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

To elucidate the possible role of thyroid hormone in somatomedin-C (SmC)/insulin-like growth factor I regulation in diabetes mellitus and starvation, plasma SmC, liver SmC, and kidney SmC concentrations were measured in streptozotocin-induced (60 mg/kg) diabetic and starved (for 72 h) rats. Triiodothyronine (T3, 5.0 micrograms/kg every 24 h) was subcutaneously injected into diabetic rats for 7 days and into starved rats at 12, 36, and 60 h after starvation. Plasma T3, plasma SmC, liver SmC, and kidney SmC concentrations were significantly decreased in diabetic and starved rats. T3 administration restored plasma T3 levels to the normal value in diabetic and starved rats. Plasma SmC and kidney SmC concentrations were significantly increased in T3-treated starved rats, while they were not increased in T3-treated diabetic rats. These results suggest that thyroid hormone may have some role in SmC regulation during starvation, but may have no role in diabetes mellitus in the rat.
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PMID:Possible role of thyroid hormone in decreased somatomedin-C levels in diabetic and starved rats. 233 Nov 41

Synthesis of alpha 2u globulin and its mRNA has been used as an index to monitor the effect of thyroxine on specific gene expression in the liver of hypoinsulinemic male rats. Administration of a physiological dose of thyroxine can partially reverse (to approximately 30% of the normal control) the marked reduction (more than 90%) in the hepatic levels of alpha 2u globulin and its mRNA during streptozotocin-induced diabetes. Estimation of newly synthesized alpha 2u globulin RNA transcripts from the native chromatin of isolated liver nuclei by "nuclear runoff experiments" showed that thyroxine can elevate the rate of transcription of alpha 2u globulin gene in the diabetic rat. Hypoinsulinemic diabetes is also found to be associated with an approximately 35% reduction in the thyroid hormone receptor level as compared to the normal control. The stimulatory effect of thyroxine on the synthesis of alpha 2u globulin and its mRNA was also evident in spontaneous diabetic Wistar "BB" rats. From these studies it can be concluded that severe hypoinsulinemia can cause a decrease in thyroid hormone action at the level of specific gene expression.
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PMID:Partial reversal of alpha 2u globulin gene expression by thyroxine in the liver of diabetic rats. 242 95

The effect of altered thyroid function on serum fructosamine concentrations was investigated in 31 untreated hyperthyroid patients, 18 short-term hypothyroid patients (i.e., 20 days after withdrawal of thyroid hormone suppressive therapy for thyroid cancer), 7 untreated long-term hypothyroid patients, and 25 age-matched normal controls. No differences in serum fructosamine concentrations were observed between hyperthyroid patients and normal controls; conversely, serum fructosamine concentrations were significantly higher both in short-term and in long-term hypothyroid patients than those found in normal controls. Furthermore, long-term hypothyroid patients showed significantly higher serum fructosamine concentrations than short-term hypothyroid patients. L-Thyroxine (L-T4), replacement therapy in two hypothyroid patients, resulted in a marked decrease in serum fructosamine concentrations. In seven hyperthyroid patients, the restoration of euthyroidism with antithyroid drug therapy was associated with no significant changes in serum fructosamine concentrations. The results of the present study indicate that hypothyroidism is associated with a marked increase in serum fructosamine concentrations. This alteration does not appear to be the consequence of gross abnormalities in plasma protein or glucose metabolism. The duration of hypothyroidism seems to be an important factor, even though the mechanism underlying this alteration remains at present unexplained. These results also suggest that caution must be used in the interpretation of elevated serum fructosamine concentrations as an index of the metabolic control of diabetes mellitus in the presence of hypothyroidism.
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PMID:The effect of altered thyroid function on serum fructosamine concentrations. 245 10

The influence of thyroxine treatment on the altered reactivity of the isolated perfused mesenteric vasculature from streptozocin-induced diabetic rats was examined and compared with that of insulin. After 8 weeks of diabetes, the time when the decreased response to isoproterenol appeared, treatment with thyroxine reversed this decreased response to control levels. However, thyroxine replacement did not reverse the decreased responsiveness to norepinephrine, 5-hydroxytryptamine, acetylcholine, and isoproterenol after 12 weeks of diabetes. On the other hand, insulin replacement improved the vascular responsiveness to these agonists at 8 and 12 weeks. Insulin treatment also reversed the attenuated response to nerve stimulation found in diabetic rats, whereas thyroxine treatment did not improve it. Insulin treatment reversed the decreased plasma thyroid hormone levels similarly as thyroxine treatment. These results suggest that thyroid hormone deficiency is likely to be involved partly in the altered reactivity of the rat mesenteric vasculature at the early period of diabetes. On the other hand, adrenergic neuropathy is not induced by hypothyroidism.
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PMID:Reversal effect of thyroxine on altered vascular reactivity in diabetic rats. 247 Sep 87

Thyroxine and T3 induced oxygen consumption and glucose uptake were studied in vitro in mononuclear blood cells isolated from patients with non-insulin-dependent diabetes mellitus (NIDDM) and from non-diabetic control persons. Cellular oxygen consumption and glucose uptake were promptly increased by physiological and supraphysiological concentrations of T3 and T4 in a dose-dependent manner (50-5000 nmol/l), whereas rT3 and T2 had no stimulatory effect. The effect of T3 and T4 was independent of new protein synthesis in that it was not blocked by tunicamycin (1 mg/l) and tiothepa (75 mg/l). Examination of stimulation of cells from control subjects and patients with NIDDM revealed an identical oxygen consumption, whereas the thyroid hormone-induced glucose uptake was significantly increased in cells from patients with NIDDM. T4 (5 mumol/l) stimulation in controls: 1.34 +/- 0.23 mmol.l-1 (mg DNA)-1.h-1, in NIDDM: 3.24 +/- 0.77 mmol.l-1.(mg DNA)-1.h-1, P less than 0.05 (mean +/- SD). These studies indicate that T4 as well as T3 increases cellular oxygen consumption and glucose uptake and that this stimulation is independent of new protein synthesis. Examination of cells from patients with NIDDM revealed an increased thyroid hormone induced glucose uptake, indicating increased thyroid hormone sensitivity. This observation contrasts the well known insulin insensitivity, suggesting separate mechanisms for glucose uptake elicited by insulin and thyroid hormones.
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PMID:Thyroid hormone stimulated glucose uptake in human mononuclear blood cells from normal persons and from patients with non-insulin-dependent diabetes mellitus. 249 51

The effects on cardiac function of feeding a diet high in sucrose to male Wistar rats over an extended period of time (15 months) was examined. This diet produced a diabetic condition which resembled noninsulin dependent diabetes mellitus. Resting hyperglycemia, high circulating insulin and triglyceride levels were observed in these animals. Further, the sucrose fed animals were overweight in comparison to chow fed control animals. Contractile protein Ca2+-ATPase activity was measured as a biochemical estimate of cardiac contractile function. Myosin and actomyosin Ca2+-ATPase activities of isolated myofibrillar fractions from hearts of experimental animals were depressed in comparison to chow fed control rats. Myosin K+-EDTA activity was also altered. The results demonstrate for the first time a defect in contractile protein Ca2+-ATPase activity in rat hearts using a model of noninsulin dependent diabetes mellitus. As the animals were euthyroid, thyroid hormone alterations in these animals were unlikely to influence the results. The results also demonstrate that insulin could not be a direct factor associated with cardiac pathology in diabetes. Instead, cardiac dysfunction may be associated with other, as yet undefined, metabolic abnormalities which accompany the diabetic state.
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PMID:Cardiac contracile protein ATPase activity in a diet induced model of noninsulin dependent diabetes mellitus. 252 35

The mechanism of glucose intolerance in thyrotoxicosis was investigated in 119 patients with Graves's disease with careful consideration of the age-related deterioration of glucose tolerance. Before and after treatment of thyrotoxicosis with antithyroid drug, changes of blood glucose (BG) and serum immunoreactive insulin (IRI) in response to 50 g oral glucose tolerance test (OGTT) and insulin binding to red blood cell (RBC) were evaluated. In control subjects, the sigma IRI/sigma BG ratio after 50-g OGTT decreased progressively with age without significant change in absolute sigma IRI value, suggesting the occurrence of age-related insulin resistance. Glucose intolerance was much more apparent in hyperthyroid patients because of age-related relative decrease of insulin secretion. Such a decrease of insulin secretion was not found in age-matched postgastrectomy patients with a similar degree of hyperglycemia, however. Maximal binding of labeled insulin and number of insulin receptors of RBC were decreased in old patients but binding affinity was unchanged. Elevation of BG was partially suppressed when serum thyroxine (T4) and triiodothyronine (T3) were reduced to moderately supernormal levels, whereas sigma BG, sigma IRI, sigma IRI/sigma BG ratio, and insulin binding to RBC were all returned to normal when normal serum thyroid hormone concentration was maintained. Our data indicate that insufficient insulin secretion and reduced insulin action at the target cell are responsible, at least in large part, for age-related glucose intolerance in hyperthyroid patients.
Diabetes Care
PMID:Effects of antithyroid drug therapy on blood glucose, serum insulin, and insulin binding to red blood cells in hyperthyroid patients of different ages. 258 47

The heart is a major target organ for insulin and thyroid hormone action, and marked changes in cardiac function occur in patients with hyper- or hypothyroidism and diabetes mellitus. Cardiac contractility is increased in the hyperthyroid state and decreased in hypothyroidism, and changes in specific proteins mediating cardiac contraction accompany these alterations. Changes in thyroid status mediate their influence on cardiac function by a combination of direct thyroid hormone effects on the heart, alterations in the responsiveness of the cardiac sympathoadrenal system, and hemodynamic effects generated in the periphery. Cardiovascular complications of diabetes mellitus are a major contributor to mortality and morbidity in the diabetic population. In addition to cardiac small and large vessel disease, an autonomic neuropathy and a cardiomyopathy occur in diabetic patients. The cardiomyopathy results in congestive failure and is independent of large vessel disease. Studies in diabetic animal models point to a metabolic basis for the cardiomyopathy, which is accompanied by changes in specific contractile proteins.
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PMID:Diabetes and thyroid-hormone-induced changes in cardiac function and their molecular basis. 265 57

In insulin-dependent diabetes mellitus (IDDM) several organ-specific autoantibodies are found in addition to pancreatic islet cell autoantibodies. In the present study we researched the presence of thyroid microsomal antibodies (anti-TMS) in 33 young patients with IDDM and evaluated contemporaneously their thyroid function. 5 patients (15.4%) are found with significant levels of circulating anti-TMS, among them 4 (12.1%) were also subclinical hypothyroid. However 6 other patients are found with mildly altered thyroid hormone pattern in absence of circulating anti-TMS. Basal and TRH-stimulated TSH were significantly higher, whereas serum FT4 was significantly lower, in patients with IDDM and circulating anti-TMS than in patients with IDDM but without anti-TMS. These observations indicate a significant incidence of mild or subclinical hypothyroidism in patients with IDDM and anti-TMS. Thus the screening for anti-TMS is recommended in all patients with IDDM, then thyroid hormone pattern of anti-TMS positive patients must be periodically followed.
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PMID:[Thyroid hormone anomalies in patients with insulin-dependent diabetes mellitus and circulating antithyroid microsomal antibodies]. 274 68

In the present study, isolated atrial function in spontaneously diabetic BB Wistar rats maintained for 12 weeks on a low (BB-LI) and a high (BB-HI) dosage of insulin was examined. Basal atrial rates were unchanged in the diabetic animals, relative to nondiabetic littermates (ND-BB) or Wistar controls. The BB-HI animals were euglycemic and responded to isoproterenol in a similar manner to the ND-BB and Wistar control animals. In contrast, BB-LI animals remained hyperglycemic and exhibited lower responses to the maximum chronotropic effects of isoproterenol. Plasma thyroid hormone levels were unaltered in the BB-diabetic animals. These results therefore reveal an absence of bradycardia and hypothyroidism in spontaneously diabetic BB rats, in contrast to previous observations in streptozotocin diabetic rats. However, a decrease in chronotropic response to isoproterenol was still noted in the BB-LI animals. These findings suggest that decreased positive chronotropic effect of isoproterenol in diabetes may not be a direct consequence of altered thyroid status.
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PMID:Chronotropic function in spontaneously diabetic BB rats. 276 97


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