Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The responsiveness to vasoactive agents in the perfused mesenteric vascular bed of streptozocin-induced diabetic rats was examined and compared with that of propylthiouracil-induced hypothyroid rats. Diabetic rats at 4 and 8 weeks after the induction of diabetes showed a significant decrease in isoproterenol-induced vasodilatation. In addition, the contractile responses to norepinephrine and 5-hydroxytryptamine and the vasodilative response to acetylcholine were significantly decreased in 12-week-diabetic rats. The contractile response to nerve stimulation was markedly decreased at 8 and 12 weeks. On the other hand, hypothyroid rats showed a decreased response to isoproterenol, but they did not show any change in the response to nerve stimulation. A decrease in plasma thyroid hormone levels in diabetic rats at any time period was similar in extent to that in hypothyroid rats. The data indicate that the progressive changes in vascular reactivity in diabetic rats may be divided into two stages. In the early stage, the altered reactivity of vasculature is likely to be mediated by hypothyroidism, whereas in the later stage, it is induced by other factors, e.g. hyperglycemia and hypoinsulinemia. Adrenergic neuropathy is not caused by hypothyroidism.
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PMID:Changes in vascular reactivity in experimental diabetic rats: comparison with hypothyroid rats. 316 24

Previous studies of patients with end-stage renal disease (ESRD) indicate that the prevalence of goiter varies from 0 to 58% while that of hypothyroidism ranges from 0 to 9.5%. In addition, altered serum thyroid hormone levels are present in euthyroid patients with ESRD and may be related to nonthyroidal disorders including malnutrition. To examine these issues further, 306 patients with ESRD were compared to 139 hospitalized patients without renal disease (control population). Goiter was present in 43% with ESRD compared to 6.7% of controls (P less than 0.001). Goiter frequency was greater (49.6%, P = 0.047) and serum parathyroid hormone levels higher (mean: 238.6 microlitersEq/ml, P less than 0.001; normal: less than 15 microlitersEq/ml) in 115 patients dialyzed for longer than 1 year than in 191 dialyzed for less than 1 year or not at all (38.7%, and 61.5 microlitersEq/ml, respectively). In addition, goiter was more common in females (50.0%) than in males (35.1%, P = 0.008) with ESRD. No significant relationships were observed between goiter frequency and age, race, diabetes mellitus, or elevated antimicrosomal antibody titers. The prevalence of primary hypothyroidism was higher in ESRD (2.6%) than in 2122 in- and out-patients (1.1%) (P = 0.024). Compared to the total group of ESRD patients, the hypothyroid patients were predominantly female (88% vs. 50%) and had a higher frequency of positive antimicrosomal antibody titers (50% vs. 6.7%, P = 0.029). The frequency of hyperthyroidism was not significantly different, being 1.0% in ESRD compared to 0.3% in the general population (P = 0.057). There was a higher frequency of reduced free T4 index values in the 287 euthyroid patients with ESRD (12.9%) than in controls (3.6%) (P = 0.002). Similarly, free T3 index values were reduced below 100 in 65.5% with ESRD compared to 33.8% of controls (P less than 0.001). In addition, serum albumin levels were lower in euthyroid patients with ESRD (3.5 g/dl, P less than 0.001) than in controls (3.8 g/dl). Serum T3 levels correlated directly with both serum albumin (r = 0.57, P less than 0.001) and transferrin (r = 0.54, P less than 0.001) levels in ESRD as well as in controls (r = 0.74, P less than 0.001, and r = 0.69, P less than 0.001, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The thyroid in end-stage renal disease. 325 81

The liver and kidney nuclear T3 content and the maximal nuclear T3-binding capacity (MBC) were measured 1 month after streptozotocin administration and compared with values in controls either fed ad libitum (C) or offered a restricted diet (FR). A group of insulin-treated diabetic (D+I) rats was also included. Plasma T4 and T3 concentrations decreased to low levels in diabetic (D) rats. Plasma T3 levels were decreased in FR rats, whereas circulating T4 was in the normal range for C animals. The MBC (nanograms of T3 per mg DNA) for liver and kidney nuclear T3 was determined by an in vivo saturation technique. The respective results for all groups were as follows (asterisks denote values differing from C with P values less than 0.05): C, 0.601 and 0.414; FR, 0.583 and 0.369; D, 0.310 and 0.220; D+I, 0.630 and 0.394. Nuclear T4 and T3 concentrations were determined by an isotopic equilibrium technique. Nuclear T3 (nanograms per mg DNA) for liver and kidney were, respectively, 0.298 and 0.176 for C, 0.208 and 0.135 for FR, 0.109 and 0.070 for D, and 0.270 and 0.168 for D+I rats. The decreased liver and kidney nuclear T3 content in D rats appears to be due to a marked reduction of their available intracellular T4 pool, from which T3 could be generated, but most likely represents a decreased T3 uptake into liver and kidney nuclei, as the nuclear to plasma ratios of labeled T3 were decreased in D rats. The low levels of T3 in nuclei of FR rats could be attributed to an inhibition of T4 to T3 conversion, since the intracellular pool of T4 appears to be normal. The possibility that diabetes and food restriction might affect the thyroid activity was examined by measurement of the activities of alpha-glycerophosphate dehydrogenase and cytosol malic enzyme, two liver and kidney enzymes regulated by thyroid hormone. Furthermore, although the measurements made in FR rats excluded the possibility that the alterations in MBC found in D animals were nutrition dependent, the reduced nuclear T3 content concomitant with food restriction may account for some of the quantitative changes in the alpha-glycerophosphate dehydrogenase and cytosol malic enzyme activity found in D rat tissues. In conclusion, the present findings suggest that the observed changes in indices of thyroid hormone action in liver and kidney of D rats could be related to alterations in nuclear T3 receptor concentrations and the concentration of T3 bound to the receptor.
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PMID:Diabetes decreases liver and kidney nuclear 3,5,3'-triiodothyronine receptors in rats. 355 32

We investigated the serial changes in the plasma levels of anti-thyroglobulin antibody (ATA) by solid-phase enzyme immunoassay, thyroid hormones and blood glucose, since spontaneous occurring lymphocytic thyroiditis (LT) has been found in spontaneously diabetic Bio Breeding/Worcester (BB/W) rat. We also observed the correlation between these levels and histological findings in the thyroid gland. The incidence of diabetes was 0% in 5 week old rats (group A), 70% in 11 week old rats (group B), and 86% in 20 week old rats (group C), while LT was observed in 0% in group A, 20% in group B and 48% in group C. Although the incidence of both increased with age, there was no link between LT and diabetes. Plasma ATA levels were 91.4 +/- 28.5 (OD492 X 1,000, mean +/- SEM) in the control (14 week old Wistar Furth) rats. 49.5 +/- 15.4 in group A, 197.8 +/- 41.5 in group B, and 376.7 +/- 48.7 in group C, again showing a clear increase with age. In group C, the plasma levels of ATA in rats with LT were significantly higher than those without LT. In addition, 6 out of 11 rats without LT had abnormaly high ATA levels. In group C, the plasma levels of free 3,5,3'-triiodothyronine (FT3) and total thyroxine (TT4), and also the FT3/TT4 ratio were significantly lower and the plasma levels of blood glucose were higher than in the other groups. There was no difference between the plasma thyroid hormone levels in rats with LT and those without LT. These studies suggest that LT may occur independently of insulitis, namely diabetes, ATA levels and the incidence of LT increase with age, the site of ATA production may not be confined to the thyroid gland, and the derangement of glucose metabolism may be one of the factors in the decrease in plasma thyroid hormone. The BB/W rat is not only a useful animal model to use in exploring the pathogenesis of human insulin-dependent diabetes mellitus, but also spontaneous autoimmune thyroiditis.
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PMID:Spontaneous autoimmune thyroiditis in Bio Breeding/Worcester (BB/W) rat. 355 49

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.
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PMID:Serum reverse T3 assay for predicting glucose intolerance in uremic patients on dialysis therapy. 358 26

Several previous studies have reported that serum T3 and reverse T3 (rT3) concentrations are altered in uncontrolled diabetes mellitus and their normalization occurs when euglycemia is achieved. Therefore, this study was undertaken to examine the usefulness of serum T3 and rT3 levels as indices of metabolic control in diabetes mellitus. Serum T3, rT3, T4, Free T4, TSH and T3 resin uptake were determined in 18 normal subjects and 35 patients with newly discovered diabetes mellitus before initiation of therapy and reassessed after normalization of glycosylated hemoglobin (HbA1) concentration. These thyroid hormone concentrations were compared to the well established parameters of metabolic control such as fasting plasma glucose (FPG), peak plasma glucose (PPG), area under the curve of the oral glucose tolerance test (sigma G), 24 hr urinary glucose level (UG), HbA1 as well as glycosylated protein (GlyPr) and glycosylated albumin (GlyAlb) concentrations. Serum T4, T3RU, Free T4 and TSH concentrations in patients with diabetes mellitus prior to treatment were not significantly different from normal subjects and were not significantly correlated with any of the parameters of diabetic control. Serum T3 was significantly lower and serum rT3, significantly higher in diabetic patients prior to treatment as compared to normal subjects and both T3 and rT3 normalized in 20 patients studied when adequate metabolic control was achieved as reflected by normalization of HbA1 (less than 8.2%). Furthermore, significant negative and positive correlations were noted between parameters of metabolic control and serum T3 and rT3 levels respectively. Therefore, this study demonstrates that serum T3 and rT3 may be reliable indices of metabolic control in diabetes mellitus.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Res 1986 Oct
PMID:Serum T3 and reverse T3 concentrations: indices of metabolic control in diabetes mellitus. 381 44

Euthyroid sick syndrome is characterized by low serum T3 and raised reverse T3 (rT3). Most of the states with this syndrome are also documented to manifest hyperglucagonemia. Furthermore, several recent studies have suggested that glucagon may play a role in T4 monodeiodination in some of these states such as starvation and uncontrolled diabetes mellitus. Therefore, hyperglucagonemia was induced by intravenous glucagon administration in euthyroid healthy volunteers and thyroid hormone levels were determined at frequent intervals up to six hours. Plasma glucose and insulin rose promptly on glucagon administration, thus establishing the physiologic effect of glucagon. Serum T4, free T4, T3 resin uptake, and TSH concentrations remained unaltered throughout the study period. Serum T3 declined to a significantly low level (P less than 0.05) between 60-90 minutes. Serum rT3 rose significantly (P less than 0.05) by four hours and the rise was progressive till the end of the study period. Therefore, these results suggest that hyperglucagonemia may be one of the factors responsible for lowering of T3 and a rise in rT3 in euthyroid sick syndrome.
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PMID:Glucagon administration induces lowering of serum T3 and rise in reverse T3 in euthyroid healthy subjects. 391 May 31

We have previously established the value of 2-dimensional electrophoretic mRNA activity profiles for investigating the hepatic genomic response to several metabolic perturbations, such as thyroid hormone or GH treatment, diabetes, high carbohydrate diet, starvation, and uremia. We now report the effects of adrenalectomy and dexamethasone treatment, and compare these with alterations due to thyroidectomy and T3 treatment. Total rat hepatic RNA was isolated and translated in a reticulocyte lysate system. The [35S]methionine-labeled translated products were separated by 2-dimensional gel electrophoresis and quantified with computerized videodensitometry. Of 200 consistently quantifiable products, 14 (7%) were altered by adrenalectomy and dexamethasone, including 4 products (46, 47, 56, and 57) which have not been observed to change in previous studies from this laboratory. Adrenalectomy increased 5 and decreased 2 products, whereas dexamethasone increased 1 and decreased 8 products. Two products maintained the same directional shift in the transitions form adrenalectomy to control and from control to the dexamethasone-treated state. Thyroidectomy and T3 altered 13 products. Thyroidectomy increased 2 and decreased 7 products, whereas T3 treatment increased 6 and decreased 3 products. Four products maintained the same directional shift in the transitions from thyroidectomy to control and from control to the T3-treated state. In all of the manipulations performed (adrenalectomy, thyroidectomy, dexamethasone treatment, and T3 treatment), a total of 20 separate products changed. One third were affected by alterations of both the steroidal and thyroidal states. However, when adrenalectomy and thyroidectomy were compared, only 7% of the shifts were concordant, whereas 30% of the shifts were concordant when treatment with dexamethasone and T3 were compared. These results demonstrate that the mRNA activity response is highly specific for each hormonal manipulation. In addition, unanticipated interrelationships between steroidal and thyroidal states were observed. In some, the presence of T3 appears necessary for the suppressive effect of dexamethasone. Others show that T3 appears to inhibit a stimulatory effect of dexamethasone. Specificity of response to dexamethasone is emphasized by the lack of response to vitamin D, deoxycorticosterone, and dihydrotestosterone and by a different response to estradiol from dexamethasone.
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PMID:Hepatic messenger ribonucleic acid activity profile of rats subjected to alterations in thyroidal and adrenocortical states: evidence for significant interaction. 399 30

A large prospective study investigated prenatal and perinatal antecedents of chronic motor dysfunction (cerebral palsy [CP]), evaluating approximately 400 characteristics of the mothers, pregnancies, or deliveries. In addition to confirming some, but not all, of the classic risk factors for CP, this study observed relatively large increases in the CP rate in association with maternal mental retardation, seizure disorders, hyperthyroidism, or with the administration of thyroid hormone and estrogen in pregnancy. Some risk factors were predictive of CP only insofar as they were associated with low birth weight or low Apgar scores. Among factors not significantly related to CP rate were maternal age, parity, socioeconomic status, smoking history, maternal diabetes, first trimester vaginal bleeding, kidney or bladder infection, moderate hypertension, long cord, use of anesthetic agents, or use of oxytoxics for initiation or augmentation of labor. Duration of labor, whether precipitate or prolonged, was not a risk factor for CP.
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PMID:Antecedents of cerebral palsy. I. Univariate analysis of risks. 403 90

After mentioning insulin deficiency diabetes in animals produced by drugs such as Alloxan, Diazoxide or Streptozotocin only drugs are discussed, which are used in elderly patients and may either provoke diabetes mellitus (or temporary hyperglycemia) or may change the clinical course of diabetes. In the first group endocrine products such as corticosteroids, estrogens, somatotrophic hormone, thyroid hormone, glucagon, somatostatin, catecholamines and hormones with anabolic effects are listed. The second group comprises saluretics, salicylates, amphetamines, pentamidine, nicotinic acid and its derivatives, beta-receptor blockers and finally laxatives. Hypopotassemia alone can also be the cause of hyperglycemia. Speaking of the sulfonylureapreparations, their interaction with alcohol, with phenylbutazone, with some sulfonamides and the effect of the sulfonylureas on peripheric insulin-receptors is discussed. In case of severe diabetic vascular disease the use of anticoagulants may lead to hemorrhages. If such an hemorrhage occurs in the eyes, it may lead to blindness. In diabetic nephropathy the use of phenacetine and its derivatives should be substituted by another medication. This review is not at all complete but should only show some of the problems in the treatment of elderly diabetic patients.
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PMID:[Iatrogenic diabetes mellitus (side effects and interactions of drugs during clinical diabetes mellitus (author's transl)]. 612 38


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