ABSTRACT
Myoglobin acts as an oxygen store and a reactive oxygen species acceptor in muscles. We examined myoglobin mRNA in rat cardiac ventricle and skeletal muscles during the first 42 days of life and the impact of transient neonatal hypo- and hyperthyroidism on the myoglobin gene expression pattern. Cardiac ventricle and skeletal muscles of Wistar rats at 7-42 days of life were quickly removed, and myoglobin mRNA was determined by Northern blot analysis. Rats were treated with propylthiouracil (5-10 mg/100 g) and triiodothyronine (0.5-50 µg/100 g) for 5, 15, or 30 days after birth to induce hypo- and hyperthyroidism and euthanized either just after treatment or at 90 days. During postnatal (P) days 7-28, the ventricle myoglobin mRNA remained unchanged, but it gradually increased in skeletal muscle (12-fold). Triiodothyronine treatment, from days P0-P5, increased the skeletal muscle myoglobin mRNA 1.5- to 4.5-fold; a 2.5-fold increase was observed in ventricle muscle, but only when triiodothyronine treatment was extended to day P15. Conversely, hypothyroidism at P5 markedly decreased (60%) ventricular myoglobin mRNA. Moreover, transient hyperthyroidism in the neonatal period increased ventricle myoglobin mRNA (2-fold), and decreased heart rate (5%), fast muscle myoglobin mRNA (30%) and body weight (20%) in adulthood. Transient hypothyroidism in the neonatal period also permanently decreased fast muscle myoglobin mRNA (30%) and body weight (14%). These results indicated that changes in triiodothyronine supply in the neonatal period alter the myoglobin expression program in ventricle and skeletal muscle, leading to specific physiological repercussions and alterations in other parameters in adulthood.
Subject(s)
Animals , Male , Hyperthyroidism/metabolism , Hypothyroidism/metabolism , Muscle, Skeletal/metabolism , Myocardium/metabolism , Myoglobin/genetics , RNA, Messenger/metabolism , Animals, Newborn , Antithyroid Agents , Blood Pressure , Blotting, Northern , Gene Expression , Heart Rate , Heart Ventricles/metabolism , Hyperthyroidism/chemically induced , Hypothyroidism/chemically induced , Myoglobin/metabolism , Organ Size , Propylthiouracil , Random Allocation , Rats, Wistar , Reactive Oxygen Species , TriiodothyronineABSTRACT
Differently from most hormones, which commonly are specialized molecules able to influence other cells, tissues and systems, thyroid hormones (TH) are pleiotropic peptides, whose primordial function is difficult to identify. The complex action of TH on human economy can be easily witnessed by examining the diverse consequences of TH excess and deficiency during development and after maturity. In particular, different manifestations in bone modeling and remodeling reflect the circumstantial consequences of thyroid disturbances, which are age dependent. While hyperthyroidism during childhood enhances bone mineralization and accelerates epiphyseal maturation, in adults it induces bone loss by predominant activation of osteoclast activity. Furthermore, the syndrome of TH resistance is a multifaceted condition in which different sites exhibit signs of hormone excess or deficiency depending on the configuration of the TH receptor isoform. The investigation of the impact of TH resistance on the skeleton still remains to be elucidated. We present here a thorough review of the action of TH on bone and of the impact of thyroid disorders, including hyper- and hypothyroidism and the syndrome of TH resistance, on the skeleton.
Diferentemente da maioria dos hormônios, que usualmente são moléculas especializadas capazes de influenciar outras células, tecidos e sistemas, os hormônios da tireoide (HT) são peptídeos pleiotrópicos, cuja função primordial é difícil de identificar. A ação complexa dos HT na fisiologia humana pode ser facilmente reconhecida ao observar as diversas consequências do excesso e da deficiência de HT durante e após o pleno desenvolvimento. Em particular as diferentes manifestações na modelação e remodelação óssea refletem que as consequências esqueléticas das disfunções tireoidianas dependem das circunstâncias e variam com a idade. Enquanto o hipertireoidismo durante a infância aumenta a mineralização óssea e acelera a maturação epifisária, em adultos induz a perda óssea pela ativação predominante da ação osteoclástica. Além disso, a síndrome de resistência ao HT é uma condição multifacetada na qual diferentes tecidos apresentam sinais de excesso ou deficiência hormonal, dependendo da predominância da expressão das diversas isoformas do receptor de HT. O impacto da resistência ao HT sobre o esqueleto ainda é motivo de investigação. Apresentamos aqui uma revisão abrangente sobre as ações ósseas dos HT e o impacto no esqueleto dos distúrbios da tireoide, incluindo hipo e hipertireoidismo e síndrome de resistência ao HT.
Subject(s)
Animals , Humans , Bone and Bones/metabolism , Hypothyroidism/metabolism , Minerals/metabolism , Thyroid Hormone Resistance Syndrome/metabolism , Thyrotoxicosis/metabolism , Calcification, Physiologic/physiology , Calcium/metabolism , Databases, Bibliographic , Epiphyses/growth & development , Osteoclasts/metabolism , Osteoporosis/etiology , Phosphorus/metabolism , Thyroid Diseases/metabolism , Thyrotoxicosis/complications , Thyroxine/metabolism , Triiodothyronine/metabolismABSTRACT
The actions of thyroid hormone (TH) on pancreatic beta cells have not been thoroughly explored, with current knowledge being limited to the modulation of insulin secretion in response to glucose, and beta cell viability by regulation of pro-mitotic and pro-apoptotic factors. Therefore, the effects of TH on proinsulin gene expression are not known. This led us to measure: a) proinsulin mRNA expression, b) proinsulin transcripts and eEF1A protein binding to the actin cytoskeleton, c) actin cytoskeleton arrangement, and d) proinsulin mRNA poly(A) tail length modulation in INS-1E cells cultured in different media containing: i) normal fetal bovine serum - FBS (control); ii) normal FBS plus 1 µM or 10 nM T3, for 12 h, and iii) FBS depleted of TH for 24 h (Tx). A decrease in proinsulin mRNA content and attachment to the cytoskeleton were observed in hypothyroid (Tx) beta cells. The amount of eEF1A protein anchored to the cytoskeleton was also reduced in hypothyroidism, and it is worth mentioning that eEF1A is essential to attach transcripts to the cytoskeleton, which might modulate their stability and rate of translation. Proinsulin poly(A) tail length and cytoskeleton arrangement remained unchanged in hypothyroidism. T3 treatment of control cells for 12 h did not induce any changes in the parameters studied. The data indicate that TH is important for proinsulin mRNA expression and translation, since its total amount and attachment to the cytoskeleton are decreased in hypothyroid beta cells, providing evidence that effects of TH on carbohydrate metabolism also include the control of proinsulin gene expression.
Subject(s)
Animals , Cattle , Rats , Actin Cytoskeleton/metabolism , Eukaryotic Initiation Factor-1/metabolism , Hypothyroidism/metabolism , Insulin-Secreting Cells/metabolism , Proinsulin/genetics , RNA, Messenger/metabolism , Gene Expression , Hypothyroidism/genetics , Proinsulin/biosynthesis , RNA, Messenger/geneticsABSTRACT
A 15-mth-old male child of consanguineous parents, presented with classical features of congenital hypothyroidism. Serum total thyroxine (T4), total triiodothyronine (T3) and TSH were low. There was no evidence of deficiency of other pituitary hormones. Magnetic resonance imaging of the pituitary was normal. TSHB gene sequencing revealed a homozygous missense mutation due to single base substitution G?A at codon 85 resulting in change from Glycine to Arginine. This mutation in TSHB gene has been reported earlier in three cases with similar phenotype from Japan.
Subject(s)
Brain/pathology , Humans , Hypothyroidism/genetics , Hypothyroidism/metabolism , Hypothyroidism/pathology , Infant , Magnetic Resonance Imaging , Male , Mutation, Missense/genetics , Thyrotropin, beta Subunit/genetics , Thyroxine/metabolism , Triiodothyronine/metabolismABSTRACT
O hipotireoidismo congênito (HC) é uma das doenças metabólicas mais comuns na infância, com incidência de HC é de 1:3.000 a 1:5.000 nascidos-vivos. Quando primário, o HC caracteriza-se por altos níveis de TSH podendo ser originado por disormonogênese, deficiente produção hormonal ou decorre de disgenesia tireoidiana, defeito embriológico que leva a agenesia, hemiagenesia ou ectopia. Na ausência do tratamento hormonal, o HC leva a grave retardo mental, além de outras alterações clínicas. A interação do hormônio TSH com o seu receptor (TSHR) tem importante função biológica estimulando o crescimento, diferenciação e função tireoidiana. Mutações no gene do TSHR têm sido identificadas como causa de HC hereditário ou congênito, mas parecem ser raras. Objetivos: 1) Obter genealogia das famílias afetadas para determinação do padrão de herança, identificação de afetados e possíveis portadores; 2) Descrever as características clínica- emográficas dos pacientes com HC; 3) Determinar a distribuição mutacional no gene do receptor do hormônio estimulante da tireoide (TSHR) nos afetados; 4) Sugerir ações de saúde pública e de otimização do aconselhamento genético. Foram estudados 12 pacientes provenientes de Monte Santo-BA, sendo oito diagnosticados pela triagem neonatal e quatro diagnosticados tardiamente durante expedição à cidade. Estes últimos foram identificados durante a coleta dos dados genealógicos das famílias dos afetados. Todos foram investigados para mutações no gene do TSHR. Toda a região codificadora do gene foi amplificada através do DNA genômico, seguido de SSCP e sequenciamento. À época da primeira avaliação, os pacientes apresentaram níveis elevados de TSH, confirmando o caráter primário da doença, associados a sinais e sintomas do HC. Observou-se grande heterogeneidade clínica entre os pacientes mesmo aqueles com grau de parentesco muito próximo. Nenhuma mutação patogênica foi encontrada no gene TSHR. Conclusão: a análise das genealogias permitiu observar a heterogeneidade clínica e genética da doença. Não foi encontrada nenhuma mutação no gene TSHR. O estudo de outros genes poderá ajudar no esclarecimento do HC na região.
Subject(s)
Humans , Thyroid Diseases/pathology , Hypothyroidism/metabolism , Mutation/genetics , Receptors, Antigen, T-Cell, gamma-delta/immunologyABSTRACT
INTRODUCTION: Severe cognitive impairment follows thyroid hormone deficiency during the neonatal period. The role of nitric oxide (NO) in learning and memory has been widely investigated. METHODS: This study aimed to investigate the effect of hypothyroidism during neonatal and juvenile periods on NO metabolites in the hippocampi of rats and on learning and memory. Animals were divided into two groups and treated for 60 days from the first day of lactation. The control group received regular water, whereas animals in a separate group were given water supplemented with 0.03 percent methimazole to induce hypothyroidism. Male offspring were selected and tested in the Morris water maze. Samples of blood were collected to measure the metabolites of NO, NO2, NO3 and thyroxine. The animals were then sacrificed, and their hippocampi were removed to measure the tissue concentrations of NO2 and NO3. DISCUSSION: Compared to the control group's offspring, serum thyroxine levels in the methimazole group's offspring were significantly lower (P<0.01). In addition, the swim distance and time latency were significantly higher in the methimazole group (P<0.001), and the time spent by this group in the target quadrant (Q1) during the probe trial was significantly lower (P<0.001). There was no significant difference in the plasma levels of NO metabolites between the two groups; however, significantly higher NO metabolite levels in the hippocampi of the methimazole group were observed compared to controls (P<0.05). CONCLUSION: These results suggest that the increased NO level in the hippocampus may play a role in the learning and memory deficits observed in childhood hypothyroidism; however, the precise underlying mechanism(s) remains to be elucidated.
Subject(s)
Animals , Female , Rats , Hippocampus/metabolism , Hypothyroidism/metabolism , Learning Disabilities/metabolism , Memory Disorders/metabolism , Nitric Oxide/metabolism , Antithyroid Agents , Hypothyroidism/chemically induced , Methimazole , Nitric Oxide Synthase/metabolism , Nitric Oxide/blood , Rats, Wistar , Time Factors , Thyroxine/analysisABSTRACT
Apoptose, proliferação e histomorfometria do baço foram investigados em ratas Wistar adultas ovariectomizadas e não-ovariectomizadas, mantidas em hipotireoidismo induzido pela administração diária de propiltiouracil (PTU) por 120 dias. Dois grupos eutireóideos ovariectomizados e não-ovariectomizados serviram como controle. Foi colhido o plasma para dosagem de T4 livre e o baço para análise da histomorfometria, do índice apoptótico e da expressão imunohistoquímica de caspase 3 e CDC47. Valores de T4 livre foram menores nas ratas tratadas com PTU (p < 0,05). Nos grupos hipotireóideos houve redução do peso do baço, do número e do tamanho dos folículos linfóides e aumento do índice apoptótico e da expressão de caspase 3 (p < 0,05). Porém, o baço de ratas hipotireóideas ovariectomizadas apresentou aumento menos acentuado do índice apoptótico e da expressão de caspase 3 do que o baço de ratas hipotireóideas não-ovariectomizadas (p < 0,05). O grupo eutireóideo ovariectomizado apresentou hiperplasia da polpa branca em relação ao grupo eutireóideo não-ovariectomizado. Não houve diferença na expressão de CDC47 entre os grupos. Conclui-se que a hipofunção tireoidiana e gonadal apresentam efeitos distintos no baço e que na associação hipotireoidismo-hipogonadismo há aumento menos acentuado do índice apoptótico e da expressão de caspase-3 esplênica do que no hipotireoidismo isolado.
Apoptosis, proliferation and histomorphometry of spleen were investigated in ovariectomized and non-ovariectomized adult Wistar rats maintained in hypothyroidism induced by daily administration of propylthiouracil (PTU) during 120 days. Two groups ovariectomized euthyroid and non-ovariectomized euthyroid were used as controls. Plasma was collected for free T4 dosage and the spleen for histomorphometry analysis, apoptosis index and the immunohistochemistry expression of caspase 3 and CDC47. Values of free T4 were lower in rats treated with PTU (p<0.05). In the hypothyroid groups there was some decrease in the spleen weight as well as the number and size of lymphoid follicles and there was some increase in the apoptotic index and the caspase 3 expression (p<0.05). However, the increase in the apoptosis index and the expression of caspase 3 in ovariectomized hypothyroid rats spleen was less accentuated than non-ovariectomized hypothyroid ones (p<0.05). The ovariectomized euthyroid group presented white pulp hyperplasia in comparison to the non-ovariectomized euthyroid group. There was no difference in the CDC47 expression between groups. It was concluded that the thyroid and ovarian hypofunction have distinct effects on the spleen and that in the hypothyroidism-hypogonadism association, the increase in the apoptosis index and in the expression of splenic caspase 3 is not as much as in isolated hypothyroidism.
Subject(s)
Animals , Female , Rats , Apoptosis , Cell Proliferation , Hypothyroidism/metabolism , Ovariectomy , Spleen , Thyroid Gland/metabolism , Antithyroid Agents , Adenosine Triphosphatases/analysis , Adenosine Triphosphatases/metabolism , /analysis , /metabolism , Disease Models, Animal , DNA-Binding Proteins/analysis , DNA-Binding Proteins/metabolism , Hypogonadism/metabolism , Hypothyroidism/blood , Hypothyroidism/chemically induced , Lymphoid Tissue/metabolism , Lymphoid Tissue/pathology , Propylthiouracil , Rats, Wistar , Spleen/cytology , Spleen/metabolism , Spleen/pathology , Thyroid Gland/cytology , Thyroxine/bloodABSTRACT
O estado somatotrófico é modulador importante dos eixos tirotrófico e corticotrófico. Enquanto a reposição somatotrófica em pacientes com deficiência de GH aumenta a conversão do hormônio inativo (T4) na sua forma ativa (T3), aumentando dessa forma a ação biológica do hormônio tireoidiano, a mesma reposição induz no eixo corticotrófico a conversão de cortisol, hormonalmente ativo, em cortisona, que é biologicamente inativa. Nessa revisão, foram discutidos os efeitos do GH nesses dois eixos hormonais, os possíveis mecanismos e as implicações clínicas no manejo dos pacientes com hipopituitarismo.
Somatotrophic status is a major determinant of both thyrotrophic and corticotrophic axis. In growth hormone deficient patients, somatotrophic replacement increases the conversion rate of the inactive form of the thyroid hormone (T4) to its active form (T3), whereas the same replacement induces the conversion of cortisol, which is hormonally active, in cortisone, its inactive form. This review details the effects of GH on these two hormonal axis, possible mechanisms and clinical implications for the management of hypopituitary patients.
Subject(s)
Humans , Adrenal Glands/metabolism , Human Growth Hormone/therapeutic use , Hypothyroidism/drug therapy , Thyroid Gland/metabolism , Human Growth Hormone/deficiency , Hypothyroidism/metabolism , Thyroxine/metabolism , Triiodothyronine/metabolismABSTRACT
The effect of the hormones triiodothyronine (T3) and melatonin on antioxidant defense system was studied in 6-propyl thiouracil (6-PTU)-treated or photoperiod-exposed teleost Anabas testudineus. 6-PTU (2 microg/g) treatment or photoperiod exposure (24 h) increased malondialdehyde (MDA) and conjugated dienes (CD) concentrations, indicating increased lipid peroxidation (LPO) in the experimental conditions. T3 or melatonin (10(-6) M) treatment for 15 min in vitro in PTU-treated fish reversed the activity of superoxide dismutase (SOD), catalase and glutathione content. T3-treated group showed no change in glutathione peroxidase (GPx) activity, whereas melatonin treatment decreased its activity. T3 inhibited glutathione reductase (GR) activity. Photoperiod exposure (physiological pinealotomy) induced a stressful situation in this teleost, as evidenced by LPO products and antioxidant enzyme activities. Melatonin and T3 treatment for 15 min in vitro also reversed the effect of photoperiod on peroxidation products and the SOD and catalase activities. GR activity decreased in photoperiod-exposed group and melatonin and T3 treatment reversed the activities. The antioxidant enzymes responded to the stress situation after 6-PTU treatment and photoperiod exposure by altering their activities. The study suggested an independent effect of T3 and melatonin on antioxidant defence mechanism in different physiological situations in fish.
Subject(s)
Animals , Antioxidants/metabolism , Fishes , Free Radicals , Glutathione Peroxidase/metabolism , Hypothyroidism/metabolism , Light , Lipid Peroxidation , Liver/metabolism , Melatonin/metabolism , Pineal Gland/metabolism , Propylthiouracil/chemistry , Thyroid Gland/metabolism , Triiodothyronine/pharmacologyABSTRACT
Insulin receptor substrate-1 (IRS-1) is the main intracellular substrate for both insulin and insulin-like growth factor I (IGF-I) receptors and is critical for cell mitogenesis. Thyrotropin is able to induce thyroid cell proliferation through the cyclic AMP intracellular cascade; however, the presence of either insulin or IGF-I is required for the mitogenic effect of thyroid-stimulating hormone (TSH) to occur. The aim of the present study was to determine whether thyroid IRS-1 content is modulated by TSH in vivo. Strikingly, hypothyroid goitrous rats, which have chronically high serum TSH levels (control, C = 2.31 ± 0.28; methimazole (MMI) 21d = 51.02 ± 6.02 ng/mL, N = 12 rats), when treated with 0.03 percent MMI in drinking water for 21 days, showed significantly reduced thyroid IRS-1 mRNA content. Since goiter was already established in these animals by MMI for 21 days, we also evaluated IRS-1 expression during goitrogenesis. Animals treated with MMI for different periods of time showed a progressive increase in thyroid weight (C = 22.18 ± 1.21; MMI 5d = 32.83 ± 1.48; MMI 7d = 31.1 ± 3.25; MMI 10d = 33.8 ± 1.25; MMI 14d = 45.5 ± 2.56; MMI 18d = 53.0 ± 3.01; MMI 21d = 61.9 ± 3.92 mg, N = 9-15 animals per group) and serum TSH levels (C = 1.57 ± 0.2; MMI 5d = 9.95 ± 0.74; MMI 7d = 10.38 ± 0.84; MMI 10d = 17.72 ± 1.47; MMI 14d = 25.65 ± 1.23; MMI 18d = 35.38 ± 3.69; MMI 21d = 31.3 ± 2.7 ng/mL, N = 9-15 animals per group). Thyroid IRS-1 mRNA expression increased progressively during goitrogenesis, being significantly higher by the 14th day of MMI treatment, and then started to decline, reaching the lowest values by the 21st day, when a significant reduction was detected. In the liver of these animals, however, a significant decrease of IRS-1 mRNA was detected after 14 days of MMI treatment, a mechanism probably involved in the insulin resistance that occurs in hypothyroidism. The increase in IRS-1 expression during goitrogenesis may represent...
Subject(s)
Animals , Male , Rats , Adaptor Proteins, Signal Transducing/metabolism , Goiter/metabolism , Hypothyroidism/metabolism , Thyroid Gland/cytology , Thyrotropin/metabolism , Adaptor Proteins, Signal Transducing/drug effects , Goiter/chemically induced , Hypothyroidism/chemically induced , Mitosis , Methimazole/pharmacology , Rats, Wistar , Reverse Transcriptase Polymerase Chain Reaction , RNA, Messenger/analysis , Thyroid Gland/drug effects , Thyrotropin/drug effectsABSTRACT
O hipotireoidismo é comum entre pessoas idosas, especialmente entre as mulheres. A suspeita diagnóstica deve se basear na presença de sinais e sintomas clássicos e a detecção pode ser feita pela elevação dos níveis do hormônio tireo-estimulante (TSH). Anormalidades lipídicas na presença de hipotireoidismo sub-clínico são de menor impacto. Entretanto, a reposição específica de hormônio tireoideano é tão mais importante quanto a magnitude do distúrbio glandular. Na vigência de doença hepática, alguns agentes hipolipemiantes podem levar a um agravamento do quadro, entretanto, estudos recentes têm mostrado que as estatinas podem ser utilizadas na presença de esteatose hepática. Terapia hipolipemiante combinada pode induzir aumentos de enzimas hepáticas e o monitoramento cuidadoso é recomendado nestes pacientes.
Subject(s)
Humans , Male , Female , Liver Diseases/drug therapy , Hypothyroidism/drug therapy , Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use , Age Factors , Azetidines/adverse effects , Azetidines/metabolism , Azetidines/therapeutic use , Clofibrate/adverse effects , Clofibrate/metabolism , Clofibrate/therapeutic use , Drug Interactions , Dyslipidemias/complications , Dyslipidemias/drug therapy , Liver Diseases/etiology , Liver Diseases/metabolism , Hypothyroidism/etiology , Hypothyroidism/metabolism , Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects , Hydroxymethylglutaryl-CoA Reductase Inhibitors/metabolism , Sex Factors , Thyrotropin/bloodABSTRACT
Las enfermedades tiroideas constituyen una heterogénea colección de anormalidades asociadas a mutaciones en los genes responsables en el desarrollo de la tiroides: factor de transcripción tiroideo 1 (TTF-1), factor de transcripción tiroideo 2 (TTF-2) y PAX8, o en uno de los genes que codifican para las proteínas involucradas en la biosíntesis de hormonas tiroideas como tiroglobulina (TG), tiroperoxidasa (TPO),sistema de generación de peróxido de hidrógeno (DUOX2), cotransportdor de Na/I (NIS), pendrina (PDS), TSH y receptor de TSH. El hipotiroidismo congénito ocurre con una prevalencia de 1 en 4.000 nacidos. Los pacientes coneste síndrome pueden ser divididos en dos grupos: con hipotiroidismo congénito sin bocio (disembriogénesis) o con bocio (dishormonogénesis). El grupo de disembriogénesis, que corresponde al 85% de los casos, resulta de ectopía,agenesia o hipoplasia. En una minoría de estos pacientes, el hipotiroidismo congénito está asociado con mutaciones en los genes TTF-1, TTF-2, PAX-8, TSH o TSHr. La resencia de bocio congénito (15% de los casos) se ha asociado a mutaciones en los genes NIS, TG, TPO, DUOX2 o PDS. El hipotiroidismo congénito por dishormonogénesis es trasmitido en forma autonómica recesiva. Mutaciones somáticas en el TSHr han sido identificadas en adenomas tiroideos hiperfuncionantes. Otra enfermedad tiroidea bien establecida es la resistencia a hormonas tiroideas(RTH). Es un síndrome de reducida respuesta tisular a la acción hormonal causado por mutaciones localizadas en el gen del receptor de hormonas tiroideas (TR). Mutantes de TRinterfieren con la función del receptor normal por un mecanismo de dominancia negativa. En conclusión, la identificación de mutaciones en los genes de expresión tiroidea ha permitido un mayor entendimiento sobre la relación estructura-función de los mismos. La tiroides constituye un excelente modelo para el estudio molecular de las enfermedades genéticas.
Subject(s)
Humans , Goiter/genetics , Hyperthyroidism/genetics , Hypothyroidism/genetics , Goiter/metabolism , Hyperthyroidism/metabolism , Hypothyroidism/congenital , Hypothyroidism/metabolism , Iodide Peroxidase/genetics , Iodide Peroxidase/metabolism , Mutation , Receptors, Thyrotropin/genetics , Thyroid Hormones/biosynthesis , Thyroid Hormones/geneticsABSTRACT
Thyroid hormones exert an enormous range of effects on lipid metabolism. The composition and the transport of lipoproteins are seriously disturbed in thyroid diseases.The aim of this study is to look for a significant statistical correlation between thyroid hormones and levels of serum lipids in attempt to use such a correlation in the clinical diagnosis of thyroid disorders. Significant elevated levels of total cholesterol, phospholipids and VLDL cholesterol were observed in hypothyroidism with a slight increase in the serum triglyceride. However in hyperthyroidism, an insignificant decrease of total cholesterol, phospholipids and VLDL cholesterol concentrations was observed as well as plasma triglycerides The results of the present study suggests that the use of classical methods for the determination of lipid profile as a preliminary step in the diagnosis of thyroid disorder is to be of great importance, wherever radioimmunoassay assay kits of thyroid hormone are not available as in remote urban medical sites or in unfavorable circumstances
Subject(s)
Humans , Male , Female , Thyroid Diseases/blood , Thyroid Diseases/physiopathology , Lipids/blood , Thyroid Function Tests , Hypothyroidism/blood , Hypothyroidism/metabolism , LipoproteinsABSTRACT
Sufficient data relating urinary iodine excretion in children to other iodine deficiency indicators are lacking in Egypt. We assayed urinary iodine concentration and serum levels of thyroid stimulating hormone [TSH], thyroglobulin, free triiodothyronine [T3] and free tetraiodothyronine in 99 school-aged Egyptian children. Goitre was found in 25 children. Median urinary iodine concentration was 70 micro g/L. We found mild iodine deficiency [50-99 micro g/L] in 60.6% of the children and moderate to severe deficiency [< 50 micro g/L] in 31.3%.The latter showed a high frequency of goitre and elevated mean serum free T3, TSH and thyroglobulin levels. Individual urinary iodine excretion rates vary, therefore these other indicators could help in screening for iodine deficiency at an individual level, especially in moderate to severe deficiency
Subject(s)
Adolescent , Child , Female , Humans , Male , Iodine/deficiency , Goiter, Endemic/metabolism , Health Status Indicators , Hypothyroidism/metabolism , Mass Screening/methods , Population Surveillance , Prevalence , Severity of Illness IndexABSTRACT
Fifty obese subjects with body weight above 120% of the ideal weight for that height or body mass index greater than 27.8 kg/m2 in men or 27.3 kg/m2 in women were studied for thyroid hormone profile. Nearly three-fourths obese subjects had body mass index of 30-40 kg/m2. Eighty-six per cent subjects were clinically and biochemically euthyroid. Fourteen per cent of the subjects had hypothyroidism; out of them, 8% were clinically and biochemically hypothyroid while 6% were only biochemically hypothyroid. None of the hypothyroid subjects had morbid obesity (greater than 40 kg/m2 body mass index). Duration of obesity in hypothyroid subjects was less than 10 years in nearly three-fourths of cases.
Subject(s)
Adult , Body Mass Index , Female , Humans , Hypothyroidism/metabolism , Male , Middle Aged , Obesity/metabolism , Thyroid Hormones/metabolismABSTRACT
Effect of excess folate on the metabolism of folate and plasma lipids in thyroid stressed animals was studied. Administration of excess dietary folate to hyperthyroid rats did not affect the decreased in vivo histidine oxidation in these animals, but it increased the hepatic tetrahydrofolate content. Hypothyroid rats had higher plasma total cholesterol (TC), high density lipoprotein cholesterol (HDLC) and trigylcerides (TG) with no change in post heparin lipolytic activity (PHLA). In hyperthyroidism both TC and HDLC were decreased in plasma and PHLA levels were elevated. On administration of excess dietary folate to hyperthyroid rats HDLC levels were not altered but PHLA and TC levels became near normal, while TG levels remained elevated.
Subject(s)
Animals , Folic Acid/administration & dosage , Histidine/metabolism , Hyperthyroidism/metabolism , Hypothyroidism/metabolism , Lipid Metabolism , Liver/metabolism , Male , Oxidation-Reduction , Rats , Rats, WistarABSTRACT
Las hormonas tiroideas son imprescindibles para el desarrollo y maduracion cerebral normales. El hipotiroidismo congenito es una de las causas mas frecuentes y evitable de retardo mental. Los sintomas clinicos son inespecificos y progresan con la evolucion del hipotiroidismo congenito porque antes del primer mes de vida, etapa en la que se debe iniciarse el tratamiento solamente un 5 por ciento de los niños afectados serian diagnosticados clinicamente, la incidencia mundial es de 1 en 3000 niños. Por estas razones se hace necesario realizar de forma rutinaria el programa de deteccion precoz de HCN, atraves del metodo de Screening neonatal para evitar tales casos
Subject(s)
Humans , Child , Pregnancy , Female , Infant, Newborn , Hypothyroidism , Hypothyroidism/congenital , Hypothyroidism/diagnosis , Hypothyroidism/embryology , Hypothyroidism/physiopathology , Hypothyroidism/metabolism , Thyroid Hormones/analysis , Thyroid Hormones/adverse effects , Thyroid Hormones/physiology , Thyroid Hormones/metabolism , Thyroid HormonesABSTRACT
Introducción. La finalidad del examen de tamiz neonatal es la detección precoz de las alteraciones congénitas del metabolismo que ocasionan retraso mental; de ellas la más común es el hipotiroidismo congénito (HTC). El objetivo de estudio fue conocer la incidencia del HTC detectado por tamiz neonatal en el Instituto Nacional de Perinatología. Material y métodos. Se revisaron los casos corroborados de HTC en el período de 1990 a 1993, que fueron identificados a través del programa de tamiz neonatal del Instituto. Resultados. En el período de estudio se tamizaron 13,510 recién nacidos (RN), se detectaron 10 casos de HTC, lo que proporcionó una incidencia de 1 caso por cada 1,428 niños tamizados. Se tamizó en promedio el 74.4 por ciento del total de RN vivos. Conclusiones. La incidencia de HTC fue superior a otros estudios realizados en México. Es necesario incrementar la capacitación de RN en el programa de tamiz neonatal