RESUMO
Amphibians inhabiting montane riparian zones in the Neotropics are particularly vulnerable to decline, but the reasons are poorly understood. Because environmental contaminants, endocrine disruption, and pathogens often figure prominently in amphibian declines it is imperative that we understand how these factors are potentially interrelated to affect montane populations. One possibility is that increased precipitation associated with global warming promotes the deposition of contaminants in montane regions. Increased exposure to contaminants, in turn, potentially elicits chronic elevations in circulating stress hormones that could contribute to montane population declines by compromising resistance to pathogens and/or production of sex steroids regulating reproduction. Here, we test this hypothesis by examining contaminant levels, stress and sex steroid levels, and nematode abundances in male drab treefrogs, Smilisca sordida, from lowland and montane populations in Costa Rica. We found no evidence that montane populations were more likely to possess contaminants (i.e., organochlorine, organophosphate and carbamate pesticides or benzidine and chlorophenoxy herbicides) than lowland populations. We also found no evidence of elevational differences in circulating levels of the stress hormone corticosterone, estradiol or progesterone. However, montane populations possessed lower androgen levels, hosted more nematode species, and had higher nematode abundances than lowland populations. Although these results suggested that nematodes contributed to lower androgens in montane populations, we were unable to detect a significant inverse relationship between nematode abundance and androgen level. Our results suggest that montane populations of this species are not at greater risk of exposure to contaminants or chronic stress, but implicate nematodes and compromised sex steroid levels as potential threats to montane populations.
Assuntos
Anuros/parasitologia , Disruptores Endócrinos/toxicidade , Poluentes Ambientais/toxicidade , Animais , Anuros/sangue , Anuros/fisiologia , Corticosterona/sangue , Costa Rica , Disruptores Endócrinos/metabolismo , Glândulas Endócrinas/efeitos dos fármacos , Glândulas Endócrinas/fisiopatologia , Poluentes Ambientais/metabolismo , Aquecimento Global , Hormônios Esteroides Gonadais/sangue , Interações Hospedeiro-Parasita , Masculino , Nematoides/isolamento & purificação , Nematoides/patogenicidade , Dinâmica Populacional , Estresse Fisiológico , Clima Tropical/efeitos adversosRESUMO
AIM: Conflicting results regarding testicular function in adults with type 1 diabetes (T1D) have been reported, but little is known about Leydig and Sertoli cell function during puberty in boys treated with multiple daily insulin doses. Our aim was to assess testicular function in boys with T1D. METHODS: Pubertal boys with T1D (n = 71) and healthy control boys (Control group; n = 104) who were 10-18 years were studied. Both groups were matched by pubertal stage, age, and BMI. Total testosterone (TT), calculated free testosterone (cfT), SHBG, inhibin B, AMH, and gonadotropin levels were determined. RESULTS: At the beginning of puberty, the T1D group had higher levels of SHBG (p = 0.003) and similar androgen levels than the Control group. At the end of puberty, higher TT, and cfT were observed in T1D compared to the Control group (p < 0.01 and p < 0.001, respectively). Gonadotropins and AMH were similar in both groups. Regression analysis showed that T1D was a significant factor, even after adjusting for Tanner stage and BMI-SDS, affecting TT, cFT, and SHBG levels. BMI-SDS was a significant factor affecting TT and SHBG levels. Higher HbA1c had a negative effect on total testosterone and cFT and a positive effect on SHBG levels in T1D boys. CONCLUSION: Adolescents with T1D do not exhibit hypogonadism, as shown by normal gonadotropin, testosterone, inhibin B, and AMH levels. However, in T1D boys, HbA1c and BMI-SDS had a negative association with testosterone levels. Elevated testosterone levels are observed during late puberty, which were not present earlier.
Assuntos
Diabetes Mellitus Tipo 1/complicações , Glândulas Endócrinas/fisiopatologia , Doenças do Sistema Endócrino/complicações , Hipogonadismo/complicações , Modelos Biológicos , Puberdade , Testículo/fisiopatologia , Adolescente , Biomarcadores/sangue , Criança , Chile , Diabetes Mellitus Tipo 1/sangue , Diabetes Mellitus Tipo 1/tratamento farmacológico , Diabetes Mellitus Tipo 1/fisiopatologia , Glândulas Endócrinas/efeitos dos fármacos , Glândulas Endócrinas/metabolismo , Doenças do Sistema Endócrino/induzido quimicamente , Doenças do Sistema Endócrino/prevenção & controle , Hemoglobinas Glicadas/análise , Hospitais Públicos , Hospitais Urbanos , Humanos , Hipoglicemiantes/efeitos adversos , Hipoglicemiantes/uso terapêutico , Hipogonadismo/induzido quimicamente , Hipogonadismo/prevenção & controle , Insulina/efeitos adversos , Insulina/uso terapêutico , Masculino , Puberdade/efeitos dos fármacos , Análise de Regressão , Testículo/efeitos dos fármacos , Testículo/metabolismo , Testosterona/análise , Testosterona/metabolismoRESUMO
BACKGROUND: There is a high prevalence of depression in individuals with type 2 diabetes mellitus. Depressive disorders are associated with increased medical morbidity and mortality in individuals with diabetes. It has been demonstrated that there is a higher prevalence of diabetic complications among individuals with diabetes and depression compared to those without depression. Several biological alterations have been reported in individuals with depressive disorders, particularly abnormal levels of endocrine-inflammatory markers.This study aims to determine the prevalence of major depressive disorder (MDD) in type 2 diabetes patients, the prevalence of cardiovascular events in individuals with and without MDD and to compare the endocrine-inflammatory profile between groups. METHODS: The study was approved by the "Comité de Etica de Protocolos de Investigación del Departamento de Docencia e Investigación del Hospital Italiano de Buenos Aires" with the number "1262" and included only patients who provided written informed consent. The study was conducted in accordance with the Declaration of Helsinki and the Habeas Data law on protection of personal data (Law Nª 25326, Argentina).Type 2 diabetes patients (n = 61) were included and they were classified as having MDD or not according to DSM-IV. Macrovascular disease was obtained from the medical history. Additionally, the intima-media thickness of the common carotid, carotid bifurcations and internal carotid arteries was measured non-invasively by two-dimensional ultrasound imaging. Fasting glucose, fasting lipid profile, inflammatory (CRP, TNF-α) and endocrine (urine free cortisol and saliva cortisol) markers. Student t tests were used to compare means for normally distributed variables and Mann-Whitney test for variables without normal distribution. Relative frequencies were calculated and a chi-square analysis was conducted. Data were expressed as mean ± standard deviation (SD) or median and interquartile range. Multivariable logistic regression was used to determine the relative odds of clinical cardiovascular disease in individuals with compared to those without depression. Differences were considered significant using a two-sided p < 0.05. RESULTS: 21 patients (34%) had MDD and 40 patients (66%) didn't have MDD. Diabetic patients with MDD had significantly higher CRP levels (4.1(1.9-7.6) vs 1.5(0.5-4.4) mg/l; p = 0.02) and 24-hour urine free cortisol (71.4 ± 21.3 vs 59.8 ± 29.3 ug/24 h; p = 0.03). The other metabolic and inflammatory parameters were not statistically different between groups. There was a significantly higher prevalence of cardiovascular events in individuals with MDD: 38% for the depressive group vs 15% for non-depressive group, p = 0.04). Patients with MDD had a 3.5-fold greater odd of having cardiovascular disease. CONCLUSIONS: Diabetic patients with depression are more likely to have cardiovascular events, and different factors can determine this high association.
Assuntos
Transtorno Depressivo Maior/complicações , Diabetes Mellitus Tipo 2/fisiopatologia , Glândulas Endócrinas/fisiopatologia , Inflamação/complicações , Idoso , Doenças Cardiovasculares/complicações , Diabetes Mellitus Tipo 2/complicações , Feminino , Humanos , Masculino , Pessoa de Meia-IdadeRESUMO
Eventos ou estímulos no início da vida podem afetar o desenvolvimento do indivíduo; dentre esses o tabagismo materno. A exposição materna isolada à nicotina, principal componente do cigarro, causa na prole alterações metabólicas, em curto e longo prazo, como aumento da adiposidade, resistência à leptina, e disfunção tireoideana e adrenal. Entretanto é sabido que na fumaça de cigarro estão presentes outros componentes com potenciais efeitos tóxicos. Assim propomos comparar o efeito de duas formas de exposição neonatal à fumaça do cigarro sobre o perfil endócrino-metabólico da prole em curto e longo prazo. Para isso, no 3º dia após o nascimento, ratos lactentes foram submetidos a dois modelos: Modelo I (exposição pelo leite materno), ninhadas separadas em: exposição à fumaça (EF; n=8) lactantes expostas à fumaça de cigarros 2R1F (1,7 mg de nicotina/cigarro por 1h, 4 vezes ao dia), separadas de suas proles e grupo controle (C; n=8), onde as mães foram separadas de suas proles e expostas ao ar filtrado; Modelo II (exposição direta à fumaça), ninhadas separadas em: exposição à fumaça (EF; n=8) mães e proles expostas à fumaça de cigarros 2R1F e controle (C; n=8) mães e proles expostas ao ar filtrado. A exposição ao tabaco ocorreu até o desmame. Mães sacrificadas aos desmame e proles aos desmame e aos 180 dias de idade. As mães lactantes expostas à fumaça (EF) apresentaram hipoleptinemia (-46%), hiperprolactinemia (+50%), hipoinsulinemia (-40%) e diminuição de triglicérides (-53%). Quanto a composição bioquímica do leite, as lactantes EF mostraram aumento de lactose (+52%) e triglicérides (+78%). No modelo I, as proles EF apresentaram ao desmame: diminuição da gordura corporal total (-24%), aumento de proteína corporal total (+17%), diminuição da glicemia (-11%), hiperinsulinemia (+28%), hipocorticosteronemia (-40%) e aumento de triglicérides (+34%). Quando adultas, as proles EF apresentaram somente alteração da função adrenal onde observou-se menor ...
Events or stimuli during early life can affect the development; among these events, there is the maternal smoking. Children born from smoking mothers showed low birth body weight and overweight in childhood and adolescence. Maternal nicotine exposure, the main cigarette component, causes in the offspring several metabolic changes in short- and long-term, such as increase in adiposity, hyperleptinemia, leptin resistance as well as thyroid and adrenal dysfunction. However, it is known that there are other toxic components in tobacco smoke. Then, we compared the effects of two models of tobacco smoke exposure on endocrine-metabolic profile in offspring at short- and long-term. For this, in the 3rd day of birth, suckling rats were submitted to two different experiments: Model I (through breast milk exposure), in which litters were separated into, smoke exposure (SE; n=8) lactating mothers exposed to 2R1F cigarettes smoke (1.7 mg nicotine/cigarette/1h, 4 times per day) separated from their offspring; and control (C; n=8) mothers were separated of their pups and exposed to filtered air. Model II (direct exposure), in which litters were separated into: Smoke exposure (SE; n=8) lactating mothers and their offspring were exposed to 2R1F cigarettes smoke; and control (C; n=8) mothers and their pups were exposed to filtered air. The smoke exposure occurred until the weaning, when mothers and half of pups were killed. The other offspring were killed at 180 days-old. SE dams presented hypoleptinemia (-46%), hyperprolactinemia (+50%), hypoinsulinemia (-40%) and lower triglycerides (-53%). Concerning milk compositon, SE dams showed higher lactose (+52%) and triglycerides (+78%). In model I (through breast milk exposure), EF offspring showed at weaning lower total body fat (-24%) and higher total body protein (+17), lower serum glucose (-11%), hyperinsulinemia (+28%), hypocorticosteronemia (-40%) and higher triglycerides (+34%). In adulthood, these parameters were ...
Assuntos
Animais , Feminino , Ratos , Exposição Materna/efeitos adversos , Lactação , Lactação/metabolismo , Tabagismo/complicações , Glândulas Endócrinas , Glândulas Endócrinas/fisiopatologia , Hormônios/metabolismo , Troca Materno-Fetal , Nicotina/efeitos adversos , Nicotina/toxicidade , Obesidade/metabolismo , Efeitos Tardios da Exposição Pré-Natal , Sistema Endócrino/metabolismoRESUMO
La primera descripción anatómica de las glándulas paratiroides fue expuesta por Richard Owen en 1850 cuando realiza la disección de un rinoceronte indio, publicando su hallazgo en 1862. Remak, en 1855, evidencia estas estructuras en gatos y las asocia con un posible desarrollo embriológico relacionado con el timo. Virchow en 1863 describe estas glándulas como linfonódulos perdidos entre material conectivo en cara posterior de la tiroides. Sin embargo, el hallazgo e identificación de las paratiroides le es designado al sueco Ivar Sandstrõm en 1880, quien las describe primero en perros, luego en otros mamiferos y en el hombre, y además, es el primero en describirlas histológicamente. Así reciben la nominación de "glandulae parathyroidea". Gley en 1892 redescubre las glandulas y establece su importancia como estructuras endocrinas y su relación fisiopatológica con la tetania y la muerte tras tiroidectomías en perros. Kohn en 1895 establece la anatomía, histología y embriología de las paratiroides totalmente independientes de la tiroides. Erdheim (1903) enfatiza su autonomía histológica y realiza nuevas descripciones histólógicas. McCallum y Voegtlin en 1908 relacionan las paratiroides con el control sanguíneo del calcio. Collip, entre 1922-1923, establece el papel fisiológico de las paratiroides sobre la regulación de la calcemia. La primera paratiroidectomía terapéutica es realizada en 1925 por Felix Mandl sobre "Albert", quien padecia problemas óseos. La segunda paratiroidectomía se registra en el Hospital General de Massachussets sobre el capitán Martell en 1926, y tras múltiples intervenciones se realiza el hallazgo de un adenoma paratiroideo mediastinal.
Assuntos
Humanos , Animais , Cálcio/análise , Glândulas Endócrinas/fisiopatologia , Glândulas Paratireoides/anatomia & histologia , Glândulas Paratireoides/embriologia , Paratireoidectomia/história , Glândula Tireoide/anatomia & histologia , Tecido Conjuntivo/anatomia & histologiaRESUMO
The main endocrine-regulated processes of crustaceans have been reviewed in relation to the effects of endocrine-disrupting compounds (EDCs). Molting has been shown to be inhibited by several organic pollutants, such as xenoestrogens and related compounds, as well as by some pesticides. Most of these disrupters are thought to interfere with ecdysone at target tissues, although only for a few has this action been demonstrated in vitro. The heavy metal cadmium appears to inhibit some ecdysone secretion. Juvenoid compounds have also been shown to inhibit molting, likely by interfering with the stimulatory effect of methyl farnesoate. A molt-promoting effect of emamectin benzoate, a pesticide, has also been reported. As for reproduction, a variety of organic compounds, including xenoestrogens, juvenoids and ecdysteroids, has produced abnormal development of male and female secondary sexual characters, as well as alteration of the sex ratio. Cadmium and copper have been shown to interfere with hormones that stimulate reproduction, such as methyl farnesoate, as well as with secretion of the gonad inhibiting hormone, therefore affecting, for example, ovarian growth. Several heavy metals were able to produce hyperglycemia in crustaceans during short times of exposure; while a hypoglycemic response was noted after longer exposures, due to inhibition of secretion of the crustacean hyperglycemic hormone. The ecological relevance of EDCs on crustaceans is discussed, mainly in relation to the identification of useful biomarkers and sentinel species. New experimental approaches are also proposed.
Assuntos
Crustáceos/efeitos dos fármacos , Crustáceos/fisiologia , Disruptores Endócrinos/toxicidade , Glândulas Endócrinas/efeitos dos fármacos , Poluentes Ambientais/toxicidade , Animais , Glândulas Endócrinas/fisiopatologia , Sistema Endócrino/fisiologia , Reprodução/efeitos dos fármacosRESUMO
Circulating leptin levels, proinflammatory and T helper cells type 1 (Th1), Th2 cytokine production, and lymphoproliferative response were measured in 15 infants with primary moderate protein calorie malnutrition on admission and after recovery of 10% of weight. Sixteen healthy, well nourished infants of comparable age served as controls. A significant deficit in the z-score of weight for age, weight for height, body mass index, and circulating leptin and growth factors were detected in malnourished infants on admission compared with controls (P < 0.05). These deficits were associated with a significant suppression of the lymphoproliferative response, Th1, and proinflammatory cytokine production (P < 0.05). After a 10% weight gain, a significant increase in circulating leptin levels was produced in parallel with a significant increase in Th1 activity, as revealed by an enhancement in interferon-gamma and a suppression in IL-4 production. Concomitantly, the lymphoproliferative response became similar to that detected in control infants. Furthermore, a significant increase in IL-1 and TNFalpha production compared with that at admission was shown. These findings suggest an association between the increase in leptin and the immunological recovery observed following refeeding of malnourished infants.
Assuntos
Leptina/sangue , Distúrbios Nutricionais/sangue , Distúrbios Nutricionais/imunologia , Antropometria , Formação de Anticorpos , Divisão Celular/efeitos dos fármacos , Citocinas/biossíntese , Glândulas Endócrinas/fisiopatologia , Feminino , Humanos , Lactente , Mediadores da Inflamação/metabolismo , Masculino , Mitógenos/farmacologia , Monócitos/metabolismo , Monócitos/patologia , Distúrbios Nutricionais/patologia , Células Th1/metabolismo , Células Th2/metabolismoRESUMO
Methods for assessment, e.g., anthropometric indicators and imaging techniques, of several phenotypes of human obesity, with special reference to abdominal fat content, have been evaluated. The correlation of fat distribution with age, gender, total body fat, energy balance, adipose tissue lipoprotein lipase and lipolytic activity, adipose tissue receptors, and genetic characteristics are discussed. Several secreted or expressed factors in the adipocyte are evaluated in the context of fat tissue localization. The body fat distribution and the metabolic profile in nonobese and obese individuals is discussed relative to lipolysis, antilypolysis and lipogenesis, insulin sensitivity, and glucose, lipid, and protein metabolism. Finally, the endocrine regulation of abdominal visceral fat in comparison with the adipose tissue localized in other areas is presented.
Assuntos
Tecido Adiposo/metabolismo , Tecido Adiposo/patologia , Obesidade/metabolismo , Obesidade/patologia , Pele , Vísceras , Abdome , Adipócitos/metabolismo , Glândulas Endócrinas/fisiopatologia , Hormônios/metabolismo , Humanos , Obesidade/fisiopatologia , Valores de ReferênciaRESUMO
We tested the hypothesis that the llama fetus has a blunted cardiovascular chemoreflex response to hypoxemia by investigating the effects of acute hypoxemia on perfusion pressure, heart rate, and the distribution of the combined ventricular output in 10 chronically instrumented fetal llamas at 0.6-0.7 gestation. Four llama fetuses had the carotid sinus nerves sectioned. In the intact fetuses, there was a marked bradycardia, an increase in perfusion pressure, and a pronounced peripheral vasoconstriction during hypoxemia. These cardiovascular responses during hypoxemia in intact fetuses were accompanied by a pronounced increase in plasma vasopressin, but not in plasma angiotensin II concentrations. Carotid denervation prevented the bradycardia at the onset of hypoxemia, but it did not affect the intense vasoconstriction during hypoxemia. Plasma vasopressin and angiotensin II levels were not measured in carotid-denervated fetuses. Our results do not support the hypothesis that the carotid chemoreflex during hypoxemia is blunted in the llama fetus. However, they emphasize that other mechanisms, such as increased vasopressin concentrations, operate to produce an intense vasoconstriction in hypoxemia. This intense vasoconstriction in the llama fetus during hypoxemia may reflect the influence of chronic exposure to the hypoxia of high altitude on the magnitude and gain of fetal cardiovascular responses to a superimposed acute episode of hypoxemia.