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Effects of thyroid hormones in individual tissues are determined by many factors beyond their serum levels, including local deiodination and expression and activity of thyroid hormone transporters. These effects are difficult to examine by traditional techniques, but a novel approach that exploits the existence of common genetic variants has yielded new and surprising insights. Convincing evidence indicates a role of type 1 iodothyronine deiodinase (D1) in determining the serum T(4):T(3) ratio and a role of phosphodiesterase 8B in determining TSH levels. In addition, studies of type 2 iodothyronine deiodinase (D2) variants have shown that thyroid hormones contribute to osteoarthritis and these variants influence Intelligence quotient alterations associated with iodine deficiency. Preliminary evidence suggests associations between TSH-receptor variants and fasting glucose level, D1 variants and insulin-like growth factor I production, and D2 variants and hypertension, psychological well-being and response to T(3) or T(4) treatment. Intriguingly, most of these associations are independent of serum thyroid hormone levels, which highlights the importance of local regulation of thyroid hormones in tissues. Future research might reveal novel roles for thyroid hormones in obesity, cardiovascular disease, osteoporosis and depression and could have implications for interpretation of thyroid function tests and individualization of thyroid hormone replacement therapy.
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PMID:Novel insights into thyroid hormones from the study of common genetic variation. 1935 19

Micronutrients, mostly iodine and selenium, are required for thyroid hormone synthesis and function. Iodine is an essential component of thyroid hormones and its deficiency is considered as the most common cause of preventable brain damage in the world. Nowadays about 800 million people are affected by iodine deficiency disorders that include goiter, hypothyroidism, mental retardation, and a wide spectrum of other growth and developmental abnormalities. Iodine supplementation, under form of iodized salt and iodized vegetable oil, produced dramatic improvements in many areas, even though iodine deficiency is still a problem not only for developing countries. In fact, certain subpopulations like vegetarians may not reach an adequate iodine intake even in countries considered iodine-sufficient. A reduction in dietary iodine content could also be related to increased adherence to dietary recommendations to reduce salt intake for preventing hypertension. Furthermore, iodine intakes are declining in many countries where, after endemic goiter eradication, the lack of monitoring of iodine nutrition can lead to a reappearance of goiter and other iodine deficiency disorders. Three different selenium-dependent iodothyronine deiodinases (types I, II, and III) can both activate and inactivate thyroid hormones, making selenium an essential micronutrient for normal development, growth, and metabolism. Furthermore, selenium is found as selenocysteine in the catalytic center of enzymes protecting the thyroid from free radicals damage. In this way, selenium deficiency can exacerbate the effects of iodine deficiency and the same is true for vitamin A or iron deficiency. Substances introduced with food, such as thiocyanate and isoflavones or certain herbal preparations, can interfere with micronutrients and influence thyroid function. Aim of this paper is to review the role of micronutrients in thyroid function and diseases.
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PMID:Role of iodine, selenium and other micronutrients in thyroid function and disorders. 1959 17

The clinical research of the Department of Gerontology and Geriatrics of the Leiden University Medical Center focuses on the causes of health and disease in old age. We examine, amongst others, the genetic mechanisms of longevity by comparing children of long-living parents with their partners. At a mean age of 60 years, the children of the long-living parents have a lower prevalence of several cardiometabolic diseases, among which are myocardial infarction, diabetes, and hypertension. The children of the long-living parents also have a more favourable cardiometabolic risk profile, with lower values of glucose, insulin, triglycerides, and thyroid hormone, and a better insulin sensitivity. Moreover, over the past years we have shown that traditional cardiovascular risk factors, such as an increased cholesterol and hypertension, do not automatically apply to the very old. For the very old it must be taken into account that risk profiles for various diseases differ from those of younger populations. The choice of treatment must therefore be based on the 'best available evidence'. In absence of randomized clinical trials this is currently the knowledge on the pathofysiology of health and disease in old age.
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PMID:[Causes of health and disease in old age: new insights from the Leiden Research Program on Ageing]. 2007 72

Diseases of the thyroid gland are common in many zoo species, but there are few descriptions of thyroid dysfunction in Mustelidae. A 7-yr-old, captive-bred female fisher (Martes pennanti) with progressive alopecia was diagnosed with clinical hyperthyroidism based on persistent elevation of both total and free serum thyroxine and triiodothyronine, ultrasound examination, and histologic evidence of adenomatous hyperplasia. Four additional geriatric adult fishers (two male and two female) were identified with thyroid adenomatous hyperplasia in a review of 23 postmortem records. Banked sera were available for thyroid hormone testing from three of the four necropsy cases. Total and free thyroxine were elevated in four of four animals tested, and triiodothyronine was elevated in two of three animals tested. Necropsy findings in four cases identified cardiac hypertrophy, congestive heart failure, and vascular lesions consistent with hypertension; complete tissues were not available from the remaining case. Clinical and subclinical hyperthyroidism may be a common but overlooked condition of captive fishers.
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PMID:Proliferative thyroid lesions and hyperthyroidism in captive fishers (Martes pennanti). 2059 22

Sarcopenia, the age-related decline in muscle mass, affects the muscle strength and muscle quality, and these changes decrease functional capacity. The prevalence of thyroid dysfunction increases with age, and changes in thyroid hormone level lead to neuromuscular deficits. We investigated the effects of subclinical hypothyroidism on the muscle mass, strength or quality in elderly people. One thousand one hundred eighteen subjects aged > or = 65 yr were randomly selected from a local population and classified into a euthyroid (280 men and 358 women), subclinically hypothyroid (61 men and 75 women), or overtly hypothyroid (7 men and 16 women) group. Although women with subclinical hypothyroidism had a higher prevalence of sarcopenia, defined according to the ratio of appendicular skeletal muscle mass to the square of height, muscle mass, strength or quality did not differ in relation to thyroid status in men or in women. Multivariate analysis including age, diabetes, hypertension, acute coronary event, alcohol, smoking, presence of pain, physical activity score, and lipid profile, showed that thyroid-stimulating hormone level was not associated with muscle mass, strength or quality. In conclusion, subclinical hypothyroidism has little influences on muscle mass, strength or quality, and may not be associated with sarcopenia.
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PMID:Subclinical hypothyroidism has little influences on muscle mass or strength in elderly people. 2067 29

Subclinical hypothyroidism (SH) is a frequent condition affecting millions of people around the world. Defined by increased thyrotropin-stimulating hormone (TSH) and accompanied by normal thyroid hormone levels, SH reflects a mild tissue hypothyroidism that has been associated with metabolic derangements and-although this issue is still contentious-possibly with increased cardiovascular risk. Depending on the degree of TSH elevation, SH has accordingly been associated with hyperlipidemia, arterial hypertension, and cardiovascular disease (CVD), as well as, increasingly, newly emerging CVD risk factors such as serum C-reactive protein and retinol binding protein 4 levels. There have also been reports of abnormalities in glucose metabolism and of hemostatic parameters, mainly underscored by the increased activity of factor VII. This review discusses the results of the latest studies on the various parameters affected by SH while highlighting the need for timely treatment with levothyroxine.
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PMID:New insights into subclinical hypothyroidism and cardiovascular risk. 2124 2

Renal phosphate transport is mediated by the abundance and activity of the sodium-dependent phosphate transporters, Npt2a, Npt2c, and PiT-2, present within the apical brush border membrane of the proximal tubule. Recent studies have demonstrated differential expression and activity of these sodium-dependent phosphate transporters within the proximal tubule. In general, phosphate transport is regulated by a variety of physiological stimuli, including parathyroid hormone, glucocorticoids, vitamin D3, estrogen, and thyroid hormone. Phosphatonins are now recognized as major regulators of phosphate transport activity. Other factors that affect phosphate transport include dopamine, dietary phosphate, acid-base status, lipid composition, potassium deficiency, circadian rhythm, and hypertension. Studies have shown that the PDZ-containing sodium/hydrogen exchanger regulatory factor (NHERF) proteins, specifically NHERF-1 and NHERF-3, play a critical role in the physiological regulation of phosphate transport, particularly in response to dietary phosphate. In addition, recent studies have found that NHERF-1 is also important in both the parathyroid hormone- and dopamine-mediated inhibition of phosphate transport. This review will detail the various hormones and agents involved in the regulation of phosphate transport as well as provide a brief summary of the signaling pathways and cytoskeletal proteins active in the transport of phosphate in the renal proximal tubule.
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PMID:The regulation of renal phosphate transport. 2140 91

Although veterinary clinicians commonly rely on panels of laboratory tests with individual results flagged when abnormal, care should be taken in interpreting normal test results as well. There are several examples of this in evaluating patients with endocrine disease. The finding of a normal leukogram (absence of a stress leukogram) can be indicative of adrenal insufficiency in dogs, and this disorder can be especially elusive when there are no overt indicators of mineralocorticoid deficiency. Cats with hyperthyroidism can have normal serum thyroid hormone concentrations, normal hematocrits, and normal serum concentrations of creatinine despite the presence of disease that affects these parameters. A normal serum phosphorus concentration, in the face of azotemia, isosthenuria, and hypertension can point a clinician toward a diagnosis of primary hyperaldosteronism rather than primary renal disease. A normal serum parathyroid hormone concentration in the face of hypercalcemia is inappropriate and can indicate the presence of primary hyperparathyroidism. Similarly, hypoglycemia accompanied by a normal serum insulin concentration can be found in cases of hyperinsulinism. These normal findings in abnormal patients, and their mechanisms, are reviewed.
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PMID:When normal is abnormal: keys to laboratory diagnosis of hidden endocrine disease. 2159 44

In recent years, tyrosine kinase inhibitors (TKIs) have emerged as a new class of anti-cancer therapy with proven efficacy in several types of carcinoma. Although generally considered less toxic than cytotoxic chemotherapy, TKIs do have significant side effects including fatigue and hypertension. In addition, TKI-induced thyroid dysfunction is now recognized as a common toxicity that is associated with some TKI inhibitors. Detection of TKI-induced thyroid dysfunction requires routine monitoring of thyroid function and, in some cases, may require treatment. This review provides a comprehensive assessment of literature evaluating TKI-induced thyroid dysfunction, focusing on the potential mechanisms that result in this toxicity, whether the development of thyroid dysfunction is clinically meaningful, and controversies regarding treatment with thyroid hormone therapy.
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PMID:Tyrosine kinase inhibitor-induced hypothyroidism: incidence, etiology, and management. 2210 6

Childhood obesity is a worldwide health problem and its prevalence is increasing steadily and dramatically all over the world. Obese subjects have a much greater likelihood than normal-weight children of acquiring dyslipidemia, elevated blood pressure, and impaired glucose metabolism, which significantly increase their risk of cardiovascular and metabolic diseases. Elevated TSH concentrations in association with normal or slightly elevated free T4 and/or free T3 levels have been consistently found in obese subjects, but the mechanisms underlying these thyroid hormonal changes are still unclear. Whether higher TSH in childhood obesity is adaptive, increasing metabolic rate in an attempt to reduce further weight gain, or indicates subclinical hypothyroidism or resistance and thereby contributes to lipid and/or glucose dysmetabolism, remains controversial. This review highlights current evidence on thyroid involvement in obese children and discusses the current controversy regarding the relationship between thyroid hormonal derangements and obesity-related metabolic changes (hypertension, dyslipidemia, hyperglycemia and insulin resistance, nonalcoholic fatty liver disease) in such population. Moreover, the possible mechanisms linking thyroid dysfunction and pediatric obesity are reviewed. Finally, the potential role of lifestyle intervention as well as of therapy with thyroid hormone in the treatment of thyroid abnormalities in childhood obesity is discussed.
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PMID:Thyroid function in childhood obesity and metabolic comorbidity. 2213 Mar 12


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