Endocrine Block 1 Lecture Dr. Usman Ghani - ppt video online download
Serum levels of free T3 and T4, serum prolactin, testosterone, serum gonadotropins, . To investigate the relationship between serum thyrotropin ( TSH), insulin are now evolving from augmentation media vehicles to meme media vehicles. TSH increases the uptake of iodide into thyroid cells, moving to the apical liver, and some other peripheral tissues, T3 is formed from T4 by T4ORD due to ( Mann-Whitney; p>) and no significant relationship between length and saluer tous mes amis qui m'ont encouragé au cours de ces derniers mois, de même. A STUDY OF THYROID HORMONES (T3, T4 & TSH) IN PATIENTS OF TSH was increased than normal in % of the patients and all these A possible relationship of hypothyroidism with neurotic depression but not with dementia.
The small, butterfly-shaped gland pumps thyroid hormone straight into your bloodstream, where it circulates throughout your body to influence practically every system in your body. So when it goes on the fritz -- and it has for 20 million Americans -- everything suffers, and get this: According to the University of Maryland Medical Centerwomen over 50 are at the greatest risk for thyroid disorders.
Your Thyroid Not at Work Thyroid disease, generally, comes in two flavors: An underactive thyroid, called hypothyroidism, however, is a whole different story. According to the U. National Library of Medicinean underactive thyroid can lead to fatigue, brain fogirregular menstrual periods, weight gaindepression, constantly feeling cold, and even hair loss --all of which also can occur during perimenopause and into menopause.
Five to eight times as many women have hypothyroidism than hyperthyroidism. Is It Menopause or a Thyroid Disorder? There are no symptoms that could be absolutely not related to thyroid. We are all different and we change as individuals over time.
The 411 on Diabetes + Thyroid Disease
After all, in the end, the only surefire way to tell if your symptoms come from a lack of thyroid hormone or a lack of estrogen is to get your hormones tested, Einhorn indicates. Usually all that stands in their way of knowing is a simple blood test. In the case of an underactive thyroid, TSH levels will be markedly elevated, while low levels can be caused by several conditions, meaning that more testing will be needed to determine if the cause is an overactive thyroid.
A T3 test, which measures another thyroid hormone called triiodothyronine, is sometimes performed, but is generally not necessary for diagnosis, he says. Luckily, in most cases, simply taking thyroid meds can result in complete symptom resolution. Family history may be the greatest indicator of troubles ahead, but since so many people are undiagnosed, you could have a family history of thyroid disease and have no clue about it. Also, while the thyroid needs iodine in tiny amounts to churn out thyroid hormone, today, so many foods contain iodine that hypothyroidism due to iodine deficiency is extremely rare, he says.
Low-iodine diet LID is known to greatly increase the serum levels of TSH, which through its activation of TSHR, leads to increased proliferation of thyroid follicular cells and enlargement of the thyroid gland 47. The relative thyroid weight increased 2-fold, and the thyroid follicular cells became hypertrophic Figure 2, C, H, and Iwhich is typically associated with goiter Regulation of cell proliferation genes by GLIS3.
Gene ontology GO and pathway analysis http: In addition to cell cycle—regulatory genes, a number of ECM-related genes, including several collagen genes, e. These data suggest that, in addition to enhanced proliferation, thyroid glands from WT-LID mice display an increased fibrotic and inflammatory response and that these responses are suppressed in Glis3KO mice.
Previous studies have linked the LID-induced proliferation of thyroid follicular cells as well as thyroid follicular carcinoma cells to activation of the mTORC1 pathway 4 It is well known that TSH induces the expression of many genes involved in TH biosynthesis, particularly the expression of Pds and Nis and, to a lesser extent, that of Tpo and Duoxa2 67910 However, despite the high TSH levels in Glis3KO mice, the expression of Pds was reduced rather than increased Supplemental Table 3and Figure 5Awhile the expression of Tpo was slightly elevated, that of the monocarboxylate transporter 8 Mct8 also referred to as Slc16a2 moderately lower, and that of Nis, Tg, Duoxa2, Duoxa1, and Tshr not significantly altered.
The expression levels of Pax8, Ttf1 also referred to as Nkx2. GAPDH was used as a loading control. Data in E and F are derived from triplicate samples and representative of 2 independent experiments.
A STUDY OF THYROID HORMONES (T3, T4 & TSH) IN PATIENTS OF DEPRESSION
Since the uptake of iodide through NIS is a critical first step in TH biosynthesis and because its regulation is well studied 9we focused on the effect of GLIS3 on Nis expression in more detail. Together, these data support the hypothesis that GLIS3 plays a critical role in the regulation of Nis expression and is required for its optimal induction by TSH.
A Pie chart showing the position of GLIS3-binding regions on the genome of the mouse thyroid gland relative to their nearest gene identified by Chipset analysis. The promoter is defined as the region up to 5 kb upstream of the TSS. Tshr and Ccnb1 are included as negative controls. GO analysis identified transport-related genes that included Nis and Pds as among the top categories of downregulated genes directly regulated by GLIS3 Supplemental Table 5Cwhereas no highly significant correlation was found between a specific pathway and upregulated genes.
Discussion GLIS3 deficiency in humans is associated with the development of congenital hypothyroidism; however, the underlying mechanism is poorly understood 24 — In this study, we show that loss of GLIS3 function in mice also leads to the development of congenital hypothyroidism, as indicated by the significant decrease in serum TH concentration and greatly elevated serum TSH levels Figure 1, A and B.
Although in the first week after birth, the average size of the thyroid follicles in Glis3KO mice is smaller, thyroid morphology and serum TH levels are not significantly different from those in WT mice Figure 2A and Supplemental Figure 3. This, together with our data showing that the expression of genes critical for thyroid development, including Pax8, Ttf1 Nkx2. Therefore, the development of hypothyroidism in Glis3KO mice appears to be related to dyshormonogenesis.
Therefore, it is possible that in a different genetic background, GLIS3 deficiency might also affect embryonic thyroid development.
The expression of Tshr was not significantly changed in thyroid glands of Glis3KO mice, suggesting that the decreased expression of Pds and Nis is not due to the reduction in Tshr expression. Genetic variants and mutations in Nis, Pds, Tpo, and Duoxa2 have been linked to hypothyroidism 920 — 2340 ; the observed decrease in the expression of these genes is therefore, at least in part, responsible for the development of hypothyroidism in Glis3KO mice and would explain the development of congenital hypothyroidism in the group of GLIS3 patients with dyshormonogenesis 24 — 28 The mechanisms that regulate the transcription of Nis and Pds gene expression are not yet fully understood.
Nis expression is under complex control and regulated at both the transcriptional and posttranscriptional levels 9 Another study indicated that PAX8 regulates Nis transcription by binding directly to the NUE promoter region, which is critical for Nis transcriptional regulation 46while TTF1 has been reported to play a role in the regulation of Pds transcription Future studies need to determine in what ways these 2 transcription factors cooperate in regulating Nis transcription.
In addition to the critical function of GLIS3 in TH biosynthesis, our study demonstrates that it also has a key role in the regulation of thyroid follicular cell proliferation. The reduced proliferation of thyroid follicular cells is supported by gene profiling analysis showing decreased expression of a number of key cell cycle—regulatory genes Supplemental Table 3 and Figure 3D. However, in Glis3KO mice, in which TSH is greatly elevated, TSH-mediated induction of cell proliferation and cell cycle—regulatory genes and goiter development were not observed.
The difference in thyroid follicular cell proliferation between thyroid glands of WT and Glis3KO mice became even more distinct in mice fed a LID Supplemental Table 3 and Figure 3, C and Dand differences in the expression of cell cycle—regulatory genes between WT and Glis3KO mice were magnified under these conditions.
As they are proliferation-regulatory genes, though a few direct target genes were identified by ChIP-Seq analysis, the regulation of these genes by GLIS3 is largely mediated by an indirect mechanism Figure 6D and Supplemental Table 3.
The mTORC1 pathway plays a critical role in promoting proliferation in many cell systems and has been implicated in several cancers, including follicular thyroid cancer 50 We previously reported that GLIS3 undergoes a number of posttranslational modifications, including phosphorylation and ubiquitination, that can regulate GLIS3 transcriptional activity 54 Moreover, the recurrent positive- and negative-feedback regulation of TH biosynthesis may require tight regulation of GLIS3 transcription activity.
Similarly, such posttranslational modifications of GLIS3 might also play a role in its regulation of the mTORC1 pathway and, consequently, the expression of several cell cycle genes and thyroid follicular cell proliferation. These functions also provide a mechanism explaining why GLIS3 deficiency leads to neonatal hypothyroidism and prevents the development of goiter.
Elucidation of upstream pathways that regulate the transcriptional activity of GLIS3 may lead to new therapeutic strategies in the management of some thyroid gland—associated pathologies. Measurement of serum and tissue TH levels. Serum T3, T4, and TSH levels and free and thyroglobulin-bound T3 and T4 contents in thyroid gland were measured by radioimmunoassay as described in detail previously 40 The anti-NIS antibody was provided by N.
Anti-chicken or anti-rabbit Alexa Fluor — or Alexa Fluor —conjugated antibodies 1: Alexa Fluor —conjugated wheat germ agglutinin WGA 1: Fluorescence was observed with a Zeiss LSM confocal microscope.Thyroid Function Test :-T3,T4,TSH -thyroid symptoms and types in Hindi-DOCTOR Lab
Proliferation of thyroid follicular cells was analyzed by the EdU incorporation assay.