Effect of insulin on osmoregulation of vasopressin

1987 ◽  
Vol 252 (4) ◽  
pp. E538-E548 ◽  
Author(s):  
T. P. Vokes ◽  
P. R. Aycinena ◽  
G. L. Robertson
Keyword(s):  
Plasma Osmolality ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Plasma Sodium ◽  
Diabetic Patients ◽  
Intravenous Insulin ◽  
Plasma Vasopressin ◽  
Insulin Dependent ◽  
Vasopressin Secretion ◽  
Hypertonic Dextrose

Patients with uncontrolled insulin-dependent diabetes mellitus have elevations in plasma vasopressin that cannot be completely accounted for by recognized stimuli. To determine whether insulin deficiency per se increases plasma vasopressin, we investigated the effect of acute insulin depletion on the osmoregulation of plasma vasopressin in insulin-dependent diabetics. When intravenous insulin infusion was stopped, plasma vasopressin, osmolality, and glucose increased over the ensuing 5 h, whereas plasma sodium decreased, and blood volume and pressure did not change. This increase in vasopressin was not due to a loss of osmoregulation, because changes in plasma osmolality and sodium, induced by infusion of hypertonic saline or water loading, induced appropriate vasopressin responses under insulin deplete as well as replete conditions. However, when plasma osmolality and glucose were raised by infusion of hypertonic dextrose, plasma vasopressin increased significantly in diabetic patients under insulin-deplete but not under insulin-replete conditions and actually decreased in healthy controls. These results indicate that acute insulin depletion increases vasopressin secretion by sensitizing the osmoreceptor to stimulation by hyperglycemia. This change in osmoreceptor specificity may be explained by postulating that glucose transport by osmoreceptor neurons as insulin dependent.

Regulation of plasma vasopressin in insulin-dependent diabetes mellitus

1985 ◽  
Vol 249 (3) ◽  
pp. E317-E325 ◽  
Author(s):  
R. L. Zerbe ◽  
F. Vinicor ◽  
G. L. Robertson
Keyword(s):  
Diabetes Mellitus ◽  
Plasma Osmolality ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Plasma Sodium ◽  
Diabetic Patients ◽  
Plasma Vasopressin ◽  
Insulin Dependent ◽  
Vasopressin Secretion

Patients with uncontrolled insulin-dependent diabetes mellitus have elevations in plasma vasopressin that cannot be accounted for totally by recognized osmotic or nonosmotic stimuli. To investigate the possibility that regulation of vasopressin secretion is abnormal in this disease, we characterized the vasopressin response to osmotic and hemodynamic stimuli in five uncomplicated, well-controlled insulin-dependent diabetics, and compared the results with those found in nondiabetic volunteers. During osmotic stimulation with hypertonic saline, plasma vasopressin increased in close linear correlation with plasma osmolality or sodium in both groups. However, in the diabetics, the lines describing the relationships between plasma sodium and vasopressin were shifted significantly to the left of normal, suggesting resetting of the osmostat. This shift was not due to abnormal stimulation by hyperglycemia, because increasing plasma glucose and osmolality by intravenous infusion of hypertonic dextrose produced no increase in plasma vasopressin in diabetics or normals. Tilt tests produced a slightly exaggerated increase in plasma vasopressin in diabetics, but their basal and upright pulse rate, blood pressure, plasma renin activity, norepinephrine, and hematocrit were all normal. The results indicate that in diabetic patients the osmoreceptor for osmotic regulation of vasopressin secretion is reset in such a way that higher plasma vasopressin levels are observed at comparable levels of plasma sodium. The exact cause and consequence of this abnormality remain to be determined.

Effect of blood glucose concentration on osmoregulation in diabetes mellitus

1989 ◽  
Vol 256 (3) ◽  
pp. R597-R604 ◽  
Author(s):  
C. J. Thompson ◽  
S. N. Davis ◽  
P. H. Baylis
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Blood Glucose Concentration ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Plasma Sodium ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Insulin Dependent ◽  
Vasopressin Secretion

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.

Diabetic Ketoacidosis in Children and the Role of Outpatient Management

1990 ◽  
Vol 11 (10) ◽  
pp. 297-304 ◽  
Author(s):  
H. Peter Chase ◽  
Satish K. Garg ◽  
David H. Jelley
Keyword(s):  
Diabetic Ketoacidosis ◽  
Hospital Admissions ◽  
Insulin Dependent Diabetes Mellitus ◽  
The United States ◽  
Absolute Number ◽  
Dependent Diabetes Mellitus ◽  
National Commission ◽  
Diabetic Patients ◽  
Intravenous Insulin ◽  
Insulin Dependent

Diabetic ketoacidosis (DKA) is a common complication among children with diabetes, accounting for 14% to 31% of all diabetes-related hospital admissions.1,2 Extrapolation of data from the National Commission on Diabetes3 suggests that there are approximately 160 000 admissions to private hospitals each year in the United States for DKA. The cost of hospitalizations for DKA is over one billion dollars annually. Sixty-five percent of all patients admitted are less than 19 years of age. The incidence of DKA is believed to be declining. However, because the numbers of subjects with insulin-dependent diabetes mellitus is increasing, the absolute number of hospitalizations for DKA is still increasing. It is the single most common cause of death in diabetic patients under 24 years of age.2 The treatment of DKA has changed in recent years, particularly with the use of low-dose continuous intravenous insulin infusion and with the availability of blood pH levels. Severe DKA has been defined as "a state of ketoacidosis with serum bicarbonate decreased to 10 mmol/L or less," or more recently, as a "pH of 7.1 or less."4 The mortality from DKA has been reported to be in the range of 0.5 to 15.4%.3,5 Previous mortality figures were as high as 38%.2

Hepatic drug metabolism is increased in poorly controlled insulin-dependent diabetes mellitus

1990 ◽  
Vol 123 (5) ◽  
pp. 550-556 ◽  
Author(s):  
Steven Goldstein ◽  
Anna Simpson ◽  
Paul Saenger
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Dependent Diabetes Mellitus ◽  
Diabetic Control ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Diabetic Patients ◽  
Hepatic Drug Metabolism ◽  
Hepatic Drug ◽  
Insulin Dependent ◽  
Cytochrome P 450

Abstract. In addition to increased glycosylation of hemoglobin, abnormalities of other heme proteins such as cytochrome P-450 might also occur in patients with insulin-dependent diabetes mellitus. Antipyrine is a useful marker drug for cytochrome P-450 dependent hepatic drug metabolism. Antipyrine kinetics and urinary excretion of antipyrine metabolites were measured in 14 patients with insulin-dependent diabetes mellitus in poor metabolic control. Improvement in diabetic control in 9 patients, as measured by more normal HbA1 values, led to normalization of plasma antipyrine half-time (t½) and metabolism: the mean antipyrine t½ slowed from 4.7±0.2 (sem) initially to 7.8±0.3 h in these 9 patients and was thus nearly identical to that of normal subjects 8.6±1.0. Antipyrine plasma clearance improved in the 9 diabetic patients whose diabetic control improved. The apparent volume of distribution was normal on both occasions in the diabetic patients. These findings provide a new argument for tight metabolic control in patients with insulin-dependent diabetes mellitus.

scholarly journals FTIR Spectroscopic Investigation of Mineral Structure of Streptozotocin Induced Diabetic Rat Femur and Tibia

2003 ◽  
Vol 17 (2-3) ◽  
pp. 627-633 ◽  
Author(s):  
Handan Boyar ◽  
Belma Turan ◽  
Feride Severcan
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Diabetic Rat ◽  
Carbonate Content ◽  
Diabetic Patients ◽  
Type I ◽  
Mineral Density ◽  
Insulin Dependent

Diabetes mellitus (DM) can be accepted as a heterogenous multi organ disorder that can affect various systems of the human body. Disorders include retinopathy, neuropathy, cardiomyopathy, musculoskeletal abnormalities such as diminished bone formation and bone healing retardation. Low bone mineral density is often mentioned as a complication for patients with insulin dependent diabetes mellitus (type I DM). Streptozotocin (STZ) induced diabetic rats are good models for investigation of the complications of insulin dependent diabetes. In the present study, the effects of STZ induced diabetes on the mineral environment of rat bones namely femur and tibia were studied by Fourier transform infrared (FTIR) spectroscopic technique. The results revealed that mineral crystal sizes increased and carbonate content decreased for diabetic femur and tibia. These changes can be due to the formation of osteoporosis which is widely seen in diabetic patients.

Dissociation of in vitro sensitivities of glucose transport and antilipolysis to insulin in NIDDM

1987 ◽  
Vol 253 (3) ◽  
pp. E300-E304 ◽  
Author(s):  
H. Yki-Jarvinen ◽  
K. Kubo ◽  
J. Zawadzki ◽  
S. Lillioja ◽  
A. Young ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Transport ◽  
American Indians ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Binding ◽  
Dependent Diabetes Mellitus ◽  
Diabetic Patients ◽  
Insulin Dependent ◽  
Obese Subjects

It is unclear from previous studies whether qualitative or only quantitative differences exist in insulin action in adipocytes obtained from obese subjects with non-insulin-dependent diabetes mellitus (NIDDM) when compared with equally obese nondiabetic subjects. In addition, the role of changes in insulin binding as a cause of insulin resistance in NIDDM is still controversial. We compared the sensitivities of glucose transport and antilipolysis to insulin and measured insulin binding in abdominal adipocytes obtained from 45 obese nondiabetic (% fat, 41 +/- 1), 25 obese diabetic (% fat, 40 +/- 1), and 15 nonobese (% fat, 30 +/- 1) female southwestern American Indians. Compared with the nonobese group, the sensitivities of glucose transport and antilipolysis were reduced in both the obese nondiabetic and obese diabetic groups. Compared with the obese nondiabetic subjects, the ED50 for stimulation of glucose transport was higher in the obese patients with NIDDM (171 +/- 38 vs. 92 +/- 10 pM, P less than 0.005). In contrast, the ED50s for antilipolysis were similar in obese diabetic patients (32 +/- 6 pM) and obese nondiabetic subjects (27 +/- 3 pM). No difference was found in insulin binding in patients with NIDDM when compared with the equally obese nondiabetic subjects. These data indicate 1) the mechanism of insulin resistance differs in NIDDM and obesity, and 2) the selective loss of insulin sensitivity in NIDDM precludes changes in insulin binding as a cause of insulin resistance in this disorder.

Impaired Endothelium-Dependent and Independent Dilatation of Forearm Resistance Arteries in Men with Diet-Treated Non-Insulin-Dependent Diabetes: Role of Dyslipidaemia

1996 ◽  
Vol 91 (5) ◽  
pp. 567-573 ◽  
Author(s):  
G. F. Watts ◽  
S. F. O'brien ◽  
W. Silvester ◽  
J. A. Millar
Keyword(s):  
Sodium Nitroprusside ◽  
Density Lipoprotein ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Diabetic Patients ◽  
Resistance Arteries ◽  
Control Subjects ◽  
Vasodilatory Response ◽  
Insulin Dependent

1. We measured endothelium-dependent and independent dilatation of forearm resistance arteries in 29 men with diet-treated non-insulin-dependent diabetes mellitus and 18 age- and sex-matched control subjects. None of the diabetic patients had hypercholesterolaemia, overt hypertension or microproteinuria. 2. We examined endogenous and exogenous nitric oxide-mediated vasodilatation by measuring forearm blood flow with venous occlusive plethysmography after administration of acetylcholine (7.5 and 15 μg/min) and sodium nitroprusside (3 and 10 μg/min), respectively, into the brachial artery. NG-monomethyl-l-arginine was also infused to study the inhibition of basal and stimulated release of nitric oxide. 3. The vasodilatory response to acetylcholine, expressed as area under curve, was significantly decreased in the diabetic patients compared with the control subjects (P = 0.019). NG-monomethyl-l-arginine significantly reduced basal (P < 0.001) and acetylcholine-stimulated blood flow (P < 0.02) in both groups. The vasodilatory response (also expressed as area under curve) to sodium nitroprusside was significantly less (P = 0.044) in the diabetic patients than in the control subjects. 4. In the diabetic patients, impaired vasodilatory responses to acetylcholine were significantly correlated with higher serum triacylglycerols (P = 0.048) and lower high-density lipoprotein-cholesterol concentrations (P = 0.007); the association with high-density lipoprotein was independent of age, glycated haemoglobin and blood pressure. Sodium nitroprusside responses were not correlated with lipid and lipoprotein concentrations. 5. We conclude that there is impaired endothelial and smooth muscle cell function in men with diet-treated non-insulin-dependent diabetes mellitus uncomplicated by overt hypertension or microproteinuria. Endothelial dysfunction may be related to diabetic dyslipidaemia and associated metabolic disturbances.

Islet cell transplantation for insulin-dependent diabetes mellitus: perspectives from the present and prospects for the future

2000 ◽  
Vol 2 (6) ◽  
pp. 1-28 ◽  
Author(s):  
Derek W.R. Gray ◽  
Nicolas Titus ◽  
Lionel Badet
Keyword(s):  
Diabetes Mellitus ◽  
Immune Modulation ◽  
Insulin Dependent Diabetes Mellitus ◽  
Human Islet ◽  
Insulin Dependent Diabetes ◽  
Current Status ◽  
Dependent Diabetes Mellitus ◽  
Diabetic Patients ◽  
Islet Cell Transplantation ◽  
Insulin Dependent

The long-term complications of insulin-dependent diabetes mellitus have become a major health care problem, and it is now clear that they arise from inadequate homeostatic control of blood glucose by injected replacement insulin. Transplantation of pancreatic islets is arguably the most logical approach to restoring metabolic homeostasis in people with diabetes. This review looks at the current status of human islet transplantation and the problems that remain. These include: (1) the limited supply of human islet tissue available for transplantation; (2) the adverse effects of current immunosuppressive protocols on diabetic patients; (3) the problems of primary nonfunction of the transplanted islets; (4) the rejection of islets; and (5) the recurrence of autoimmune diabetic disease. Some of the approaches that might solve these problems are then examined: (1) immune modulation to reduce or prevent immune attack by the recipient's immune system; (2) immunoisolation to prevent recognition of the islet graft; (3) induction of tolerance; (4) xenotransplantation using islets derived from animals; and (5) gene therapy.

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