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Query: UMLS:C0011849 (diabetes)
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The manifestations of endocrine derangements in the musculoskeletal system in infancy and childhood are disturbances in growth and maturation and in adulthood are disturbances in maintenance and metabolism. Hypercortisolism during skeletal immaturity suppresses growth. In the adult, hypercortisolism leads to osteoporosis, osteonecrosis, and muscle wasting. Deficiency of growth hormone during skeletal development results in short stature. An excess of growth hormone in a skeletally immature individual results in gigantism, an excess in a skeletally mature individual results in acromegaly. Patients with gigantism have extreme height with normal body proportions. Musculoskeletal manifestations of acromegaly include soft-tissue thickening, vertebral body enlargement, characteristic hand and foot changes, and enthesal bony proliferation. Hyperthyroidism causes catabolism of protein and loss of connective tissue, which manifest as muscle wasting. Deficient levels of thyroid hormone cause defects in growth and development. Severe growth retardation from congenital hypothyroidism is rare because neonatal screening recognizes the disorder and leads to early treatment. The skeletal manifestation of hypergonadism in children is precocious growth and early skeletal maturation. Although the initial precocious growth spurt results in a tall child, early closure of the growth plates results in a short adult. Hypogonadism in the prepubertal child results in delayed adolescence and delayed skeletal maturation. Diabetes mellitus in childhood results in decreased growth, a phenomenon presumed to be secondary to nutritional abnormalities. Generalized osteoporosis and short stature are common. In the adult, generalized osteoporosis may accompany insulin-dependent diabetes mellitus if obesity is absent. Calcification of interdigital arteries of the foot is common in diabetics and uncommon in other conditions. Additional skeletal manifestations relate to complications of diabetes such as peripheral neuropathy and diabetic foot disease.
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PMID:Radiologic manifestations in the musculoskeletal system of miscellaneous endocrine disorders. 198 24

Thyroid hormone picture of 28 patients (15 males and 13 females), mean age 56.6 yr (range 45-65 yr), with seriously decompensated type II diabetes mellitus has been studied. In each patient the study was repeated after 3 months of treatment of diabetes. The patients showed significantly lower serum T3 levels and significantly higher serum rT3 levels (P less than 0.001), in comparison with a group of 16 normoglicemic subjects. After 3 months of strict control of diabetes T3 and FT3 significantly increased (P less than 0.01), whereas significant variations of rT3 were not found. Among the whole group of diabetics 5 patients had low levels of serum T4 (P less than 0.01 vs. controls), high levels of serum TSH (P less than 0.001 vs. controls) and an exaggerated responsiveness to exogenous TRH (P less than 0.001 vs. controls). After the 3 months of treatment these patients showed a significant decrease of rT3 (P less than 0.02) and of delta-TSH (P less than 0.01). In the whole group of diabetics significant statistical correlations between glycometabolic and thyroid parameters were not found. The study, on the whole, showed in patients with seriously decompensated type II diabetes, a hormone picture like the low-T3 syndrome, in some cases, however, pituitary TSH secretion suggested the existence of incipient failure of thyroid hormones. A connection between alterations in thyroid hormone picture and glycometabolic imbalance, even statistically labile, is however indicated by improvement of thyroid function when diabetes is carefully controlled.
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PMID:[Changes in the thyroid hormone picture that may be found in severely decompensated type II diabetics]. 200 Jan 80

Prolonged hypoglycemia induced by acetohexamide (AH) in a patient with noninsulin dependent diabetes mellitus accompanied by primary hypothyroidism was presented. A 74-year-old man who had been treated with AH (500mg, daily) for diabetes mellitus since 1973 was admitted to our hospital in Oct. 1988 because of hypoglycemic coma. On admission, the level of blood glucose was 20mg/dl. Continuous intravenous administration of 10 per cent glucose solution led to improvement in the mental state on the second day. However, the level of blood glucose remained between 30 to 45mg/dl for four days after admission. On the fifth day, a fasting blood glucose level finally reached 75mg/dl. In a thyroid function test, the serum levels of thyroid hormone showed the following decreases: T3 68ng/dl, T4 2.8 micrograms/dl, free T4 0.3ng/dl, while basal TSH levels increased to 50.3 microU/ml. Since anti-thyroid microsomal antibody was positive and thyroid 99mTc-pertechnetate uptake was slightly elevated, the hypothyroidism in this patient was considered to be caused by chronic thyroiditis. Urinalysis was positive for protein. In a renal function test, the blood urea nitrogen was 26.7mg/dl and creatinine 1.7mg/dl, and creatinine clearance decreased to 22ml/min. After thyroid function returned to euthyroid, creatinine clearance improved (41 ml/min). To clarify the relationship between hypothyroidism and the metabolism of AH, the serum levels of AH and its metabolite hydroxyhexamide (HH) following oral administration of AH (500mg) were evaluated before and after thyroxine replacement therapy. The blood glucose level before therapy was lower than that after therapy, and hypoglycemic symptoms were observed early in the second and third morning after AH administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A case of acetohexamide-induced hypoglycemia: the influence of hypothyroidism on the metabolism of acetohexamide. 201 45

Serum thyroid hormone concentrations, 1-thyroxine (T4), free T4 and 3,5,3'-l-triiodothyronine (T3) were measured in 213 patients of diabetes and analyzed their correlation with metabolic parameters, hyperglycemia and body weight. Haemoglobin A1 (HbA1) was used as an index of hyperglycemia. Body weight was expressed by relative body weight (body weight/standard weight). Among the thyroid hormones, only T3 had significant correlation with HbA1 and body weight (r = -0.476, P less than 0.01 and r = 0.369, P less than 0.01, respectively). Multivariable analysis of serum T3 by HbA1 and relative body weight gave the following regression equation. Serum T3 (ng/dl) = 108 + 0.362 x relative body weight (%) - 3.88 x HbA 1 (%). Though relative body weight had inverse correlation with HbA1, the contribution of the two metabolic parameters to the serum T3 was independent from each other. Our results confirm the previous reports that low T3 in diabetes correlates with severity of hyperglycemia and we report for the first time that serum T3 of diabetic patients has positive correlation with body weight, probably due to still available carbohydrate in spite of disturbances in the metabolism.
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PMID:Multivariable analysis of serum 3,5,3'-L-triiodothyronine concentration in patients of diabetes mellitus by blood glucose level and body weight. 211 9

Thyrotrophin (TSH) secretion was studied in 63 patients with Cushing's syndrome (53 patients with pituitary dependent Cushing's disease, eight with adrenocortical tumours, and two with the ectopic ACTH syndrome). Prior to treatment, TSH response to 200 micrograms of TRH intravenously was significantly decreased compared to controls; TSH response was 'flat' (increment less than 2 mU/l) in 34 patients (54%). Patients with a flat response to TRH had significantly higher morning and midnight cortisol levels than patients with a TSH response of 2 mU/l and more; this was not due to differences in serum thyroid hormone levels. Basal TSH, TSH increment after TRH, and stimulated TSH value, but not serum triiodothyronine, were correlated with cortisol measurements (0800 h serum cortisol, midnight cortisol, and urinary free corticoid excretion). After exclusion of 40 patients with additional disease (severe systemic disease, diabetes mellitus, or goitre), cortisol-TSH correlations were even more pronounced (r = -0.73 for midnight cortisol and stimulated TSH levels), while in the patients with additional complications, these correlations were slight or absent. Successful treatment in 20 patients was associated with a rise in thyroid hormone levels and the TSH response to TRH. These results indicate that (1) the corticoid excess but not serum T3 is the principal factor regulating TSH secretion in Cushing's syndrome, (2) a totally flat response to TRH is rare, and (3) TSH suppression and lower than normal serum thyroid hormone levels are reversible after treatment. Since factors like severe systemic disease, diabetes mellitus and goitre also affect TSH secretion, they tend to obscure the statistically significant correlations between cortisol excess and TSH secretion.
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PMID:TSH secretion in Cushing's syndrome: relation to glucocorticoid excess, diabetes, goitre, and the 'sick euthyroid syndrome'. 212 25

Diabetes impairs cardiac performance more extensively in hypertensive rats than it does in nonhypertensive strains. A "low thyroid state" may contribute to the adverse cardiovascular effects of diabetes in spontaneously hypertensive rats (SHR). We tested this hypothesis by comparing the effects of thyroid hormone with those of insulin treatment on cardiac performance of diabetic SHR. Diabetes was induced with streptozotocin (45 mg/kg). Subsets of diabetic rats were treated with either insulin (10-20 units/kg/day) or triiodothyronine (8-10 micrograms/kg/day). Heart rate and systolic arterial pressure were obtained at weekly intervals. After 8 weeks, cardiac function was assessed using an isolated working heart preparation. Diabetes reduced arterial pressure and heart rate in vivo and markedly depressed cardiac performance under volume and pressure loading conditions ex vivo, confirming previous observations. As expected, insulin treatment prevented the bradycardia and depressor effect in vivo and the impairment of cardiac performance ex vivo caused by diabetes. The triiodothyronine treatment duplicated the effects of insulin on the hemodynamic measurements in vivo, and corrected nearly all depressed indexes of performance of diabetic SHR hearts ex vivo. Both treatment regimens successfully reduced 8-week mortality when compared with the untreated diabetic group. The results support the hypothesis that a low thyroid state may contribute to the cardiovascular dysfunction in diabetic SHR. Left ventricular hypertrophy may be an important factor in this phenomenon.
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PMID:Insulin, thyroid hormone, and heart function of diabetic spontaneously hypertensive rat. 214 Aug 15

Diabetes mellitus causes a more profound reduction of left ventricular weight (LVW) in the spontaneously hypertensive rat (SHR) than it does in nonhypertensive strains. Diabetes also depresses the activity of cardiac ornithine decarboxylase (ODC), an index of cell growth. We measured ODC activity, of ventricular homogenates obtained from diabetic SHR and nonhypertensive WKY rats, with and without chronic treatment with insulin or triiodothyronine (T3). Left ventricular ODC activities of nondiabetic SHR and WKY rats were not different from each other. Streptozotocin-induced diabetes (8 weeks) reduced left ventricular ODC activity of SHR and WKY rats to the same extent; the effect was characterized by a reduction in apparent Vmax with no change in apparent Km. Both T3 and insulin therapy prevented the decline in ventricular ODC activity in both strains, although only the effect of insulin was correlated with LVW. The results suggest that the effects of diabetes on LVW and ODC activity are independent of attendant reductions in serum thyroid hormone levels. However, the results did not reveal any strain-selective effects of diabetes on ODC activity which might have contributed to the pronounced loss of LVW in the SHR strain.
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PMID:Cardiac ornithine decarboxylase of diabetic spontaneously hypertensive rat: effects of insulin and thyroid hormone treatment. 214 35

Four-week-old Wistar and Wistar-Kyoto (WKY) and 12-year-old Wistar rats treated with streptozotocin (55 or 65 mg/kg) were studied to assess the relationship between diabetes-induced alterations in lipid and thyroid hormone concentrations and myocardial tissue function. In the Wistar rats, both doses of streptozotocin resulted in hyperlipidemia and hypothyroidism. However, the higher dose was associated with: greater increases in plasma lipid levels in both age groups; larger increases in plasma lipid levels in older rats; and decreases in myocardial sensitivity to isoproterenol and beta-adrenoceptor density. The diabetic state in WKY rats, while also accompanied by hypothyroidism, was not differentially affected by the two doses of streptozotocin, nor associated with severe hyperlipidemia, nor associated with alterations in the myocardial beta-adrenoceptor system. These findings, as expected, reveal that the dose of streptozotocin and the age and strain of rat influence the diabetic state. Furthermore, these data do not suggest a direct correlation between diabetes-induced alterations in myocardial inotropic sensitivity and associated changes in plasma lipid or thyroid hormone concentrations.
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PMID:Myocardial and metabolic abnormalities in streptozotocin-diabetic Wistar and Wistar-Kyoto rats. 215 89

Organ specific autoimmune diseases are relatively common immunological disorders in man which include thyroid autoimmune disease, insulin-dependent diabetes mellitus and myasthenia gravis. The target autoantigens in some of these diseases have recently been characterised. In thyroid autoimmune disease this includes the key enzyme, thyroid peroxidase (TPO), which is involved in the generation of thyroid hormone. Structural knowledge about autoantigens such as thyroid peroxidase will allow a greater understanding of the interaction between autoantigens and the aberrant immune response, and facilitate the development of strategies for antigen-specific therapeutic manipulation. We report here a prediction of the secondary structure of thyroid peroxidase, together with the results of circular dichroic spectroscopy of a homologous purified enzyme. A combination of 3 secondary structure prediction programs has been used, following multiple sequence alignment, and TPO has been found to consist mainly of alpha-helical conformation, with little beta-sheet present. This structure prediction, together with knowledge of the exon-intron boundaries allows a model for the domain organisation of the TPO molecule to be proposed.
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PMID:Prediction of domain organisation and secondary structure of thyroid peroxidase, a human autoantigen involved in destructive thyroiditis. 216 85

Aminoglycoside nephrotoxicity in experimental animals can be reduced by calcium loading, inducing diabetes, and giving thyroid hormone, while a potassium deficient diet enhances aminoglycoside nephrotoxicity. This study investigated whether potassium loading protects against gentamicin nephrotoxicity in the rat. In part I, group GK ate a diet containing 3.5% potassium and drank 0.2 mol/L KCl. Pair-fed rats eating a standard diet, group G, ate a 1% potassium diet and drank water. After 10 days, each group received gentamicin subcutaneously, 60 mg/kg twice daily for 8 days. The control groups, K and C, received the high or normal potassium diet, respectively. To control for a protective effect from a high solute load, the effect of equimolar NaCl loading was studied in group GNa and Na. At the end of the 8 days of gentamicin, inulin clearance was significantly higher in GK compared with G(0.6 +/- 0.1 v 0.3 +/- 0.1 mL/min per 100 g body weight [BW], P less than 0.05), but group GNa (0.4 +/- 0.1 mL/min per 100 g BW) was not different from group G. Morphological studies demonstrated that potassium-loaded rats (group GK) had significantly less proximal tubular necrosis compared with rats on a standard potassium diet, group G. Sodium loading did not protect against cellular necrosis. Part II studied renal function, cortical Na,K-adenosine triphosphatase (ATPase) and gentamicin accumulation after 2 days of gentamicin to determine the early functional and biochemical effects of potassium loading before overt renal functional impairment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of KCl loading in gentamicin nephrotoxicity. 216 23


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