. It can be concluded that astrocytes and microglia play important roles as mediators of the effects of THs in CNS development and function. However, further analysis is needed to acknowledge other key factors and TH signaling mechanisms influencing the gene expression in neuroglia.

Three experiments were conducted to determine the effect of energy, protein, sex, and time on serum T4 and T3 concentrations. All sampling periods occurred at 28-day intervals. In the first experiment, (March-February) 7 adult bucks were placed on 2 feed levels, ad libitum or 25% restricted. Feed consumption of ad libitum deer was highest (P≤0.05) from June-October, fell in November, and remained low through March. Body weights of both groups were highest (P≤0.05) from September-October; lowest from March-April. Serum T4 was highest (P≤0.05) in May and July, and lowest in November. From November-February, restricted deer had lower T4 concentrations (P<0.01) than did ad libitum deer. Serum T3 was highest from May-August; lowest in November. Ad libitum had higher T3 concentrations (P<0.01) than the restricted animals. The second experiment compared the effects of energy and protein on body weight, and serum T4 and T3 of 24 fawns (12 male) from October-May. Feed intake fell gradually to low levels maintained from January-March, then increased slightly. Body weight gain was initially rapid (P<0.01), minimal from November-March, and slow through May. Serum T4 was highest in late April; lowest in October and February. Maximum serum T3 concentrations occurred in April; lowest values in February. Females had higher T4 and T3 values than did males. The third experiment involved 1 adult buck. Blood samples were drawn every 2 hours for a 24-hour period via a jugular catheter. Serum T4 and T3 concentrations were highest from 1600-2000 hours (EST), lowest at 1000 hours. / M.S.