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)

Endocrinologic disorders occasionally manifest themselves by their associated or induced cutaneous abnormalities. In some instances the initial and most prominent complaints of the patient are related to alterations in the skin, and thus the dermatologist will at times be the first physician consulted. In this article we describe the cutaneous lesions that occur in patients with acromegaly, hypopituitarism, hypothyroidism, hyperthyroidism, diabetes mellitus, glucagonomas, hypercalcemia, hypoparathyroidism, and fibrous dysplasia. In addition, we also discuss the role of the skin in vitamin D metabolism. Whenever possible and where known, we have attempted to point out the pathophysiologic mechanisms that account for the cutaneous changes.
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PMID:Endocrine-skin interactions. Cutaneous manifestations of pituitary disease, thyroid disease, calcium disorders, and diabetes. 332 73

The study of hormonal alterations due to exercise is of growing interest because of the implications for adaptation, performance, and health. The influence of the sympathoadrenal response on energy metabolism and fluid and electrolyte balance has been of primary interest in past research. Interpretation of results, however, is difficult because of the numerous factors which need to be controlled. Limitations in the interpretation of hormone levels exist because of changes in plasma volume and/or clearance rate and the influences of timing and method of blood sampling. Other factors which must be considered are the design of exercise protocols, and various subject characteristics (sex, age, fitness level, training history, diet, emotional status, diurnal and menstrual variations). Hormonal alterations during acute exercise occur primarily because of sympathoadrenal secretion of the catecholamines which initiate mobilisation of glucose and free fatty acids. This response, in turn, stimulates other endocrine glands and cells (anterior and posterior pituitary, adrenal cortex, thyroid, parathyroid, liver, pancreas, kidney) to secrete secondary hormones which potentiate fuel mobilisation and regulate water and electrolyte concentrations. As duration of exercise increases, nutrient and ion concentrations also influence hormonal responses. In recent years, research has focused on the effect of exercise-induced hormonal alterations on reproductive functioning and various endocrine-related diseases (hypopituitarism, diabetes, osteoporosis, cardiovascular disease). These topics, as well as a better understanding of mechanisms of action via receptor activity, influences on training adaptations, and implications (if any) of hormonal alterations for the growth and development of children, provide challenges for future research.
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PMID:Hormonal alterations due to exercise. 352 82

The polypeptide called somatomedin B was radioimmunoassayed in serum or cerebrospinal fluid from volunteers throughout the lifespan, the daily and menstrual cycles, in oral contraceptive users, and in several patients with endocrinological disorders. This peptide, of 5000 molecular weight, is said to have insulin-like growth promoting activity, but its actual origin and function are unknown. In serum, there were no significant variations between the sexes, over the ages 20-60, in the diurnal or menstrual cycle, or by height, weight or body surface. There were significant declines after the age of 60 and 70 years in serum. The serum level in 8 women aged 20-40 taking oral contraceptives was significantly higher than that of 46 drug free women (p.001). In cerebrospinal fluid, there was a diurnal variation, a nadir at 2000 hours, but there was no decline in older individuals. Somatomedin B was significantly lower in patients with hypopituitarism and diabetes mellitus, and higher in those with hyperthyroidism and Cushing's syndrome. This is the first demonstration of somatomedin B in cerebrospinal fluid.
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PMID:Immunoreactive somatomedin B (RIA-B) in the circulation of healthy adults and patients with endocrine disorders. 378 77

Dysfunction of multiple endocrine glands may develop as the result of hypopituitarism, various infiltrative disorders, or an organ-specific autoimmune mechanism. When dysfunction of two or more endocrine glands occurs in association with circulating organ-specific antibodies directed against the involved glands, the term polyglandular autoimmune syndrome is applied. Characteristics of polyglandular autoimmunity include specific patterns of disease association and frequently a family history of similar involvement. The principal endocrine components of these syndromes are adrenal insufficiency, autoimmune thyroid disease, insulin-dependent diabetes mellitus, and premature gonadal failure. In addition, primary hypoparathyroidism is a key feature of one form of polyglandular autoimmunity that occurs in children. Several nonendocrine organ-specific autoimmune disorders are also associated with polyglandular autoimmunity, of which pernicious anemia is the most frequent. The underlying abnormality responsible for polyglandular autoimmunity is most likely a defect in T suppressor cell function, but there is evidence that aberrant expression of HLA DR antigens also plays an important role in the pathogenesis of these disorders.
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PMID:Polyglandular autoimmune syndromes. 389 41

A 42-year-old man with diabetes mellitus and probably acromegaly had a pituitary apoplexy with left-sided oculomotor palsy. There was an immediate fall in blood glucose concentration. Pituitary insufficiency promptly developed. Blood glucose levels remained normal for the next two years. During the first year after the pituitary apoplexy, severe proliferative retinopathy developed in the left eye, which became almost blind. Only mild retinopathy was present on the right side. Plasma concentrations of growth hormone remained low after the apoplexy, and the acromegalic features subsided. The explanation of these findings may be that the proliferative retinal angiopathy was caused by compression of the cavernous sinus at the time of the apoplexy. This would lead to impaired venous drainage, thus resembling occlusion of the central retinal vein, which may cause retinopathy similar to that seen in diabetes mellitus.
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PMID:Pituitary apoplexy, the Houssay phenomenon, and accelerated proliferative retinopathy. 403 88

Previous studies have demonstrated that the secretion of human prolactin is regulated primarily by factors that influence catecholamines of the hypothalamus. In an effort to identify other factors that may regulate prolactin secretion, the amino acid L-tryptophan, a precursor in the synthesis of serotonin, was infused into normal human volunteers. Intravenous infusion of L-tryptophan, 5-10 g over a 20 min period, but not equivalent amounts of 17 other amino acids, induced marked increases in serum prolactin concentrations in eight normal human volunteers. Increases of 20-200 ng/ml above the control level were observed with peak values at 20-45 min after initiation of the infusion. In addition, infusion of L-tryptophan was associated with decreases in serum concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and thyrotropin in those subjects in whom the base-line serum hormone concentration was above the lower limits of assay detectability. No consistent change was observed in serum concentrations of growth hormone, cortisol, or glucose. Four subjects with juvenile diabetes demonstrated increases in serum prolactin values comparable with those observed in healthy individuals in response to infusions of L-tryptophan. Serum prolactin values in patients with surgically induced hypopituitarism were undetectable or deficient after infusion of 10 g of L-tryptophan. In this respect, infusion of L-tryptophan was equally effective in these subjects as the standard chlorpromazine stimulation test in identifying patients with hypopituitarism, indicating that the infusion of L-tryptophan may serve as a sensitive and reliable clinical test of prolactin secretory reserve. Further studies relating to the possible mechanism of action of L-tryptophan indicated that infusion of 5-hydroxytryptophan represents a much more potent stimulus for the secretion of prolactin and that premedication with the serotonin antagonist, methysergide maleate, serves to blunt the effect of L-tryptophan on prolactin secretion. These results support the concept that the effect of L-tryptophan on the secretion of human prolactin is mediated through its conversion to serotonin and are consistent with reported experimental observations that serotonin may participate in the reciprocal regulation of prolactin and gonadotropins.
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PMID:Stimulation of human prolactin secretion by intravenous infusion of L-tryptophan. 454 74

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

Endocrine disorders are important, potentially reversible causes of impotence. Impotence may be an early manifestation of hypopituitarism, nonfunctioning pituitary tumors, prolactin-secreting pituitary tumors, or hyperthyroidism. Treatment of these disorders, as well as many of the other endocrinopathies with which impotence may be associated, usually leads to restoration of libido and potency. When impotence is caused by the autonomic neuropathy of diabetes, however, treatment of the endocrinopathy rarely restores sexual function. Sex therapy or implantation of a penile prosthesis may be useful in selected patients with this cause of impotence.
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PMID:Endocrine causes of impotence. Optimistic outlook for restoration of potency. 662 11

Three women with insulin-dependent diabetes mellitus (IDDM) from childhood and early development of diabetic retinopathy are described. Insulin requirement was reduced to 5-12 IU daily in all three after relatively uncomplicated births and all had very brittle diabetes on this dosage. At re-examination 16-22 years after these births and after 34-42 years of IDDM, regression of retinopathy was observed in two patients, while the third had a light retinopathy at the same level as initially. Other diabetic complications were few and none of the patients had nephropathy. Pituitary examination revealed incomplete hypopituitarism in all cases, human growth hormone (HGH) being the sole common factor lacking. These findings and a review of four similar cases reported previously lend some support to the hypothesis of HGH as a possible pathogenetic co-determinant in the development of diabetic retinopathy.
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PMID:Long-term insulin-dependent diabetes mellitus with secondary pituitary insufficiency and regression of retinopathy. 666 30

A case of pituitary adenoma in a patient with myasthenia gravis as well as hypothyroidism, adrenocortical hypopituitarism, and diabetes mellitus is presented. The favorable response of this man's myasthenic symptoms after removal of the adenoma and a possible relationship between the symptomatic expression of myasthenia and a functional hypothalamo-hypophyseal axis are discussed. A link between myasthenia gravis and other autoimmune phenomena is hypothesized.
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PMID:Prolactin-secreting adenoma in a myasthenic patient. 738 99


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