Fekete C, Lechan RM. Central regulation of hypothalamic-pituitary-thyroid axis under physiological and pathophysiological conditions. Endocr Rev. Hypothalamus-pituitary-thyroid axis.
Compr Physiol. Activation and inactivation of thyroid hormone by deiodinases: local action with general consequences. Cell Mol Life Sci. Dentice M, Salvatore D. Deiodinases: the balance of thyroid hormone: local impact of thyroid hormone inactivation. J Endocrinol. Cellular and molecular basis of deiodinase-regulated thyroid hormone signaling.
The Type 2 Deiodinase Thr92Ala polymorphism is associated with worse glycemic control in patients with type 2 diabetes mellitus: a systematic review and meta-analysis. J Diabetes Res. J Clin Endocrinol Metab. Association analyses of variants in the DIO2 gene with early-onset type 2 diabetes mellitus in Pima Indians. Thyroid —7. Thyroid signaling, insulin resistance, and 2 diabetes mellitus: a mendelian randomization study.
J Biol Chem. FoxO1 deacetylation regulates thyroid hormone-induced transcription of key hepatic gluconeogenic genes. Malik R, Hodgson H. The relationship between the thyroid gland and the liver. QJM — Targeted disruption of the type 1 selenodeiodinase gene Dio1 results in marked changes in thyroid hormone economy in mice.
Endocrinology —9. Eur J Biochem. PubMed Abstract Google Scholar. Perinatal deiodinase 2 expression in hepatocytes defines epigenetic susceptibility to liver steatosis and obesity. The foxo1-inducible transcriptional repressor Zfp causes hepatic steatosis and hypercholesterolemia. Cell Rep. Identification of molecular mechanisms related to nonthyroidal illness syndrome in skeletal muscle and adipose tissue from patients with septic shock.
Clin Endocrinol. Oxf —7. Thyroid hormone promotes postnatal rat pancreatic beta-cell development and glucose-responsive insulin secretion through MAFA. Diabetes — Liganded thyroid hormone receptor-alpha enhances proliferation of pancreatic beta-cells. Lenzen S, Bailey CJ.
Thyroid hormones, gonadal and adrenocortical steroids and the function of the islets of Langerhans. Peripheral metabolism of thyroid hormone and glucose homeostasis.
Thyroid — Thyroxine treatment and insulin secretion in the rat. Diabetologia — Triiodothyronine T3 -mediated toxicity and induction of apoptosis in insulin-producing INS-1 cells. Life Sci. Thyroid hormone modulates glucose production via a sympathetic pathway from the hypothalamic paraventricular nucleus to the liver.
The thyroid hormone-inactivating type III deiodinase is expressed in mouse and human beta-cells and its targeted inactivation impairs insulin secretion. Impaired insulin secretion from the pancreatic islets of hypothyroidal growth-retarded mice.
Thyroxine induces pancreatic beta cell apoptosis in rats. Diabetologia —5. Integration of NPY, AGRP, and melanocortin signals in the hypothalamic paraventricular nucleus: evidence of a cellular basis for the adipostat.
Neuron — From lesions to leptin: hypothalamic control of food intake and body weight. PubMed Abstract. Starvation-induced changes in the hypothalamic content of prothyrotrophin-releasing hormone proTRH mRNA and the hypothalamic release of proTRH-derived peptides: role of the adrenal gland.
FEBS Lett. NPY and MC4R signaling regulate thyroid hormone levels during fasting through both central and peripheral pathways. Cell Metab. Type 3 deiodinase deficiency causes spatial and temporal alterations in brain T3 signaling that are dissociated from serum thyroid hormone levels. Endocrinology —8. Type 3 deiodinase role on central thyroid hormone action affects the leptin-melanocortin system and circadian activity.
They also found a strong correlation with BMI and neck circumference. In a group of 72 patients preparing for gastric bypass surgery, 25 percent were found to have undiagnosed subclinical hypothyroidismiii.
They concluded that overall, morbid obesity was associated with elevated TSH and that weight-loss after surgery generally resulted in decreasing TSH. This has lead some researchers to believe that there is another cause of the elevation of TSH that is not related to low levels of circulating thyroid hormones.
Currently, a popular theory is that insulin resistance leads to changes in the thyroid that can result in changes in the gland and possibly in TSH levels of thyroid hormone levelsvi.
Other things being examined are associations with leptin and adiponectin. There is enough evidence for undiagnosed thyroid disease in obesity, that if you have excess weight or obesity, it is probably a good idea to have your thyroid checked with your annual labs.
This is even truer if you are female or know that you have insulin resistance or diabetes, because of the increased risk. The most common tests used to evaluate the thyroid are:. To learn more about thyroid disease, you can talk to your doctor or visit the following Web sites for more information:. She is the Chief Science Officer for Catalina Lifesciences LLC, a company dedicated to providing the best of nutritional care to weight-loss surgery patients.
Her greatest love is empowering patients to better their own health. High prevalence of previously unknown subclinical hypothyroidism in obese patients referred to a sleep clinic for sleep disordered breathing. Nutr Metab Cardiovasc Dis. Prevalence of subclinical hypothyroidism in a morbidly obese population and improvement after weight loss induced by Roux-en-Y gastric bypass. Obes Surg. Obesity is associated with increased serum TSH level, independent of thyroid function.
Swiss Med Wkly ;— v Marina A. Euthyroid controls N group were sham-injected with saline. As a control for the possible stress effects of the injection itself, saline was injected ip into eu- and hypothyroid control rats.
At the extremely low dose used here, actinomycin D only inhibits the synthesis of messenger RNA The time course of the effect of T 3 on RMR was also investigated in another experiment in which deiodinase activities were acutely inhibited as above. In the and h treatment groups, PTU administration was continued until 12 h before the animal was killed.
To acquire time-course data, with respect to oxygen consumption, sequential measurements were taken 1 h before and at various intervals after the start of iodothyronine treatment.
The RMR was measured using open-circuit indirect calorimetry. Details of this set-up and of the way that measurements are made were given by Lanni et al. Briefly, the experiments done to determine the time course of the calorigenic effects of iodothyronines were run as follows. In each rat, RMR was measured just before the injection of iodothyronines time 0. In the same rat, RMR was measured at different time-points after the injection, so that time 0 represents the starting value for each rat.
The increase in RMR was obtained by comparing the value at time 0 with those at other time points, always in one and the same rat. The mean values we reported in the figures were obtained by averaging the increases in RMR observed in animals injected with one and the same iodothyronine.
After incubation of the mixtures at 0 C for 10 min, they were centrifuged, and the radioactivity in the supernatant was subsequently determined. Accordingly, 3,5-T 2 was shown to reach its highest concentrations in the liver, compared with other tissues 12 areas of the brain, pituitary glands, and heart investigated Pinna, G. Visser, A.
Jeitner, H. Grau, M. Eravci, H. Meinhold, and A. Baumgartner, submitted manuscript. By contrast, heart and skeletal muscle are two tissues that derive their intracellular T 3 directly from plasma by active transport 23 , and no deiodinase activities have been detected in these tissues in the rat Liver concentrations of T 2 s were determined after extraction from tissue samples, as reported by Pinna et al.
Each sample was assayed in triplicate. This amount of tracer did not affect the RIA measurements. Briefly, the assay was performed by adding the following in sequence: 1 experimental buffer 0.
The supernatant was discarded, and precipitated bound radioactivity was counted. The protein concentration was determined by the method of Hartree 27 , using BSA as standard. Comparison between independent means was performed using a t test. In the latter case, the dose needed was at least three times higher than that used for 3,5-T 2 ; but the effect was lower than that elicited by 3,5-T 2.
Changes in RMR in hypothyroid upper panel and euthyroid lower panel rats after administration of iodothyronines. The values are expressed as the percentage change from the value at time 0 i. The actual RMRs [lO 2 kg 0. Figure 1 lower panel illustrates the effect of the acute administration of T 3 , T 4 , or 3,5-T 2 to N rats. The simultaneous injection of actinomycin D with T 3 into N rats strongly inhibited the late part of the effect previously seen with T 3 after 24 h , whereas the early effect between 14 and 24 h was only slightly affected.
Under such conditions, the early part of the effect of T 3 was greatly reduced, indicating that deiodination is necessary for it to produce the early part of its effect in full Fig. Effect of acute inhibition of the deiodinases activity on the change in RMR seen after administration of T 3 to N rats. The graph is obtained from the mean of four rats. The increase started between 14 and 25 h and peaked at about 50 h, and the level returned to baseline 3—4 d after the injection.
Once again, the simultaneous injection of actinomycin D did not attenuate the presumable 3,5-T 2 stimulation observed between 14 and 25 h, but it did inhibit the effect seen after 25 h presumably T 3 -induced. These results support the idea that the two iodothyronines exert independent effects on RMR. D ; act. D groups, respectively. In the liver, the peak concentration of T 2 s was reached at 24 h. The maximal increase in T 2 s in the liver and the maximal increase in RMR occur at the same time at about 25 h after the injection.
The values are expressed as the percentage change from the maximal value i. The actual RMR [lO 2 kg 0. Here we report evidence that supports the hypothesis that the effect exerted by the administration of T 3 to normal euthyroid rats is not entirely attributable to T 3 itself.
We found that the pattern of change in RMR after administration of T 3 differed between euthyroid and hypothyroid rats: the maximal increase in RMR occurred 50—75 h after the injection in hypothyroid rats, but after only 25 h in euthyroid animals.
Nearly 40 yr ago, Tata 3 , studying the effect of T 3 on basal metabolic rate, reported that when T 3 was injected into euthyroid rather than hypothyroid rats, the difference in the response laid essentially in the steepness of the curves expressing the change in basal metabolic rate as a function of time.
Our observations and those of Tata could be taken to imply either: 1 that underneath the effect of T 3 elicited through the nuclear pathway lies another, more rapid, mechanism that becomes evident when the animal model used is a euthyroid rather than a hypothyroid one; or 2 that in euthyroid rats, T 3 is deiodinated to another iodothyronine with biological activity.
Indeed, deiodinase enzymes, being fully active under euthyroid conditions, have the potential to convert T 3 into a product capable of a more rapid enhancement of metabolic rate, possibly involving a cellular signaling pathway different from the nuclear one. Because we and others have shown that 3,5-T 2 is active in stimulating biochemical processes at both the mitochondrial and extramitochondrial levels 6 — 10 , 28 , this iodothyronine is a candidate for the molecule responsible for the difference between the effects seen when T 3 is injected into euthyroid rather than hypothyroid animals.
Because the effects elicited by T 3 are sensitive to actinomycin D, we thought that a simultaneous injection of actinomycin D and T 3 might help us discriminate the effects attributable to T 3 from those attributable to other products. What we found was that in N rats, administration of actinomycin D plus T 3 resulted in an inhibition predominantly of the late part of the response to T 3 after 24 h , the early phase between 14 and 24 h being much less affected.
That starts with including lean protein in your meals, says McAninch, and avoiding refined carbohydrates. Stay hydrated. However, your body needs enough water to work well, and that means getting about 2. See your doctor before starting any supplements. And some supplements, such as those that contain iodine, can worsen hypothyroidism. Some studies have suggested a connection between hypothyroidism and vitamin D deficiency. For instance, research published in in the International Journal of Health Sciences found that people with hypothyroidism were deficient in vitamin D.
Yet a analysis of the U. Get enough shut-eye. Not getting enough sleep can lower your metabolic rate, according to the National Sleep Foundation, which recommends that most adults get about seven to nine hours of sleep a night.
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