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

Altered thyroid hormone metabolism with decreased serum T3 and increased rT3 concentrations in patients with uncontrolled diabetes mellitus has been well documented. However, data regarding TSH secretion are sparse, especially the influence of glycemic control. Therefore, we examined serum T4, free T4, T3, rT3, T3 resin uptake, and TSH as well as the TSH response to TRH administration [expressed as TSH increment (delta TSH) and area under the curve (theta TSH)] in 29 newly discovered type II diabetic patients (DM) before treatment and in 12 normal subjects. The study was repeated in the DM patients after attainment of euglycemia and normalization of glycosylated hemoglobin (HbA1C) following therapy with diet and tolazamide for 8-12 weeks. Serum T4, free T4, and T3 resin uptake were not significantly different in DM compared to those in normal subjects. Serum T3 was low and rT3 was high in DM before treatment, and both normalized on achieving the euglycemic state. Basal TSH in uncontrolled DM was not significantly different from that in normal subjects and remained unchanged during treatment. However, delta TSH and theta TSH were significantly reduced (P less than 0.01) in uncontrolled DM. Both fasting plasma glucose (FBS) and HbA1C levels correlated inversely with delta TSH as well as theta TSH (FBS vs. delta TSH, r = -0.42; FBS vs. theta TSH, r = -0.38; HbA1C vs. delta TSH, r = -0.40; HbA1C vs. theta TSH, r = -0.42; P less than 0.05 for all correlations). Finally, TSH responses returned to normal on attainment of euglycemia and normal HbA1C concentrations. These studies indicate that regulation of TSH secretion is altered in DM during the decompensated state and normalizes when euglycemia is achieved.
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PMID:Impaired pituitary thyrotroph function in uncontrolled type II diabetes mellitus: normalization on recovery. 643 Sep 48

Comprehensive evaluation of thyroid hormone indices was performed in 58 children with insulin-dependent diabetes mellitus (IDDM) at the time of diagnosis and prior to insulin therapy. Two patients were found to have primary hypothyroidism, with markedly elevated TSH and very low T4, free T4, T3, and reverse T3 concentrations. The remaining 56 patients had the transient alterations in thyroid hormone indices that are characteristic of "euthyroid sick" or "low T3" syndrome. Mean TSH and reverse T3 values were significantly higher and the mean T3, T4, and free T4 levels were significantly lower than those observed in the control population. Ten of the diabetic patients had elevated TSH concentrations and normal or low free T4 values; eight had normal TSH levels and low T4 and free T4 values. The remainder of the group had thyroid indices compatible with abnormal peripheral metabolism of thyroid hormones. Elevated titers of antimicrosomal antibodies were found in 16% of the children with IDDM. We conclude that abnormal peripheral metabolism and altered hypothalamic-pituitary function are responsible for the transient changes in thyroid hormone indices in patients with untreated IDDM. The most reliable indicators of concomitant primary hypothyroidism in untreated IDDM are markedly elevated TSH and low reverse T3 values.
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PMID:Thyroid hormone abnormalities at diagnosis of insulin-dependent diabetes mellitus in children. 643 Oct 66

Several parameters of thyroid function were studied in 112 non-ketoacidotic youngsters with insulin-dependent diabetes mellitus (IDDM). Levels of thyroxine (T4), reverse triiodothyronine (rT3), thyroxine-binding globulin (TBG) and T3 were lower than in controls, whereas FT4, and FT3 were normal. T4 levels in IDDM patients were positively related to T3, rT3 and TBG, and inversely related to haemoglobin A1 (HbA1). However, only 4 patients showed biochemical hypothyroidism (T4 less than 5 micrograms/100 ml), whereas their FT4, FT3 and thyroid-stimulating hormone (TSH) levels were normal. Concurrent variations of T3 and rT3 levels were found in IDDM patients; thus, their T3/rT3 ratios were stable or higher than in controls, indicating that peripheral deiodination of T4 is preferentially oriented to production of rT3 only during ketoacidosis. Although changes in thyroid function may reflect the degree of metabolic control of diabetes in a large population, the clinical usefulness of serum thyroid hormone measurements in an individual case still appears to be limited.
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PMID:Serum TSH, T4, T3, FT4, FT3, rT3, and TBG in youngsters with non-ketotic insulin-dependent diabetes mellitus. 643 16

In order to determine whether diabetic cardiomyopathy in rats is associated with altered contractile proteins, male and female rats were made diabetic with intravenous streptozotocin (STZ). Calcium ATPase activity of cardiac actomyosin was significantly decreased after 1 week of diabetes and was depressed by 60% by 2 weeks. Rats pretreated with 3-O-methyl glucose to prevent the hyperglycemia caused by STZ had normal Ca2+-actomyosin ATPase activities, and non-diabetic rats whose food was restricted to keep their body and heart weights similar to those found in diabetic animals had only a slight fall in actomyosin ATPase activity. Ca2+-ATPase and actin-activated ATPase activities of pure myosin were similarly depressed in preparations from hearts of diabetic animals. Sodium dodecylsulfate gel electrophoresis and isoelectric focusing failed to reveal differences in the patterns of contractile proteins or light subunits between diabetics and controls, but pyrophosphate gels showed a shift in the myosin pattern. Because of depressed circulating thyroid hormone levels in diabetic animals, cardiac contractile proteins were also studied in preparations from thyroidectomized rats. Calcium activities of actomyosin and myosin ATPase were lower than values found in hearts of diabetic rats. When diabetic animals were kept euthyroid with thyroid replacement, actomyosin ATPase activity was still depressed. Thus STZ diabetes causes a significant decrease in cardiac contractile protein ATPase activity. This may be related to altered proportions of myosin isoenzymes.
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PMID:The effect of streptozotocin-induced diabetes in rats on cardiac contractile proteins. 645 19

Measurement of serum concentrations of free triiodothyronine (FT3) is considered to be an accurate index of thyroid function in the patient. In this study, we measured serum concentrations of FT3, free thyroxine (FT4) and reverse triiodothyronine (rT3) by radioimmunoassay in blood samples taken from the navel cord of 20 newborns as well as 20 nonpregnant women, 20 pregnant women, 10 patients with liver diseases, 25 patients with diabetes mellitus, 65 patients with hyperthyroidism, 30 patients with primary hypothyroidism and 29 normal subjects. In pregnant women, serum FT3 and FT4 levels gradually decreased as the pregnancy progressed. In cord blood, FT3 levels were less than a quarter of the values found during the first trimester of pregnancy or that of non-pregnant women, whereas serum rT3 levels were drastically increased. In chronic hepatitis, liver cirrhosis and diabetes mellitus, serum FT3 and FT4 levels were significantly lower than that in the controls. In thyroid diseases, serum FT3 levels varied parallel to other thyroid hormone levels. In primary hypothyroidism, however, serum FT3 levels were still lower than these in the controls after treatment with 1-thyroxine, whereas other thyroid hormone levels and TSH levels returned to control levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Circulating free T3 in pregnancy, liver diseases, diabetes mellitus and thyroid diseases]. 651 13

Infants born to diabetic mothers have decreased activity of many metabolic pathways which might be regulated by thyroid hormone. Serum TSH, T4, T3, and reverse T3 levels were measured in 22 term infants of diabetic mothers and in 9 normal term babies at 2, 12, 24, and 72 hours of age, as well as in maternal and cord sera. T4 binding index and free T4 levels were measured in 11 diabetic mothers and their babies and 5 normal mothers and babies. Mean TSH levels did not differ between diabetic and normal mothers or their infants. Mean T4 of the diabetic mothers (9.6 micrograms/dl) was significantly (p less than 0.005) less than the mean T4 of the normal mothers (12.8 micrograms/dl). Mean T4 of neonatal specimens was lower in infants of diabetic mothers for each determination, but this difference achieved statistical significance at the 12-hour sample only (p less than 0.001). Mean serum T4 binding index was similar in the neonatal specimens at each time period studied. Mean T3 of diabetic mothers (149 ng/dl) was significantly (p less than 0.001) less than that of normal mothers (217 ng/dl). At each time interval, mean T3 concentration in infants of diabetic mothers was significantly lower than that of normal infants. Levels of reverse T3 were not significantly different between normal and diabetic mothers or their neonates. These data suggest that there is an effect of maternal diabetes on T3 secretion or conversion of T4 to the more active hormone, T3, in the fetus and early newborn.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thyroid hormone levels in diabetic mothers and their neonates. 652 14

Lipoadenoma is the accepted diagnosis of a single enlarged parathyroid gland that contains large quantities of mature fat cells and focal myxoid stroma, all widely separating small parenchymal cell nests in patients with hyperparathyroidism. Here we are reporting, for the first time, on five cases of hyperparathyroidism in which all four parathyroid glands are enlarged and each gland is noted to have an admixture of fat and parenchymal cells. We will introduce the descriptive diagnosis of lipohyperplasia to name this condition and keep it in perspective with other forms of parathyroid disease. All five patients were women between the ages of 36 and 62 years who underwent neck exploration, at which time four enlarged light-tan parathyroid glands were observed. Three and one half gland resections were performed, and all patients returned to a normocalcemic state except one who had borderline serum hypercalcemia after operation. Most of the resected parathyroid glands weighed in the range of 100 to 200 mg. The largest measured gland weighed 820 mg. Parathyroid histology showed an admixture of mature fat cells with parathyroid parenchymal cells often in a 1:1 ratio. One patient who had renal failure exhibited a lower ratio of fat cells. Two patients had chronic lymphocytic thyroiditis that was severe enough to require synthetic thyroid hormone therapy. Two patients had a history of urinary tract infections. Three patients had hypertensive cardiovascular disease, and several patients had arteriosclerotic cardiovascular disease. One patient had diabetes mellitus, one had a history of pituitary adenoma, and one had polydipsia. All of these patients were first seen with parathyroid glands measuring an average of five times normal size, yet they showed the usual 50% fat/50% parenchyma pattern of normal mature parathyroid glands. This means that the enlarged glands contain a 500% increase in parathyroid tissue, justifying the diagnostic term "lipohyperplasia." This easily represents enough parathyroid tissue to generate excessive parathyroid hormone production. At this time, there is no explanation of the pathogenesis of lipohyperplasia or how it varies from other previously described forms of parathyroid hyperplasia.
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PMID:Five cases of parathyroid lipohyperplasia. 664 2

The effects of diabetes mellitus on serum thyroid hormone parameters were studied in 54 patients divided into 4 groups. Treated asymptomatic patients (group I) had normal thyroid values which did not correlate with serum or urinary glucose. Untreated nonketoacidotic patients (group II) showed a mild persistent depression in T3 and an elevation in rT3. Patients with ketoacidosis with a brief history of symptoms (group III) had a moderate T3 decrease and a mild rT3 elevation which quickly resolved with treatment. Ketoacidotic patients with a long history of symptoms (group IV) had marked depression of T3 and elevation of rT3 which was only partially rectified by treatment. Serum T4 was generally normal, except for a minimal decrease on the day after admission, probably resulting from rehydration and a subsequent increase associated with an increase in TSH. We concluded that thyroid hormone parameters were not influenced by variations in serum glucose, but seemed to reflect the effects of a preexisting catabolic state, ketoacidosis, or both.
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PMID:Pattern of recovery of thyroid hormone indices associated with treatment of diabetes mellitus. 679 65

Diabetes appears to cause a cardiomyopathy independent of atherosclerotic coronary artery disease and hypertension. Left ventricular papillary muscle function studies in rats made severely diabetic with streptozotocin have shown a slowing of relaxation and a depression of shortening velocity. However, the effects of insulin therapy on the myocardial mechanics of diabetic rats have not been studied. Therefore, rats diabetic for 6-10 weeks were treated with PZI insulin for 2, 6, 10, or 28 days and the mechanical performance of their left ventricular papillary muscles was compared to that of untreated diabetics and age-matched controls; cardiac contractile protein enzymatic activity was also measured. Neither 2 nor 6 days of therapy had any effects on the depressed cardiac muscle performance of diabetic animals, although plasma glucose concentration was restored to normal. By 10 days of therapy, recovery of mechanical performance was nearly complete, and by 28 days of therapy, complete reversal of the altered myocardial mechanics was observed. Crystalline insulin added to the bath (9 mU/ml) had no effect on myocardial mechanics in either diabetics or controls. A gradual recovery of actomyosin and myosin ATPase activity in the hearts of insulin-treated diabetic animals was also found, complementing the mechanical studies. In addition to demonstrating a gradual but complete reversibility of the abnormalities in papillary muscle function in diabetic rats (although control of hyperglycemia was less than ideal), this study confirms that this model of a cardiomyopathy is not a result of streptozotocin-induced cardiac toxicity. Additional data are provided indicating that depressed thyroid hormone levels in diabetic rats are not responsible for the mechanical changes observed.
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PMID:Reversibility of diabetic cardiomyopathy with insulin in rats. 703 May 13

An elevated plasma glucagon concentration and reduced T3 production from T4 have both been observed in several clinical disorders, including hepatic cirrhosis, uremia, diabetes mellitus, and starvation. The question of whether glucagon has a direct effect on T3 production was studied in normal rats infused iv with [125I]T4 of [125I]T3 and 3 micrograms T4/day, using implanted minipumps. The blood [125I]T4 and [125I]T3 levels maintained a plateau between the fifth and ninth days of infusion. Each animal also received a second minipump, implanted ip, that infused either a diluant solution or 30 micrograms glucagon/100 g BW . day. After 7 days of continuous infusion, the glucagon-treated animals showed a 20% increase in plasma glucose and a 4-fold increase in plasma glucagon from baseline. However, the levels of insulin, T4, and T3 remained unchanged. The MCRs and the disposal rates of T4 and T3, calculated by the constant infusion method, showed T4 and T3 MCRs to be 0.99 +/- 0.18 and 11.25 +/- 2.52 ml/h . 100 g, respectively, and T4 and T3 disposal rates to be 68 +/- 10 and 9 +/- 2 ng/h . 100 g; there was no difference between the control animals and the glucagon-infused animals. T3 production was also determined in vitro from T4 added to a liver homogenate. Compared to control animals, the liver homogenate prepared from glucagon-infused animals showed a modestly higher T3 production rate throughout the 60-min incubation period (P = 0.025--0.05). However, the concentration of nonprotein-bound sulfhydryls was similar in the liver, kidney, brain, muscle, and heart of the two animal groups. In conclusion, glucagon does not have an important regulating role on the peripheral metabolism of thyroid hormone and T3 production in rats.
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PMID:Comparison of peripheral thyroid hormone metabolism in normal rats and in rats receiving prolonged glucagon infusion. 704 21


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