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)

The binding of [125I]arginine-8-vasopressin (AVP) to hippocampal microvessels isolated from brains of normal Wistar rats, animals after water deprivation and heterozygous as well as homozygous diabetes-insipidus rats (Brattleboro strain) were measured. Data from binding experiments from the microvessels of the different groups of animals in each case revealed a single class of high affinity binding sites. However, the binding parameters between the different groups of rats were different. The affinity constants differs by a factor of 5.1, ranging from KD = 1.18 nmol X L-1 (animals after water deprivation) to KD = 6.05 nmol X L-1 (homozygous Brattleboro rats). The binding capacity, differing by a factor of 3.5, ranged from Bmax = 245 fmol X mg-1 to Bmax = 865 fmol X mg-1.
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PMID:Arginine-vasopressin binding to isolated hippocampal microvessels of rats with different endogenous concentrations of the neuropeptide. 259 15

Altogether 50 patients with diabetes mellitus, type II, with the presence of microangiopathies and 10 healthy controls were investigated to study the pathogenesis of vascular complications. An increased level of vasopressin and a normal level of beta 2-microglobulin were radioassayed in the blood plasma of the examinees. An acute furosemide test made it possible to establish 3 types of responses of vasopressin secretion in such patients: normal, paradoxical and areactive. The blood level of beta 2-microglobulin was raised in 65% of cases in the paradoxical response, in 34.5% in the normal response and in 0.6% in the areactive response. The data obtained suggested heterogeneity of the mechanisms of development of vascular complications in diabetes mellitus, type II.
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PMID:[Content of vasopressin and beta2-microglobulin in the blood in patients with diabetes mellitus type II accompanied by microangiopathy]. 265 19

A variety of age-related anatomic and functional alterations in the kidney have been described. Anatomic abnormalities in the aging kidney include a decrease in kidney size, increased glomerular sclerosis, altered tubular structure, and an altered pattern of vascular flow. These anatomic abnormalities are associated with renal functional abnormalities, including decreased renal blood flow, and glomerular filtration rate. Altered renal tubular function, including impaired handling of water, sodium, acid, and glucose, may also be present. Impaired "endocrinologic" functioning manifested by changes in the renin-angiotensin system, vitamin D metabolism, and antidiuretic hormone responsiveness have been reported. The kidney is constantly exposed to the effects of a variety of potentially toxic processes. These range from environmental toxins and drugs, to a variety of chronic medical illnesses including hypertension, diabetes, and atherosclerotic disease. In this context, differentiation of "aging" effects from nephrotoxic effects resulting from these other processes is difficult. It has been argued that hypertension is an important factor in the development and progression of renal insufficiency in the elderly. The relationship between hypertension, glomerular hyperfiltration, atherosclerosis, and progressive renal dysfunction needs further study. Further research may allow the rational recommendation of interventions designed to control age-associated changes in renal function.
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PMID:Renal function in aging. 266 87

We report a case of limbic encephalopathy clinically characterized by a progressive amnestic syndrome and many EEG seizures mainly localized on the left temporal area. Biological investigations revealed diabetes mellitus and a syndrome of inappropriate antidiuretic hormone secretion (IADH). Haemodynamic and metabolic studies by positron-emission tomography showed an important increase in cerebral blood flow (CBF) and cerebral metabolic rate of oxygen on the left anterior temporal region precisely where the electrical seizures were recorded. Nine months later, severe disorders of memory and a dramatic decrease in CBF and CMRO2 on the same area region were present. At autopsy, a small size oat cell bronchial carcinoma was found with metastases in two small adjacent lymph nodes. Neuropathological examination showed atrophy (neuronal loss, protoplasmic gliosis) in the amygdala; where there was in addition an area of nodular gliosis. The hippocampus and parahippocampal gyrus lesions were severe on the left and moderate on the right side. The authors discuss the nosology of their case in the paraneoplastic syndromes and, with a review of the literature, the role of ADH and cellular hyperactivity in the pathogenesis of specifically localized neuronal alterations.
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PMID:[Paraneoplastic limbic encephalopathy, inappropriate ADH secretion and recurrent subclinical epileptic seizures. Clinical, anatomo-pathological and metabolic correlations by positron emission tomography]. 282 90

Rats were administered streptozocin (STZ; 50 or 75 mg/kg i.v., tail vein) or vehicle. Approximately 2 wk later, venous and arterial catheters was implanted for subsequent (24 h later) vasopressin, electrolyte, and hemodynamic measurements. STZ-induced diabetic (STZ-D) rats demonstrated a dose-dependent increase in the plasma glucose concentration, plasma osmolality, and plasma vasopressin concentration. Mean arterial blood pressure (MABP) was unchanged, but heart rate was reduced. Diabetes-prone BB rats, maintained on or withdrawn from insulin treatment for 24-48 h, and diabetes-resistant rats were instrumented and studied as above. Spontaneous-diabetes-prone rats demonstrated increase in plasma glucose concentration and plasma osmolality similar to STZ-D rats but had significantly greater plasma vasopressin concentrations. The significant decrease in MABP observed in these animals probably contributed to the enhanced vasopressin response. We conclude that both osmotic and cardiovascular parameters play important roles in vasopressin secretion in diabetic rats.
Diabetes 1989 Jan
PMID:Vasopressin in rats with genetic and streptozocin-induced diabetes. 290 12

Poorly controlled insulin-dependent diabetes mellitus is associated with considerable elevations of plasma vasopressin concentrations, although well-controlled diabetics have normal osmoregulated thirst and vasopressin release. We studied the effect of blood glucose concentration on osmoregulated thirst and vasopressin secretion in insulin-dependent diabetes mellitus. Blood glucose was maintained overnight, and for the duration of the study, in either the euglycemic (4-5 mmol/l) or hyperglycemic (10-12 mmol/l) range, and patients underwent infusion of hypertonic (855 mmol/l) sodium chloride solution. Plasma sodium was lower during the hyperglycemic study, but elevation in plasma sodium concentration by infusion of saline caused progressive linear increases in both thirst and plasma vasopressin concentrations in both studies. Linear regression analysis defined lowered plasma sodium thresholds for both thirst appreciation and vasopressin release during the hyperglycemic study, although the sensitivity of the osmoreceptors remained unchanged. Analysis of the data in terms of plasma osmolality, corrected for the increase in blood glucose in the hyperglycemic study, revealed no differences in the osmotic thresholds for thirst or vasopressin release; sensitivity of the osmoreceptors also remained the same. Drinking abolished thirst and lowered plasma vasopressin concentrations before major changes in plasma sodium were observed. These results show that insulin-dependent diabetic patients osmoregulate appropriately when moderately hyperglycemic but that the threshold plasma sodium for vasopressin secretion and thirst appreciation is lowered by an unknown mechanism.
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PMID:Effect of blood glucose concentration on osmoregulation in diabetes mellitus. 292 50

Plasma vasopressin, vasopressin-induced platelet aggregation, and platelet vasopressin receptors were investigated in 10 normal subjects and 14 diabetic patients free of microangiopathy. Basal plasma vasopressin concentration was identical in two groups. Platelet aggregation induced by vasopressin as well as by epinephrine was not significantly altered in the diabetic patients. However, exploration of platelet V1-vasopressin receptors revealed in the diabetic group a dramatic reduction in the number of binding sites without alteration of the receptor affinity for tritiated vasopressin. Thus vasopressin-induced platelet aggregation in uncomplicated diabetes mellitus remains normal despite a decrease in the number of vasopressin receptors presumably due to alterations of the platelet membrane structure.
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PMID:Platelet aggregation and vasopressin receptors in patients with diabetes mellitus. 296 99

Factor VIII (FVIII) and plasminogen activator activity (PAA) rise during hypoglycaemia, and this might contribute to the vascular complications of diabetes. Similar changes in haemostasis accompany raised plasma levels of vasopressin (aVP) and adrenaline. To investigate the effects of these hormones on haemostasis during hypoglycaemia and the role of plasma insulin concentrations, eight insulin-dependent diabetic patients underwent controlled hypoglycaemia for 20 min and 13 diabetic patients were investigated during hyperinsulinaemia with blood glucose maintained at 8.0 mmol/l. During hypoglycaemia, insulin levels increased to median values of 114 mU/l, a VP rose from 0.5 to 4.4 (p less than 0.005) pg/ml and adrenaline from 0.4 to 4.4 nmol/l (p less than 0.005). FVIII coagulant activity (FVIII:C) rose from 0.75 to 1.09 IU/ml (p less than 0.01) and the ristocetin co-factor (FVIIIR:Co) and von Willebrand factor antigen (vWF:Ag) showed similar responses. PAA increased from 156 to 745 units (p less than 0.005). During hyperinsulinaemia, insulin rose following infusion from 24 to 52 and 118 mU/l, maintained for an hour at each level. Despite this, plasma aVP, FVIII:C, FVIIIR:Co, vWF:Ag and PAA remained unchanged. This study indicates that the marked changes in FVIII, vWF and PAA concentrations which accompany hypoglycaemia depend on low blood glucose and not raised plasma insulin. The response in probably mediated by increases in adrenaline and aVP, which are part of the physiological response to hypoglycaemia.
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PMID:Hormonal control of haemostasis during hypoglycaemia in diabetes mellitus. 311 5

Enhanced prostaglandin production is postulated to contribute to altered vascular reactivity and glomerular hyperfiltration in early insulin-deficient diabetes mellitus. Rats with streptozocin-induced diabetes (STZ-D) show glomerular hyperfiltration and develop renal disease. BB rats with genetic diabetes (BB-D) also hyperfilter but have only minor renal lesions. We therefore compared glomerular and mesangial prostaglandin E2 (PGE2) production and glomerular contractility in response to pressors as a reflection of in vitro vascular reactivity in these models. Glomeruli isolated from rats with 3 wk of STZ-D produced significantly more PGE2 under basal and ionophore A23187-stimulated conditions than those from control rats. Glomeruli from BB-D rats under basal and stimulated conditions, however, generated amounts of PGE2 that were comparable to either those of nondiabetic littermates or of normal Wistar rats. Mesangial cells cultured from glomeruli of STZ-D, BB-D, and control rats all had identical prostaglandin profiles judged by conversion of [14 C]arachidonic acid. They also produced comparable amounts of PGE2 under basal conditions and after stimulation with angiotensin II or A23187, as determined by radioimmunoassay. Planar surface area of glomeruli isolated from control rats showed a dose-dependent decrease in response to angiotensin II (10(-11)-10(-9) M). This response to angiotensin II was at least as great in glomeruli from STZ-D rats. Contraction of glomeruli from control and STZ-D rats was also comparable after vasopressin or norepinephrine. Similarly, glomeruli from BB-D and BB control rats contracted in a comparable fashion to angiotensin II and norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1987 Dec
PMID:Comparison of glomerular and mesangial prostaglandin synthesis and glomerular contraction in two rat models of diabetes mellitus. 311 6

Patients with diabetes mellitus have higher levels of coagulation factor VIII than the non-diabetic population. This may be a result of poor metabolic control and could contribute to the development of microvascular complications. During ketoacidosis there are acute changes in plasma concentrations of coagulation factors, some of which may be mediated by the rise in vasopressin that occurs. We have investigated the effects of hyperglycaemia without ketosis on some aspects of haemostasis by manipulating blood glucose concentrations using a Biostator. After a 1h run-in period with the blood glucose at 5 mmol/l, the blood glucose was maintained at 5, 15 and 25 mmol/l and maintained for one hour at each level in six male patients with insulin-dependent diabetes. Insulin was infused at 0.25 mu/kg/min. Venous blood samples were taken at the beginning and end of each hour after the run-in period for assays of factor VIII coagulant activity (FVIII:C), von Willebrand factor antigen (vWF:Ag), ristocetin co-factor (FVIIIR:Co), activated partial thromboplastin time (APTT) and vasopressin (aVP). There was a slight, though statistically insignificant fall in median factor VIII:C concentration at each incremental level of increase in blood glucose. Values (at the beginning and end of each hour) were: 1.0 and 1.1 iu/ml at 5 mmol/l; 0.95 and 0.79 iu/ml at 15 mmol/l; and 0.74 and 0.84 iu/ml at 25 mmol. vWF:Ag and FVIIIR:Co were unchanged. Plasma aVP fell slightly from 1.1 to 0.5 pg/ml. The results indicate that high levels of FVIII seen in diabetes are not due to short-term increases in blood glucose and that acute hyperglycaemia does not promote pro-coagulant changes in blood.
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PMID:Effect of controlled hyperglycaemia on factor VIII concentrations in insulin dependent diabetes mellitus. 313 35


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