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

The contribution of proinsulin to the total serum immunoreactive insulin (IRI) was measured in 59 patients with maturity onset diabetes (23 being treated with diet alone and 36 with oral sulfonylurea agents) and compared to that in 44 control subjects. The percentage of proinsulin was increased in 11 patients and correlated with plasma glucose, but not with IRI. There was no difference between the drug-treated group and diet-treated group, or between patients taking different sulfonylurea agents. Sequential studies in one patient showed normalization of the proportion of proinsulin following lowering of the plasma glucose level. It is probably that the increased circulating proportion of proinsulin in hyperglycemic diabetic patients is secondary to beta cell exhaustion with release of less mature granules.
Am J Med 1977 Dec
PMID:Circulating proinsulin in patients with maturity onset diabetes. 34 87

Twenty-one insulin-dependent diabetics with azotemic nephropathy were evaluated for renal transplantation by selective coronary angiography and cine left ventriculography. All had hypertension, retinopathy, neuropathy, and required salt restriction plus diuretics for volume overload. There was no clinical or electrocardiographic evidence of ischemic coronary artery disease in twenty. Ten patients (five males, five females, mean age 29.3 years; mean duration of diabetes 21.9 years; mean serum cholesterol 239 mg%) had significant coronary artery disease, seven demonstrating focal abnormalities in left ventricular wall motion. Two patients (one male, one female; mean age 36.5 years; mean duration of diabetes 28.5 years; mean serum cholesterol 250 mg%) had no significant coronary artery disease, but demonstrated diffusely abnormal left ventricular wall motion with diminished ejection fraction. Thirty-eight percent had significant coronary artery disease unpredictable by electrocardiographic or clinical data. The finding of no significant coronary artery disease in 52% of a group with severe renal-hypertensive complications of diabetes is surprising. Two patients may have a demonstrated cardiomyopathy.
Circulation 1978 Dec
PMID:Asymptomatic coronary artery disease: angiographic assessment of diabetics evaluated for renal transplantation. 36 Dec 77

Despite the best efforts of physicians and diabetic patients in the use of insulin for control of juvenile-onset (insulin-deficient) diabetes, vascular complications occur in most patients. The many advantages of the whole fetal pancreas as a donor organ make transplantation of the pancreas a promising improvement in therapy. A rat model has been developed for future application to human beings. After transplantation of one fetal rat pancreas into a diabetic recipient, maturation and growth of the transplant is adequate for complete reversal of the diabetic state of the recipient. Because of the atrophy of exocrine elements after transplantation of the fetal organ, many of the technical problems inherent in adult pancreas transplants are avoided. The small size of the fetal pancreas permits cryopreservation and permanent storage without apparent loss of function. Cryopreservation provides time for typing, matching, and preparation of the recipient to receive the donor organ and thus may alleviate rejection problems.
Ann Intern Med 1978 Dec
PMID:UCLA Conference. Pancreas transplantation for diabetes mellitus. 36 9

Plasma glucagon response to glucose in diabetic subjects was observed before and after treatment. In normal subjects, plasma glucagon concentrations decreased substantially after an oral glucose load. In all diabetic patients before treatment, plasma glucagon was not suppressed and rather tended to rise paradoxically despite pronounced hyperglycemia. In diabetics treated with sulfonylurea or insulin, basal plasma glucagon concentrations were significantly lower than those in patients who were not treated. However, plasma glucagon response to an oral glucose load was not normalized by successful treatment with sulfonylurea or insulin, in spite of improvement of glucose tolerance. These results suggest that the insensitivity of the A-cell to hyperglycemia exists after treatment, and this abnormal plasma glucagon response to glucose after treatment may be caused either by impaired response of endogenous insulin to glucose, which is sustained even after treatment, or by an intrinsic defect of the A-cell.
Diabetes 1978 Dec
PMID:Failre of suppress plasma glucagon concentrations by orally administered glucose in diabetic patients after treatment. 36 90

Functional alteration of the islet cells was investigated in dogs after the resection of different parts of the small intestine. Three weeks after jejunal or ileal resection, when the dogs might still have been in a catabolic state, insulin and pancreatic glucagon release in response to intravenously infused glucose and arginine was reduced. Three months after jejunal resection, both intravenous glucose tolerance and insulinogenic index in the intravenous glucose tolerance test were significantly below the preoperative values (P less than 0.001, P less than 0.05), while pancreatic glucagon release in response to arginine infusion release. This functional alteration three months after jejunal resection was similar to that seen in diabetes mellitus. On the other hand, three months after ileal resection, insulin and pancreatic glucagon release was almost normal. We conclude that the jejunum plays a more important role in the enteroinsular system than the ileum and that prolonged interruption of this enteroinsular axis can cause insular disorder and what could hypothetically be called enterogenic chemical diabetes, in view of the altered glucose tolerance test and the alteration in insulin secretory response.
Diabetes 1978 Dec
PMID:Functional alteration of islet cells after jejunal or ileal resection in dogs. 36 91

The rate of alloxan-induced insulin release was measured from rat islets maintained in a simple perifusion system. Insulin release during the five-minute exposure to alloxan reached its maximum rate after two to three minutes of the exposure and then rapidly declined. This insulin release was dependent upon extracellular calcium and was associated with an increased 45Ca uptake by isolated islets. Once exposed to alloxan, however, the islets did not release insulin when stimulated again with D-glucose or alloxan. These effects of alloxan on insulin release (stimulation and subsequent inhibition) and the increased 45Ca uptake were prevented by the presence of 3-0-methyl-D-glucose during the alloxan exposure. These findings indicate a close correlation between alloxan-induced insulin release and the subsequent inhibition of further insulin release. D-glucose, when present during the entire five-minute exposure to alloxan, protected competitively against alloxan inhibition of insulin release. In addition, D-glucose, when present immediately after brief (one to three minutes) alloxan exposures, reversed some of the subsequent inhibition of insulin release. These findings suggest that alloxan and D-glucose were competing for a common site on the beta-cell. The possibility of this site being a receptor responsible for the initiation of insulin release is discussed.
Diabetes 1978 Dec
PMID:Alloxan stimulation and inhibition of insulin release from isolated rat islets of Langerhans. 36 92

Fourteen juvenile-onset diabetic patients accepted for renal transplantation and maintained on chronic peritoneal dialysis during a 3-year period were compared with a similar group of 43 patients accepted for renal transplantation and maintained on hemodialysis. The 1-year survival in each group was similar (52% on chronic peritoneal dialysis; 55% on hemodialysis), but there was a striking difference in progressive morbidity. Seven patients on chronic peritoneal dialysis were blind in one or both eyes at the onset, and visual acuity improved in two, including one bilaterally blind patient who achieved 20/35 vision bilaterally; none worsened. In the hemodialysis group, 12 patients were totally blind in one or both eyes and 11 additional patients became blind or had severe deterioration in vision; none improved. Neuropathy progressed in only 1 patient on chronic peritoneal dialysis, whereas it worsened in 17 patients on hemodialysis--9 to the extent that they needed braces or canes or were nonambulatory. All patients on chronic peritoneal dialysis were home trained and were dialyzed at night, with seven being able to work full or part time; virtually none of the patients on hemodialysis were able to work. Chronic peritoneal dialysis was relatively free of technical complication, and no significant difficulty was encountered in diabetic control, in the anephric state, or during abdominal surgery. Chronic peritoneal dialysis appears to have less associated morbidity than does hemodialysis in the treatment of chronic renal failure of juvenile-onset diabetes mellitus.
Mayo Clin Proc 1978 Dec
PMID:Chronic peritoneal dialysis in juvenile-onset diabetes mellitus: a comparison with hemodialysis. 36 85

A survey is given of the literature on the influence of prostaglandins on the lipid- and carbohydrate metabolism. Some common pathobiochemical features in the development of diabetes mellitus and the ischaemic heart disease are outlined, which became apparent by examinations of the fatty acid pattern in patients. Thus a biochemical basis for that epidemiologically well known fact is given, that diabetes represents a risk factor for the ischaemic heart disease. Some of the latest results from the experimental research suggest that the vascular complications occurring in chronic diabetes are caused by a decrease in the formation of prostacyclin and possibly by an increase in the thromboxane A2 production. Similar changes in the prostaglandin metabolism occur in the ischaemic heart disease and myocardial infarction, too, as experimental results have shown.
Z Gesamte Inn Med 1978 Dec 01
PMID:[Significance of prostaglandins for fat and carbohydrate metabolism with special reference to pathogenesis of diabetes mellitus ]. 36 61

Hypophysectomy and pituitary stalk section result in dramatic morpho-functional changes in all parts of mammalian hypothalamo-hypophyseal neurosecretory system. Reorganization of the hypophyseal stalk consists of several interconnected but differing in time processes. Simultaneously with the developing traumatic changes (degeneration of the sectioned neurosecretory fibers, secretory disorders) proliferation of pituicytes with characteristic phagocytic activity is observed. A little bit later, intensive mitotic division of endothelial cells and capillary formation piercing the stalk periphery begins. At the same time, a new way for blood outflow from the capillaries of the primary portal plexus into the synuses of the brain pias is restored. Degenerated neurosecretory fibers are gradually substituted by regenerating fibers forming a dense network in heavily vascularizated stalk parts. As differentiation of endothelial cells and regeneration of neurosecretory fibers procede, axovasal contacts are gradually forming. At that time the hypophyseal stalk begins functioning as a neurohumoral organ but morpho-functionally less perfect than the posterior hypophyseal lobule. In the median eminence of the operated animals, unlike the intact ones, neurosecrete is accumulating around the capillaries of the portal plexus. Mechanical damage of neurosecretory fibers during the operation results in degeneration of a greater number of neurosecretory cells in the supraoptical and paraventricular nuclei. Preserved cells have an increased functional activity because of neurohormonal deficiency in the organism. As a result of the structural changes mentioned, diabetes mellitus develops, subsiding gradually with time course.
Arkh Anat Gistol Embriol 1978 Dec
PMID:[Changes in the hypothalamo-hyophyseal neurosceretory system of mammals following pituitary stalk transection and hypophysectomy]. 36 82

Plasma glucagon levels were determined after 50 g of oral glucose loading in eleven acromegalics and fourteen normal subjects. Basal plasma glucagon levels were significantly elevated in patients with acromegaly, as compared with those in normal subjects. Oral glucose loading caused a decrease in plasma glucagon in normal subjects but not in acromegalics. Since this non-suppressibility of plasma glucagon by orally administered glucose was observed even in acromegalics without diabetes, it is concluded that insensitivity of the pancreatic alpha cell to hyperglycaemia exists in patients with acromegaly as well as in diabetics.
Clin Endocrinol (Oxf) 1978 Dec
PMID:Acromegaly: insensitivity of the pancreatic alpha cell to hyperglycaemia. 37 62


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