UMLS:C0011849 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Target Concepts:

Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Impairment of thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) has been documented in patients with uncontrolled diabetes mellitus (DM). In acromegalic patients, however, there have been no data regarding TSH secretion studied taking the existence of DM into consideration. Therefore, we investigated the TSH response to TRH [expressed as TSH increment (delta TSH)] in 14 untreated acromegalic patients, who did not show the suprasellar extension of adenoma, divided into two groups on the basis of either presence or absence of uncontrolled DM, and in 28 normal subjects. The mean max delta TSH was significantly reduced (p less than 0.02) in acromegalic patients despite similar mean serum T4 and free T4 index (FT4l) levels. Furthermore, the mean basal and max delta TSH in 7 patients with DM (FBS, 120-300 mg/dl; HbA1, 8.8-15.2%) were significantly lower than those in 7 patients without DM (p less than 0.05 and p less than 0.02, respectively) despite similar the mean serum T3, T4, FT4l, growth hormone (GH) and prolactin (PRL) levels and sellar volume. In 4 patients with DM the TSH response to TRH 6-8 weeks after insulin therapy, when their HbA1 levels were normal, increased compared to that before insulin therapy. The mean max delta TSH after selective adenomectomy in 8 patients (3 in DM group and 5 in non-DM group), whose fasting basal GH fell to less than 5 ng/ml, was almost identical to that in normal subjects. In conclusion, the present study suggests that the abnormality in TSH secretion in acromegalic patients may be increased by the existence of uncontrolled DM.
...
PMID:The influence of diabetes mellitus on thyrotropin response to thyrotropin-releasing hormone in untreated acromegalic patients. 313 52

Previous studies demonstrated alterations of thyroidal economy in untreated diabetes mellitus both in man and experimental animals. To test the role of beta-hydroxybutyric acid (BHB) and acidosis in generating such changes, we studied the pituitary-thyroid axis of streptozotocin-diabetic rats, BHB or ammonium chloride (NH4Cl)-treated normal rats. Serum TSH, pituitary content and pituitary concentration of TSH, serum T4, T3 and free T4 (FT4), were all measured by RIA. In short term (2 days) diabetic rats the pituitary content of TSH was normal whereas the concentration (per mg of protein) was elevated (p less than 0.05 versus control group). Serum TSH (p less than 0.05), serum T4 (p less than 0.05), serum T3 (p less than 0.01) and serum FT4 (p less than 0.05) were all significantly decreased. In long term (30 days) untreated diabetic rats serum changes were similar to the short term diabetic group, though the pituitary content of TSH was significantly decreased (p less than 0.05). Animals treated with NH4Cl had no variations from controls. However, rats treated with BHB displayed a significant decrease in pituitary content of TSH (p less than 0.05), pituitary concentration of TSH (p less than 0.05) and in plasma TSH (p less than 0.01), and normal thyroid hormones in serum. No significant changes were seen in the TSH response to TRH in 2 or 30 days untreated diabetic and in BHB - treated animals. The data suggest that BHB, although not NH4Cl acidosis, may be capable of inducing a moderate depression of pituitary and plasma TSH of a lesser magnitude of that accompanying the full, long term diabetic state in the rat.
...
PMID:Effects of diabetes, beta-hydroxybutyric acid and metabolic acidosis on the pituitary-thyroid axis in the rat. 316 31

Chronic L-thyroxine administration (6 micrograms/100g BW, ip, daily) for 2 or 3 months suppressed serum TSH concentrations and decreased both the incidence of spontaneous lymphocytic thyroiditis (LT) and the serum levels of anti-thyroglobulin (anti-Tg) antibodies in the diabetes prone BB/Wor rat. This suggests that TSH may play a role in the occurrence of LT in this rat model. In contrast to these observations, L-thyroxine administration did not affect the markedly increased incidence of LT or the elevated serum anti-Tg antibodies in iodine supplemented BB/Wor rats, suggesting that TSH stimulation is not necessary for the development of iodine induced LT in this rat model. Other factors, such as the increased antigenicity of highly iodinated Tg, may be more important.
...
PMID:Effect of L-thyroxine administration on the incidence of iodine induced and spontaneous lymphocytic thyroiditis in the BB/Wor rat. 334 51

We studied serum TSH, pituitary TSH and alpha and beta-subunits of TSH and their messenger ribonucleic acids (mRNAs) in three models of nonthyroidal illness (NTI) in the rat, ie diabetes mellitus (1 wk after 65 micrograms streptozotocin/g BW IP), turpentine oil-injection (8 to 48 hours after after a dose of 5 microliter/g bw SC), and complete fasting for 72 hours. Euthyroid, hypothyroid (two months after thyroidectomy) and hyperthyroid rats (30 micrograms T4/d X 7, SC) were also studied for comparison. Pituitary TSH, alpha and beta subunits and serum TSH, T4, and T3 were measured by RIA. Pituitary mRNAs coding for common delta and TSH-beta subunits were determined by cytoplasmic dot hybridization technique using specific [32P]-cDNA probes. In all NTI models there were significant decreases in serum levels of TSH, T4, and T3, but no significant changes were observed in the pituitary content of TSH, and alpha and TSH-beta subunits. Hypothyroid rats had an increase in serum TSH, pituitary TSH, and pituitary TSH-beta subunit and a decrease in pituitary alpha subunit. On the other hand, hyperthyroid rats showed a decrease in serum TSH, pituitary TSH, and pituitary TSH-beta subunit, while there was no change in the alpha subunit. A significant reduction in the pituitary TSH-beta mRNA levels was observed in all NTI models and hyperthyroidism, while TSH-beta mRNA was increased in thyroidectomized rats. alpha-mRNA was increased only in the pituitary of hypothyroid rats; there was no appreciable change in the pituitary alpha-mRNA in the various other pituitary groups.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:A study of pituitary thyrotropin, its subunits, and messenger ribonucleic acids in nonthyroidal illness. 335 21

To evaluate the role of a circulating inhibitor of extrathyroidal conversion of T4 to T3 (IEC) in the causation of low T3 states in patients with various nonthyroidal illnesses (NTI), we measured the in vitro T3 production in the presence of ether extract of plasma. Blood samples were obtained from 22 normal subjects and 140 patients with various NTI; liver cirrhosis (LC) 37, diabetes mellitus (DM) 48, respiratory failure (RF) 15, chronic renal failure (CRF) 10 and others 30. The assay procedure of in vitro T3 production was as follows. Rat liver homogenate was incubated with 2.5 microM T4 in the presence of evaporated ether extract of plasma and the amount of T3 produced was quantified by RIA. In each assay, control plasma extracts taken from the two normal subjects were used. The results were expressed as a percentage of the control value (%T3 production), and estimated as positive IEC when %T3 production was under 72.7%, that was 2SD below the mean value of normal controls. Patients were divided into three groups; Group I (T3 greater than or equal to 80 ng/dl), Group II (80 greater than T3 greater than or equal to 50) and Group III (50 greater than T3). The %T3 productions were 88.5 +/- 22.0 in Group I, 84.9 +/- 31.5 in Group II and 78.9 +/- 34.0 in Group III respectively. The %T3 productions of each group were significantly lower than that of normal control, 101.9 +/- 14.6. IEC was positive 23.4% in Group I, 41.9% in Group II and 43.8% in Group III. There were eight nonsurvivors, and they all belonged to Group III, in which both serum T3 and T4 were subnormal. In nonsurvivors, serum concentrations of T3 (20 +/- 11 ng/dl) and TSH (1.2 +/- 1.1 microU/ml) were significantly lower than that of survivors in Group III (T3; 38 +/- 10 ng/dl p less than 0.005, TSH; 2.8 +/- 1.4 microU/ml p less than 0.05). The %T3 productions were 83.8 +/- 32.1 in survivors and 64.8 +/- 37.9 in nonsurvivors, and the incidences of positive IEC were 37.5% in survivors and 62.5% in nonsurvivors. From the standpoint of the underlying illnesses, serum concentrations of T3 (mean +/- SD ng/dl) were 49 +/- 21 in LC, 64 +/- 11 in DM, 40 +/- 22 in RF and 63 +/- 15 in CRF, and %T3 productions were 60.6 +/- 26.5 in LC, 82.5 +/- 25.8 in DM, 109.6 +/- 32.1 in RF and 97.6 +/- 24.3 in CRF.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:[An inhibitor of extrathyroidal conversion of thyroxine to 3,5,3'-triiodothyronine (IEC) in plasma of patients with various nonthyroidal illnesses]. 339 31

Spontaneous LT and elevated serum anti-Tg occur in the diabetes prone BB/W rat, but thyroid function is essentially normal in the rats with LT. Prolonged low dose MMI decreases the incidence of LT in BB/W rats. The administration of excess iodine beginning at 30 days of age markedly accelerates the occurrence of LT and anti-Tg at 90 days of age. Low iodine intake decreases the incidence of LT. Excess iodine intake did not induce LT in W-line, Wistar-Furth, and Sprague-Dawley rats. This suggests that iodine induced LT occurs only in genetically susceptible rats. Despite the increased incidence of LT during iodine administration, thyroid function remains essentially normal. This is in contrast to the frequent induction of hypothyroidism following iodine administration to euthyroid patients with Hashimoto's thyroiditis. In order to decrease thyroid reserve, rats were hemi-TX at 30 days of age. The administration of iodine markedly increased the incidence of LT and serum anti-Tg, increased the weight of the remaining lobe, and induced hypothyroidism as determined by significantly lower serum T4 and T3 concentrations and elevated serum TSH concentrations. Excess iodine administration to hemi-TX W-line rats (genetically equivalent, non-diabetes, non-LT prone BB/W rats) did not induce LT but did induce hypothyroidism, suggesting that BB/W and W-line rats are susceptible to iodine induced hypothyroidism, perhaps unrelated to the induction of LT. Excess iodine did not induce LT or affect thyroid function in hemi-TX Wistar-Furth and Sprague-Dawley rats.
...
PMID:Effect of iodine intake and methimazole on lymphocytic thyroiditis in the BB/W rat. 347 23

In order to elucidate whether or not the 'coupling defect' observed in thyroids from diabetic rats is due to a structural defect of intrathyroidal thyroglobulin (Tg), the sedimentation pattern and the stability of the thyroidal soluble iodoproteins were studied in control (C), food restricted (FR), diabetic (D) and insulin-treated diabetic (D+I) rats fed a low iodine diet either with (NID) or without (LID) iodide supplementation and labelled with 125I: acutely, 24 h prior to sacrifice and chronically, by feeding the corresponding diet labelled for 60 days. Diabetes resulted in a decrease of thyroidal weight, an increase of both thyroidal 127I content and concentration and decreased plasma TSH, irrespective of the diet. Insulin treatment reversed these alterations. Food restriction led to an intermediate situation between C and D. The iodoamino acid distribution in the acutely labelled thyroidal soluble iodoproteins showed a significant increase in the percent of organified 125I found as iodotyrosines (MIT and DIT) and a decrease of that found as iodothyronines (T3 and T4) both in D and FR. However, in the isotopically equilibrated groups, no differences were found except in LID-D where a slight increase in DIT and a decrease in T3 was found as compared to the corresponding control. The sedimentation patterns of both acutely and chronically labelled thyroidal soluble iodoproteins from all experimental groups displayed two peaks. The main one, corresponding to Tg, had a slightly lower sedimentation coefficient than the 19 S internal marker run in parallel, while the second one, relatively small, formed probably by dissociation of the main Tg peak, sedimented more slowly (12- 14 S).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Intrathyroidal thyroglobulin in streptozotocin-diabetic rats. 352 86

Sixty patients with end stage chronic renal failure (CRF) enrolled in a dialysis program underwent studies of serum thyroid hormones and carbohydrate metabolic state. The aim of the study was: 1) to evaluate whether the glucose intolerance per se represents a factor for the alteration of circulating thyroid hormones; and 2) to explore the potential usefulness of specific thyroid hormones and particularly reverse T3 (RT3) as indicators for predicting glucose intolerance. Forty-two patients received hemodialysis and 18 were on intermittent peritoneal dialysis (IPD). CRF patients had reduced serum total T4 and T3 levels, slightly decreased RT3 and TBG concentrations and normal TSH values. There was no significant difference in serum thyroid hormone indices between HD and IPD patients. Glucose intolerance was found in 25 patients. Ten had fasting hyperglycemia and diabetic response to oral glucose tolerance test (OGTT), 15 had an impaired glucose tolerance according to the criteria of the National Diabetes Data Group. In CRF patients with glucose intolerance, serum T3 and T3/T4 molar ratio were significantly lower than in those with a normal OGTT response, whereas serum RT3 and RT3/T4 molar ratio were found to be higher. In the whole group of CRF patients these serum thyroid hormones closely correlated with glucose tolerance indices. To investigate the usefulness of serum RT3 assay in predicting glucose intolerance we compared the outcome of the OGTT and serum RT3 values. Using the results of the OGTT as the true diagnosis of glucose intolerance, serum RT3 assay showed a diagnostic specificity of 94.2% and a sensitivity of 100%. In conclusion these results suggest that: 1) the glucose intolerance, which frequently occurs in uremia, may influence circulating thyroid hormones probably leading to a shift in the peripheral tissue conversion of T4 from T3 to RT3; and 2) serum RT3 assay could assume a clinical interest in assessing carbohydrate metabolic state in treated end stage renal failure independently of the type of dialysis therapy.
...
PMID:Serum reverse T3 assay for predicting glucose intolerance in uremic patients on dialysis therapy. 358 26

Serum T4, FT4, T3, and TSH were measured in a group of children with insulin dependent diabetes mellitus and a control group. In the insulin dependent diabetes mellitus group, serum T3 concentration was significantly lower than the control values. Serum T4, FT4 and TSH level did not differ. The difference in serum T3 concentration was significant between diabetic children with good or poor control. Thyroglobulin antibodies were investigated in diabetic children by Serono's "hTg antibodies" kit. Thyroglobulin antibodies were present in 14.5%. TSH concentration did not differ in antibody positive and negative cases, but one child with diabetes had evidence of moderately impaired thyroid reserve.
...
PMID:Thyroid hormones and thyroglobulin autoantibodies in insulin dependent diabetes mellitus. 359 81

We have recently reported that iodine administration (0.05% iodine in drinking water) to weanling, diabetes mellitus- and lymphocytic thyroiditis (LT)-prone Biobreeding Worcester (BB/W) rats strikingly increases the incidence of LT without occurrence of iodine-induced hypothyroidism, which frequently results when excess iodine is administered to euthyroid patients with Hashimoto's thyroiditis. Since hypothyroidism did not occur in the iodine-treated BB/W rats, hemithyroidectomy was carried out in 30-day-old BB/W rats to increase thyroid mass and functional reserve. Iodine administration for 60 days markedly increased antithyroglobulin antibodies (0.40 +/- 0.08 vs. 0.15 +/- 0.06 OD; P less than 0.02), the incidence of LT (68% vs. 13%; P less than 0.001), and thyroid weight of the residual lobe (10.5 +/- 0.7 vs. 6.3 +/- 0.3 mg/100 g BW; P less than 0.001) and induced hypothyroidism (T4, 2.5 +/- 0.2 vs. 3.0 micrograms/dL; P less than 0.05; T3, 25.1 +/- 1.9 vs. 37.5 ng/dL; P less than 0.001; TSH, 252 +/- 49 vs. 61 +/- 14 microU/mL; P less than 0.02). Hypothyroidism in the iodine-treated rats occurred primarily in those with LT. Similar studies were carried out in the non-diabetes mellitus-, non-LT-prone, genetically equivalent BB/W rats (W-line), the parent strain Wistar-Furth rats, and Sprague-Dawley rats. Iodine administration did not induce LT or antithyroglobulin antibodies in these three strains and did not affect thyroid function in Wistar-Furth and Sprague-Dawley rats. However, in the W-line rats, iodine excess did induce thyroid enlargement in the residual lobe (8.4 +/- 0.2 vs. 6.4 +/- 0.2 mg/100 g BW; P less than 0.001), a decrease in serum T3 (71.5 +/- 2.9 vs. 86.0 +/- 2.5 ng/dL; P less than 0.001), and an increase in serum TSH (344 +/- 65 vs. 69 +/- 6.0 microU/mL; P less than 0.001). It is evident, therefore, that hemithyroidectomy in BB/W rats sufficiently reduces functioning thyroid tissue, resulting in iodine-induced LT and hypothyroidism, similar to iodine-induced hypothyroidism in euthyroid patients with Hashimoto's thyroiditis. It is unclear, however, why iodine administration also induced hypothyroidism in hemithyroidectomized, genetically similar, W-line rats in the absence of LT. This observation suggests that iodine-induced hypothyroidism in rats may be genetically determined.
...
PMID:Iodine-induced thyroiditis and hypothyroidism in the hemithyroidectomized BB/W rat. 359 27

<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>