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

Thyroid autoantibodies are common in Type 1 diabetics and their first degree relatives and may be part of the autoimmune diathesis present within such families. We have measured the prevalence of microsomal (M-Ab) and thyroglobulin (Tg-Ab) autoantibodies in 84 HLA-typed families having a Type 1 diabetic child, using enzyme-linked immunosorbent assay techniques. Thyroid autoantibodies were detectable in 201/407 (49%) individuals in these families. Both autoantibodies were significantly more frequent in the subsets of parents, diabetic children and their non-diabetic siblings than in groups of control adults and children. The prevalence of these autoantibodies in the diabetic families was increased in both sexes with a female:male ratio of 1.4:1. Antigen DR5 was significantly associated with M-Ab production but only for male subjects (P = 0.005 after correction for the number of DR antigens tested). No significant associations were encountered for Tg-Ab. Within-family analyses indicated that thyroid autoantibodies occurred with increased prevalence in HLA-identical or haplo-identical siblings of autoantibody-positive index cases in comparison to control children. We conclude the DR association with thyroid autoantibody production in this diabetes-selected population was thyroiditis-related and not diabetes-related, and the DR5 association was restricted to males and the production of M-Ab. These data are consistent with the hypothesis that multiple genetic and non-genetic factors played a role in the high prevalence of thyroid autoantibodies in this population.
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PMID:Thyroid autoantibodies in HLA-genotyped type 1 diabetic families: sex-limited DR5 association with thyroid microsomal antibody. 379 56

Thyroid microsomal, gastric parietal, and adrenocortical autoantibodies were sought in 1456 Caucasian and 240 black patients with insulin-dependent diabetes mellitus (IDDM), in 1467 of the Caucasian patients' immediate family members, and in 1519 normal Caucasian control subjects. Positive clinical significances and predictive values of these autoantibodies for associated gland dysfunctions were found. In all groups, thyroid and gastric autoantibodies were more common in female subjects. In the control group, thyroid and gastric autoantibodies were more frequent with advancing age, affecting more than one-third of Caucasian women after age 60 yr. This age-augmented increase occurred very prematurely in patients with IDDM and their relatives. Among the patients with IDDM and thyroid and gastric autoantibodies, these autoantibodies appeared by the time of onset of IDDM in the large majority of cases; however, they were more common among patients with later ages of onset of IDDM. Occurrence of thyroid and gastric autoantibodies in 404 siblings of patients with IDDM was not affected by their degree of HLA-haplotype sharing with their diabetic sibling, suggesting that the inherited predisposition to thyroid and gastric autoimmunity is not HLA-related. In light of this, the increased frequencies of these antibodies in patients with IDDM and their relatives suggest that "thyroid and gastric autoimmunity genes" may also predispose to IDDM.
Diabetes Care
PMID:Thyroid, gastric, and adrenal autoimmunities associated with insulin-dependent diabetes mellitus. 405 51

Eight women with uncomplicated progressive partial lipodystrophy and two with progressive lipodystrophy and diabetes mellitus were studied. Plasma triglyceride levels were significantly elevated in the subjects with uncomplicated lipodystrophy; serum cholesterol, phospholipid, and plasma free fatty acid levels were normal. Paper electrophoresis showed increases in serum pre-beta lipoprotein and chylomicra. Thyroid function, as measured by radioiodine and stable iodine studies, was normal. Some subjects had a raised basal metabolic rate. Intravenous glucose tolerance was normal in patients with the uncomplicated disease.
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PMID:Blood lipid levels, thyroid status, and glucose tolerance in progressive partial lipodystrophy. 601 88

Increased frequencies of thyroid diseases and thyroid microsomal antibodies have been observed in insulin-dependent diabetes mellitus. However, the exact prevalence of thyroid-stimulating immunoglobulins has not been established. In the present study these antibodies were measured by both a radioreceptor and an adenylate-cyclase stimulation assay. In forty-six patients with insulin-dependent diabetes mellitus without endogeneous insulin production (C-peptide concentration less than or equal to 0.06 nmol 1(-1)) the receptor assay was positive in ten and the stimulation assay in fifteen patients. The immunoglobulins of four patients inhibited the adenylate cyclase, and one of these was positive in the receptor assay. In nine patients with post-prandial C-peptide 0.07-0.19 nmol 1(-1), five had adenylate-cyclase-stimulating antibodies, while none were positive in the receptor assay. Thyroid hormones and thyrotropin concentrations were not different in the forty-six patients without endogenous insulin production with thyroid-stimulating immunoglobulins compared with patients without these antibodies. Patients with thyroid-stimulating immunoglobulins required a daily median amount of 0.71 IE of insulin kg-1 compared to median of 0.57 IE kg-1 in patients without these antibodies (P less than 0.03), despite a similar degree of diabetic regulation. The level of tri-iodothyronine was correlated to the antibody level in patients with adenylate-cyclase-stimulating antibodies. While the prognostic and possibly pathogenetic importance of these antibodies in Graves' disease have been established, their significance in insulin-dependent diabetes mellitus remains to be demonstrated.
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PMID:Thyroid-stimulating immunoglobulins in insulin-dependent diabetes mellitus. 615 3

The effect of diabetes mellitus on the synthesis and secretion of thyroid hormone ws investigated in mice with streptozotocin-induced diabetes. Thyroid glands were labeled in vivo with 131I for 2 h. In control animals, TSH stimulated the synthesis of PB127I and 131I-labeled iodothyronines and simultaneously decreased the proportion of 131I-. These effects of TSH were not observed in diabetic animals but were demonstrable in diabetic animals treated with insulin. For studies of hormone secretion, labeled thyroid glands were cultured in vitro in medium containing 1 mM mononitrotyrosine. The rate of the hydrolysis of labeled thyroglobulin was measured as the proportion of 131I-labeled iodotyrosines and 131I-labeled iodothyronines recovered at the end of culture and was used as an index of thyroid secretion. TSH in vivo stimulated the rate of thyroglobulin hydrolysis for 6 h, with a peak occurring after 2 h. The diabetic mice had a diminished response to TSH, which improved on treatment with insulin. The addition of TSH and insulin to the culture medium significantly increased the rate of thyroglobulin hydrolysis in glands of diabetic mice over that resulting from the addition of dibutyryl cAMP alone. The generation of thyroidal cAMP in response to TSH was higher in diabetic mice than in controls. The rise in plasma T4 and T3 2 h after the administration of TSH was less in diabetic mice than in control mice or diabetic mice treated with insulin. Our studies, therefore, indicate that the thyroidal response to TSH is decreased in diabetes mellitus. The defect appears to be at a step beyond the generation of cAMP.
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PMID:Decreased thyroidal response to thyrotropin in diabetic mice. 627 30

The isolated perfused working rat heart was used to study experimental diabetes-induced alterations in the effect of isoproterenol on adenosine 3',5'-cyclic monophosphate (cAMP) content, inotropy, and phosphorylase activity. Experimental diabetes was induced by intravenous injection of either alloxan (40 mg/kg) or streptozotocin (50 mg/kg). There were no changes in either basal cAMP levels or in isoproterenol-induced cAMP levels in hearts from diabetic rats at either 3 days or 100-120 days after induction of diabetes. Maximum changes produced by isoproterenol in positive and negative dP/dt developments of diabetic rat hearts were also not different from control at either time point. However, phosphorylase was activated to a significantly greater extent by isoproterenol in hearts obtained from acute as well as chronic diabetic rats. Chronic diabetic rat hearts exhibited significantly higher total phosphorylase activity. Diabetic rat hearts had slightly but not significantly higher basal phosphorylase a activity. Furthermore, prostaglandin E1 activated phosphorylase in diabetic rat hearts but not in control rat hearts. Acute metabolic derangements and alterations in Ca2+ homeostasis caused by diabetes could be the underlying causes for this phosphorylase response. Thyroid hormone levels were depressed in diabetic rats. However, hypothyroidism is probably not responsible for the alterations in phosphorylase activity.
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PMID:Effect of experimental diabetes on rat cardiac cAMP, phosphorylase, and inotropy. 630 13

The case of a female patient with fasting hypoglycaemia before the development of Type 1 (insulin-dependent) diabetes mellitus is reported. She presented with primary hypothyroidism, partial hypopituitarism, adrenal insufficiency and glucagon deficiency. Thyroid microsomal and gastric parietal cell antibodies were detected as well as HLA-B8, whereas islet cell antibodies were not demonstrable, even 2 years after the onset of diabetes. Plasma chromatography revealed true pancreatic glucagon (IRG3500) close to undetectable in basal samples with a questionable increase from 3 to 18 pg/ml during insulin-induced hypoglycaemia. After an overnight fast, moderate hyperaminoacidaemia was found with elevations of alanine, glycine, serine, arginine and ornithine as seen in pancreatectomized patients. It is suggested that the deficient glucagon secretion in this patient might, at least in part, have been the cause of fasting hypoglycaemia and the failure of glucose recovery following insulin-induced hypoglycaemia. Possible, the A cell deficiency was part of the polyglandular failure syndrome in this patient.
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PMID:Glucagon deficiency associated with hypoglycaemia and the absence of islet cell antibodies in the polyglandular failure syndrome before the onset of insulin-dependent diabetes mellitus: a case report. 635 16

Thyroid hormones, gonadal and adrenocortical steroids, are glucoregulatory hormones. Thyroid hormones increase the provision of glucose to meet the enhanced energy demands which they impose. Glucose tolerance is decreased, associated with increased hepatic glucose production, although the glucose-raising effects of thyroid hormones are partially offset by an increased rate of glucose utilization especially in the postabsorptive state. The insulin secretory capacity of the pancreatic B cells is reduced by an excess of thyroid hormones, and the onset of diabetes may be hastened as pancreatic insulin reserves are depleted. Natural estrogens can improve glucose tolerance through a beta-cytotropic effect and enhanced insulin sensitivity. Progesterone may produce similar effects in the absence of estrogens, but progestins appear to antagonize the effects of estrogens. Testosterone exerts only marginal effects on glucose tolerance. Glucocorticoids decrease glucose tolerance by increased hepatic glucose production and impaired peripheral glucose utilization. Glucocorticoids reduce insulin sensitivity and responsiveness in peripheral tissues. However, the diabetogenic influence of glucocorticoid excess is partly compensated by a beta-cytotropic effect and a condition of diabetes develops when the functional reserve of the endocrine pancreas becomes limiting.
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PMID:Thyroid hormones, gonadal and adrenocortical steroids and the function of the islets of Langerhans. 638 Oct 36

Anterior pituitary functions and sex steroid levels were measured in 12 patients with idiopathic haemochromatosis (eight males, four postmenopausal females) and age-matched controls, 12 with diabetes mellitus and five with hepatic cirrhosis. In idiopathic haemochromatosis gonadotrophin deficiency was present in seven of 12 patients including six of seven patients who had clinical evidence of hypogonadism. Basal prolactin levels were significantly lower in the patients with idiopathic haemochromatosis compared with either of the control groups (p less than 0.02). Nine patients with idiopathic haemochromatosis exhibited subnormal prolactin responses to thyrotrophin releasing hormone. Thyroid and adrenocortical functions were normal in all patients with idiopathic haemochromatosis. Testosterone values were subnormal in five of eight males with idiopathic haemochromatosis; females with idiopathic haemochromatosis had significantly lower testosterone values compared with the diabetic females (p less than 0.05). Oestradiol values in both sexes and sex hormone binding globulin values in the males were not significantly different in patients with idiopathic haemochromatosis compared with the controls. Sex hormone binding globulin levels were significantly higher in females with idiopathic haemochromatosis compared with either diabetic or cirrhotic females (p less than 0.05). Impairment of anterior pituitary function occurs in idiopathic haemochromatosis but is selective; gonadotrophin and prolactin deficiencies are common. Clinical hypogonadism is usually hypogonadotrophic in origin.
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PMID:Endocrine abnormalities in idiopathic haemochromatosis. 668 54

Serum levels of the acid-ethanol soluble component of non-suppressible insulin-like activity (NSILA-S) have been measured by bioassay in patient with hyperprolactinaemia, hypothyroidism, thyrotoxicosis and diabetes mellitus, and in normal subjects administered prednisone, oestrogens of androgens. Hyperprolactinaemia per se did not influence serum NSILA-S, however when GH was deficient prolactin hypersecretion may have maintained serum NSILA-S. Thyroid hormones, insulin and steroids did not appear to influence serum NSILA-S. These results suggest that regulation of the serum concentration of NSILA-S is not a common effector mechanism by which these hormones influence statural growth in man.
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PMID:Endocrine influences on serum acid-ethanol soluble non-suppressible in insulin-like activity (NSILA-S). 677 55


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