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)

Autoantibodies reacting with discrete populations of cells in normal human pancreatic islets were found by immunofluorescence in 17 out of 1279 sera. A double immunofluorescence technique, with antisera to pancreatic glucagon, insulin, somatostatin, and human pancreatic polypeptide was used to show that 13 of the sera contained anitbodies reacting specifically with glucagon cells, while the other 4 reacted with somatostatin cells. These antibodies were directed against intracellular components and not against the hormones themselves. Both types of antibody occurred independently of the islet-cell antibodies which have been described in diabetes mellitus. These findings suggest selective damage to individual cell types in the pancreatic islets and raise the possibility of corresponding hormone deficiency syndromes.
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PMID:Separate autoantibodies to human pancreatic glucagon and somatostatin cells. 6 13

The effect of insulin on the serum levels of the amino-terminal propeptide of type III procollagen (PIIINP) was investigated in patients with non-insulin-dependent diabetes mellitus, whose disease was unsatisfactorily controlled by oral drugs. Before insulin therapy the PIIINP values of the patients (3.2 +/- 1.3 micrograms/l, n = 38) varied within the range of healthy subjects (3.1 +/- 0.6 micrograms/l, n = 50, NS). Insulin therapy (6-20 IU at bedtime plus the oral drugs) improved the glycemic control and increased the serum PIIINP during a 4 week (3.1 +/- 0.9 to 3.8 +/- 1.1 micrograms/l, P less than 0.01, n = 8) and an 8 week period (3.2 +/- 1.3 to 3.8 +/- 1.6 micrograms/l, P less than 0.001, n = 22). The values were still elevated after 6 months on insulin (3.5 +/- 1.5 to 4.0 +/- 1.7 micrograms/l, P less than 0.01, n = 12). Placebo-insulin did not alter the concentration of PIIINP (3.1 +/- 0.6 to 2.8 +/- 0.6 micrograms/l, NS, n = 8) whereas the glycemic control improved and body weight decreased. The PIIINP values correlated with fasting insulin before (r = 0.403, P less than 0.05, n = 30) and after the therapy (r = 0.452, P less than 0.001, n = 60). Insulin therapy, while correcting the hormone deficiency and restoring glucose and protein metabolism, seems to activate the synthesis of type III procollagen in patients with NIDDM. This may promote the atherosclerotic process.
Diabetes Res Clin Pract 1992 Sep
PMID:Effect of insulin on serum amino-terminal propeptide of type III procollagen in non-insulin-dependent diabetes mellitus. 142 60

333 consecutive patients with hypopituitarism diagnosed between 1956 and 1987 were retrospectively examined. The patients had been given routine replacement therapy. The overall mortality was higher than in an age and sex matched population. Deaths from vascular disorders were also significantly increased (60 [40 male, 20 female] versus 30.8 expected [23.5, 7.4 female]). The hazard function for vascular death was independent of age at diagnosis, time after diagnosis, calendar year of diagnosis, gender, degree of pituitary insufficiency, hypertension, and diabetes mellitus. Mortality risk was raised irrespective of whether hypopituitarism was due to pituitary adenoma or secondary to other diseases. 7 patients (3 male, 4 female) died from malignant diseases (expected 10.1 and 4.1, respectively). These observations indicate that life expectancy is shortened in patients with hypopituitarism. Growth-hormone deficiency could be a factor in this increased mortality from cardiovascular disease.
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PMID:Premature mortality due to cardiovascular disease in hypopituitarism. 197 79

Transplantation of pancreatic islets of Langerhans has been shown to prevent the development of many of the complications associated with diabetes. Transplanted islets, however, are readily rejected by the immune system. The use of artificial membranes to isolate the transplanted islets from the immune system of the host prolongs islet allografts in experimental animals. We have developed a method for encapsulating islets in semipermeable membranes composed of alginate and polylysine. The same technique can be applied to other endocrine cell types. The capsules are 700 to 800 micron in diameter with a hydrogel membrane approximately 4 micron thick. Intraperitoneal allografts of 5 x 10(3) encapsulated islets reversed diabetes in rats for up to 21 months and intact capsules with viable beta cells could be recovered from the recipients. Microencapsulation of endocrine cells for transplantation could potentially be used in the clinical treatment of hormone deficiency diseases.
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PMID:Microencapsulated cells as hormone delivery systems. 331 34

Type 1 diabetes is a disease due to hormone deficiency. Therefore treatment with insulin is hormonal substitution and should be done according to physiological data with 4 injections NPH-insulin and 3 preparandial injections of regular insulin before the main meals. Intensified insulin treatment should be separate substitution of basal and prandial insulin need. The basal insulin substitution should be tested by a fasting day over 24 h giving only basal insulin. Insulin treatment has to be supplemented by diabetes education, blood glucose self control and regulation of diet and exercise. Target values are blood glucose concentrations of 80 to 120 mg/dl fasting and before the main meals, 110 to 160 mg/dl at bedtime and above 65 mg/dl after midnight. A written plan with the algorithms of insulin substitution is helpful for the care of the diabetic patient. A successful insulin treatment is assessed by a HbA1c of 7.x without hypoglycemias.
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PMID:[Insulin therapy of type I diabetes]. 928 Dec 33

Synthesis of pituitary hormones was shown to be efficiently regulated at the transcriptional level. The specialized function of the five cell types in the anterior pituitary is controlled by ubiquitous as well as cell-specific transcription factors. Pit-1 is such a cell-specific regulator found only in lacto-, somato- and thyrotropes which could be shown to be essential for basal expression of growth hormone (GH) and prolactin (Prl) genes and the regulated expression of Prl and thyrotropin (TSH) beta-subunit genes. Identification of distinct binding sites for transcription factors and some of the mechanisms of transcriptional control shed light on the complex regulation of pituitary hormone gene expression which is exemplified for the TSH beta gene. The control of basal as well as positively and negatively regulated expression of some pituitary hormone genes becomes fairly well understood by the investigation of the role of Pit-1. Identification of different mutations in the human pit-1 gene supported the role of this protein for combined pituitary hormone deficiency (CPHD) characterized by the deficiency of GH, prolactin and TSH.
Exp Clin Endocrinol Diabetes 1997
PMID:Thyrotropin (TSH) beta-subunit gene expression--an example for the complex regulation of pituitary hormone genes. 928 5

Hypothyroidism is a recognised complication of GH therapy in GH deficient children. The mechanisms involved include direct effects on thyroid function but also result from the close interrelationship of pituitary cell-lines that differentiate during embryonic development of the anterior pituitary gland. Among numerous pituitary transcriptionfactors that orchestrate pituitary organogenesis Pit-1 was the first to be recognised and is the most extensively studied. Mutations in the Pit-1 gene account for a form of combined pituitary hormone deficiency for GH, Prolactin (Prl) and TSH (CPHD). Despite the variability of the clinical presentation of this syndrome at the time of initial diagnosis, all forms finally result in severe retardation of growth and development due to GH-deficiency and hypothyroidism. More than half of the families with a combined pituitary hormone deficiency have not disclosed any Pit-1 abnormalities. Evidence is accumulating that Prop-1, a transcriptionfactor expressed temporarily in the fetal anterior pituitary, could be a candidate for patients with a Pit-1 phenotype without any Pit-1 gene abnormalities.
Exp Clin Endocrinol Diabetes 1997
PMID:GH and TSH deficiency. 943 6

Coeliac disease does not always respond properly to a gluten-free diet, and treatment may be complicated by an underlying autoimmune endocrine disorder. We report three cases of hypopituitarism in patients with coeliac disease who seemed to have incomplete dietary response. The first patient had diabetes and suffered from hypoglygaemic events; the second had muscular atrophy of unknown origin while the third had growth failure. None had a pituitary mass, suggesting that hypopituitarism was of autoimmune origin. Overall condition improved only after replacement therapy for the underlying hormone deficiency; this association should thus be recognized.
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PMID:Autoimmune hypopituitarism in patients with coeliac disease: symptoms confusingly similar. 1134 13

Given the rapidly increasing number of women above 50 it is of pivotal importance to consider health issues related to gonadal hormone deficiency. The possibility of alleviating such symptoms by hormone replacement therapy (HRT) should be recognized by all physicians, not merely by gynaecologists. But which women should be given what therapy, and for how long? Due to the increased risk of endometrial cancer and bleeding problems when using oestrogen monotherapy, only women who have undergone hysterectomy could use this regimen unless treatment is aimed at amelioration of urogenital symptomatology only. In this case a vaginal administration of low-dose oestrogens is possible as such doses do not induce endometrial proliferation. In all other cases a combination of an oestrogen and a progestogen must be used. There are several options for doing so. During the early phase of the climacteric period when irregular and/or heavy vaginal bleeds are part of the symptomatology a cyclical therapy will often combat these problems. As women pass into the menopause a sequential regimen is often preferred until 1-3 years have elapsed since menopause. With advancing time since menopause women become more and more reluctant to experience monthly bleeds. In such cases a continuous combined regimen may be offered even though it cannot guarantee a bleed-free remedy.Non-oral, particularly transdermal, therapy is an alternative in women with co-existing morbidity such as migraine, diabetes, malfunction of the gastrointestinal tract and liver disease. Oral therapy is preferred particularly in women with elevated plasma levels of LDL-cholesterol, lipoprotein(a) or homocysteine. Oral therapy induces liver protein synthesis. This could be an advantage in cases with low plasma levels of sex hormone-binding globulin (SHBG) as low levels of SHBG may promote androgenic stigmata such as hirsutism and a lowering of the voice. However, in cases with too low an androgen influence the use of a non-oral therapy may counteract symtoms such as low libido.Tibolone could be used for the prevention (and treatment?) of osteoporosis but it will also mitigate the typical climacteric symptoms. Raloxifene is a fairly new type of drug which is classified as a selective oestrogen receptor modulator (SERM). It will reduce vertebral fractures to the same extent as bisphosphonates, albeit the increase in bone density is less. Raloxifene has no effect on climacteric symptoms. Its greatest benefit is a clear reduction of breast cancer in women, which is in contrast to HRT/ERT.There are insufficent data on tibolone and the incidence of breast cancer. Experimental data, however, are intriguing in suggesting less impact on the breast than conventional HRT/ERT.
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PMID:The role of ERT/HRT. 1209 68

Growth hormone deficiency (GHD) diagnosed in childhood may persist into adult life. After attainment of final height, retesting of the patient's growth hormone-insulin-like growth factor (GH-IGF) axis using the adult GHD diagnostic criteria should be performed after an appropriate interval of 1-3 months off GH therapy. At the time of retesting, other pituitary hormones and serum IGF-I levels should also be measured. The opportunity should be taken to assess body composition, bone mineral density, and fasting lipid and insulin levels. Patients with severe, long-standing, multiple pituitary hormone deficiency, genetic defects, or severe organic GHD can be excluded from GH retesting. When the diagnosis of adult GHD is established, continuation of GH therapy can be recommended unless there is a known risk of diabetes mellitus or malignancy. The patient's transition to GH replacement in adulthood should be arranged as a close collaboration between the pediatric and adult endocrinologists, who should discuss the reinitiation of treatment with the patient.
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PMID:Confirming the diagnosis of growth hormone deficiency (GHD) and transitioning the care of patients with childhood-onset GHD. 1279 65


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