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L H Duntas

Publications and source records attributed to L H Duntas.

15 recordsLinked to original sources
PubMed2005

Leptin TRH and ghrelin: influence on energy homeostasis at rest and during exercise.

The hypothalamus has long been recognized as a major site in the central nervous system (CNS) where a spectrum of internal and external environmental information is integrated for energy homeostasis. The isolation and sequencing of leptin in the mid 90 s, together with the demonstration of leptin administration's ability to correct the obesity syndrome in leptin-deficient ob/ob mice and humans by suppressing food intake and weight gain in laboratory rodents, confirmed the hypothesized existence of a direct humoral signal from adipose tissue to the hypothalamus, thus integrating the energy-related signals. In the 80 s, neuropeptide Y (NPY) was identified as a potent appetite-stimulating neuropeptide produced, released and acting locally within the hypothalamus. This is recognized as a major physiological appetite transducer and central neurochemical substrate receiving, interpreting and processing incoming information on energy status. More recently, ghrelin, produced in the stomach and released into the general circulation, has drawn attention as the other limb of the feedback circuit that stimulates appetite at NPY network level. Prolonged fasting suppresses serum leptin, while suppressing TSH secretion. Intervention with leptin replacement can prevent fasting-induced changes in TSH, suggesting that leptin regulates TSH. Low leptin levels in sportsmen and sportswomen as well as in recreational runners are consistent with reduction in body fat, but are also influenced by the presence of low insulin, hypothyroxemia, and elevated cortisol levels. These metabolic adaptations to chronic energy deficits indicate a role in leptin regulation. A study within the general population found that activity levels and leptin were significantly negatively associated in both sexes. Circulating ghrelin levels, however, do not change during energy expenditure.

Animals↗
PubMed2005

Iodine uptake and loss-can frequent strenuous exercise induce iodine deficiency?

Most of the daily dietary iodine intake (approximately 90 %) will be excreted in the urine; measurement of urinary iodine excretion is thus routinely used as an index of dietary iodine intake. However, urinary excretion is not the only means of iodine loss. Subjects such as athletes or those participating in vigorous exercise can lose a considerable amount of iodine in sweat, depending on environmental factors such as temperature and humidity. In areas of lower to moderate dietary iodine intake, loss in sweat can equal that in urine. Although electrolyte loss in sweat is well-recognized and replacement strategies are adopted, there is less recognition of potential iodine loss. Crude calculations reveal that if sweat iodide losses are not replaced, dietary stores could be depleted in an athlete undergoing a regular training regime. The significance of these losses could be increased in areas where dietary iodine intake is lower in the summer months. Although there is little doubt that excessive sweating can induce a relative iodine deficiency state, there is no case as yet for iodine supplementation in those that take vigorous exercise. However, sustained iodine loss may have implications for thyroid status and possibly consequences for athletic performance.

Animals↗
PubMed2005

Oxidants, antioxidants in physical exercise and relation to thyroid function.

Intensive muscular exercise promotes the production of reactive oxygen species (ROS) in the working muscles and can impair athletic performance, particularly in conjunction with inadequate recovery. Mammals are protected against oxygen toxicity by a system of ROS scavengers composed of enzymatic and non-enzymatic components. Although antioxidant supplementation has recently been considered as a means to diminish or prevent damage from ROS, the specific antioxidant requirements of athletes are not known. Since thyroid function is essential for athletic performance, thyroid control should be undertaken in cases where there is any sign of thyroid dysfunction "of unknown etiology". Hyperthyroidism and hypothyroidism have been associated with increased production of ROS as well as related inflammatory response and myopathy. There is evidence that antioxidant supplementation combined with antithyroid treatment with methimazole could be useful in decreasing the oxidative stress.

Animals↗
PubMed2003

Subclinical thyroid disorders: the menace of the Trojan horse.

This review aims at summarizing some new data regarding the so-called subclinical thyroid disease and incorporate the knowledge in order to provide a basis for a more careful approach to these morbidities. SHyper represents a considerable risk factor for atrial fibrillation in the elderly and also for osteoporosis, which is a major cause of morbidity in postmenopausal women. SHypo is not an innocuous condition. It progresses to thyroid failure in patients with positive thyroid antibodies, it affects neurobehavior, it may influence cardiac contractility at exercise and it is associated with an impaired lipid profile that may provoke atherosclerosis. Therefore, both conditions should be screened more carefully in the community and treatment should be more often considered.

Female↗
PubMed2002

Nutrition and brain function: a multidisciplinary virtual symposium.

A few months ago, the Brazilian Society for Neuroscience and Behavior (SBNeC) promoted a "virtual symposium" (by Internet, under the coordination of R.C.A. Guedes) on "Nutrition and Brain Function". The discussions generated during that symposium originated the present text, which analyzes current topics on the theme, based on the multidisciplinary experience of the authors. The way the brain could be non-homogeneously affected by nutritional alterations, as well as questions like early malnutrition and the development of late obesity and hormone abnormalities were discussed. Also, topics like the role of essential fatty acids (EFAs) on brain development, increased seizure susceptibility and changes in different neurotransmitters and in cognitive performance in malnourished animals, as well as differences between overall changes in nutrient intake and excess or deficiency of specific nutrients (e.g. iodine deficiency) were analyzed. It was pointed out that different types of neurons, possibly in distinct brain structures, might be differently affected by nutritional manipulation, including not only lack-but also excess of nutrient intake. Such differences could help in explaining discrepancies between data on humans and in animals and so, could aid in determining the basic mechanisms underlying lesions or changes in brain function and behavior.

Brain↗
PubMed2001

Lack of substantial effects of raloxifene on thyroxine-binding globulin in postmenopausal women: dependency on thyroid status.

Long-term estrogen therapy can modify thyroid hormone kinetics by increasing serum concentration of thyroxine-binding globulin (TBG). Raloxifene is a recently developed selective estrogen receptor modulator (SERM) for the treatment of osteoporosis, which possesses estrogenic and antiestrogenic properties. In a prospective and randomized study, we investigated the effects of raloxifene on TBG levels and on the serum concentrations of free thyroxine (FT4), thyroxine (T4), triiodothyronine (T3), and thyrotropin (TSH) in controls and in patients receiving TSH-suppressive doses of levothyroxine (LT4). Twenty-nine postmenopausal osteopenic (n = 14) and osteoporotic (n = 15) women were investigated over a period of 6 months. Group 1 (n = 15) included control patients and group 2 (n = 14) patients receiving TSH-suppressive dose of LT4. All patients were treated with raloxifene hydrochloride, 60 mg/d, for a period of 6 months. Serum basal TBG values were found higher in Group 1 compared to Group 2 (26.2 2 microg/mL vs. 21.4 2.1 microg/ml; p < 0.01). The TBG levels raised slightly in group 1 from 26.2 2 microg/mL to 28.6 3.1 microg/mL; p < 0.05 (in group 2 from 21.4 2.1 microg/mL to 22.2 2.3 microg/mL, not significant) after 3 months of treatment and failed to show any further significant change until the end of the study. Serum concentrations of T4, FT4, T3, and TSH levels changed insignificantly in both groups up to the completion of the study. Moreover, patients remained clinically euthyroid. Our findings may provide evidence that TBG levels, and consequently, thyroid function are not substantially affected by treatment with raloxifene. Additionally, TBG levels may also be influenced by small variations of thyroid function as subclinical hyperthyroidism.

Aged↗
PubMed2001

Prolactinomas in children and adolescents--consequences in adult life.

Prolactinomas in children and adolescents are rare. However, they represent, together with corticotropinomas, the most frequent types of pituitary tumors in adolescence. Most prolactin-secreting pituitary tumors are microprolactinomas but many, and particularly those in men, are macroadenomas. The clinical findings that would usually project into the adult life of patients, in other words the issue of transitory endocrinology from childhood to adulthood, are menstrual irregularities, infertility, short stature, osteopenia and/or osteoporosis, and sometimes psychometric abnormalities. The therapy of choice for both macro- and microprolactinomas is one of the new dopamine agonists, such as quinagolide or cabergoline. Recent evidence-based data have clearly promoted cabergoline as the first-line treatment. Cabergoline may normalize prolactin secretion, restore fertility in women and men. and induce tumor shrinkage. Today, transsphenoidal surgery should be considered only in patients with a large extrasellar extension.

Adolescent↗
PubMed1999

Disturbances of menstruation in hypothyroidism.

OBJECTIVES: Most thyroid textbooks describe hypothyroidism resulting in changes in the length of the menstrual cycle and in the amount of bleeding. Our experience at a busy thyroid clinic had given a picture which differs from that presented in the literature. The aim of this study was to determine the frequency and type of menstrual irregularities in premenopausal hypothyroid patients. DESIGN AND PATIENTS: We investigated the menstrual history, starting 6 months before the discovery of the disease, in 171 female premenopausal hypothyroid patients and 214 normal controls, with similar age and body mass index (BMI). MEASUREMENTS: TSH, TT4, TT3 and thyroid antibodies were measured by radioimmunoassay, while BMI was calculated from the ratio of body weight in kg to height in m2. RESULTS: Of the 171 hypothyroid patients, 131 (76.6%) had regular cycles and 40 (23.4%) irregular periods. Oligomenorrhoea and menorrhagia were the most common features in the latter group. No difference in BMI was found between the patients with or without menstrual abnormalities, or between patients and controls. TSH, TT4 and TT3 levels did not differ between patients with normal and abnormal menstruation. Forty-six (26.9%) out of 171 patients had subclinical hypothyroidism (group A), 42 (24.6%) mild hypothyroidism (group B) and 83 (48.5%) severe hypothyroidism (group C). Thirty-seven from group A (80.4%), 32 from group B (76.2%) and 62 from group C (74.7%) had normal periods. These differences were not statistically significant. Eighty-eight (88.9%) out of 99 patients in whom thyroid antibodies were measured had positive titres. Nineteen (21.6%) of the patients with positive thyroid antibodies had menstrual irregularities. This percentage did not differ from that found in the whole group of patients (23.4%). Out of 214 normal controls, 196 (91.6%) had normal menstruation and 19 (8.4%) irregular cycles. The latter group included mainly women with oligomenorrhoea. CONCLUSIONS: These data demonstrate that hypothyroidism in women is less frequently associated with menstrual disturbance than was previously described. Also, menstrual irregularities tend to be more frequent in sever hypothyroidism in comparison with mild cases, although this finding was not statistically significant. Oligomenorrhoea and menorrhagia are the most common menstrual disturbances.

Adult↗
PubMed1999

Incidence of sideropenia and effects of iron repletion treatment in women with subclinical hypothyroidism.

Sideropenia affects ca. 20% of the world population, and iron dependent anemia is the most frequent type of anemia worldwide. The aim of the study was to investigate the incidence of sideropenia and dependent anemia in patients with subtle changes of the thyroid function, such as subclinical hypothyroidism (SH). 57 women with SH and 61 euthyroid controls (CG) were studied. Serum concentrations of T4, T3, TSH, anti-TPO, anti-Tg, ferrum (Fe), ferritin (Frt) total iron binding capacity (TIBC) and blood count were determined. In SH 17 patients (29.8%) presented low Fe levels (<50 microg/dl). 9 (15.7%) also had decreased Frt, confirming iron deficiency, whereas 8 patients presented additionally diminished hematocrit and hemoglobin levels, suggesting manifested sideropenic anemia. In CG, 10 persons (16%) had sideropenia, 6 (9.8%) had low Fe and Frt and only 3 (4.9%) had blood count alterations suggesting manifested sideropenic anemia. In SH, anti-TPO were positive in 39 patients (68%), whereas, in CG only 2 (3.2%) were positive. 8 patients with SH and manifested sideropenic anemia were treated with ironproteinsuccinylate (I-PSL), (80 mg Fe /day, for three months), a new iron compound. The repletion treatment safely led to the clinical and laboratory correction of sideropenia and showed a good tolerability. Furthermore, iron treatment provoked a minor increase of T4 and a mild decline of TSH, but the levels were not significant. These results suggest that sideropenia is a common finding in patients with slightly decreased thyroid activity, and that determination of Frt should be routinely advised. Finally, in the assessment of sideropenia and dependent anemia, evaluation of the thyroid function must be taken into account.

Adult↗
PubMed1999

Changes in metabolism of TRH in euthyroid sick syndrome.

OBJECTIVE: The aim of this study was to examine the metabolism of a simple dose, intravenously administered TRH bolus of 200 microg, in patients with euthyroid sick syndrome (ESS). PATIENTS AND METHODS: A TRH test was performed on ten ESS patients and ten controls upon admission (d1) and after recovery (d2). Blood samples were collected at 0, 10, 20 and 30min after TRH injection. We analyzed the volume of distribution (V(d)), the plasma clearance rate (PCR), the fractional clearance rate (FCR), the half-life (t(1/2)) and the TSH response to the injection of TRH. RESULTS: All patients had lower tri-iodothyronine (T(3)) levels compared with controls (0.9 +/- 0. 1nmol/l vs 1.9 +/- 0.1 nmol/l; P < 0.0001; mean +/- S.D.; paired t-test). In addition, the V(d) (16.7 +/- 5.9/l vs 30.6 +/- 0.6/l; P < 0.0005) and PCR (2.0 +/- 0.80 l/min vs 3.3 +/- 0.25 l/min; P <0. 0005) were found statistically lowered in patients than in controls, whereas FCR (0.119 +/- 0.01 permin vs 0.110 +/- 0.01 per min; P < 0. 025) was found increased in patients as opposed to controls. The t(1/2) of exogenously administered TRH was increased in ESS compared with controls (7.2 +/- 0.7 min vs 6.3 +/- 0.6 min; P <0.005). TSH response to TRH was found significantly repressed at 10, 20 and 30 min after TRH injection. On d2, these findings had reverted to normal and no changes regarding the kinetics of TRH and the response of TSH could be detected between patients and controls. CONCLUSIONS: The results demonstrate an impairment of TRH metabolism in ESS. The findings may suggest altered enzymatic activity, responsible for TRH degradation in states of acute ESS. These changes might be involved in the pathogenesis of ESS and represent part of an adaptive mechanism to this syndrome.

Adult↗
PubMed1998

Inhibitory action of oral thyrotropin-releasing hormone on the glucoregulatory response of the oral glucose tolerance test.

Thyrotropin-releasing hormone (TRH) has been found in the gastrointestinal tract, where it mainly exerts an inhibitory action. We used oral TRH, a stable and powerful formulation, to explore the glucoregulatory response of oral glucose tolerance test (OGTT) on obese patients with impaired glucose tolerance (IGT). Seven obese patients with IGT and eight controls were investigated. Three tests were performed on three separate days. On day 1, An oral TRH test: a 40 mg TRH tablet, was given. Blood samples for blood glucose (BG), proinsulin (PI), insulin (INS), C-peptide (CP), thyroxine (T4), triiodothyronine (T3), and thyrotropin (TSH) were collected every 30 minutes for 3 hours. On day 2, an OGTT with 75 g glucose was performed. On day 3, an oral TRH test was administered 30 minutes before the OGTT, and blood was collected every 30 minutes for 3 hours. Oral-TRH had no effect on basal BG and on pancreatic hormone secretion. Oral TRH, coupled with OGTT in both controls and obese patients, led to a significant inhibition of BG (p < 0.01), of CP (p < 0.001), and of INS (p < 0.001) during the first hour of administration, and afterward, there was only a very slight increase, compared with levels after only OGTT treatment. After OGTT, PI peaked at 90 minutes (9.4+/-3 ng/mL) in controls and at 60 minutes (12.7+/-2.5 ng/mL) in obese patients. TRH application prior to OGTT inhibited PI secretion for 90 minutes in controls, whereas in obese patients PI levels were decreased, not inhibited, during the OGTT. The mechanism of the inhibitory TRH action on OGTT-induced increase of BG and pancreatic hormone secretion is not clear. It could be due to inhibition of gastric motility, and on a paracrine effect that enhances secretion of somatostatin that then suppresses INS, CP, and possibly PI levels. The partial escape of PI from the TRH blockade in obese patients with IGT might indicate a diminished functioning capability of beta-cells and that TRH cannot affect the INS processing within the beta-cells in these patients.

Adult↗