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.

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 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.

The effect of acute hyperglycemia on the plasma C-peptide response to intravenous glucagon or to a mixed meal in insulin-dependent diabetes mellitus

1991 ◽  
Vol 124 (5) ◽  
pp. 556-562 ◽  
Author(s):  
H. J. Gjessing ◽  
B. Reinholdt ◽  
O. K. Faber ◽  
O. Pedersen
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
C Peptide ◽  
Significant Difference ◽  
Insulin Dependent

Abstract. The dose-response relationships between prestimulatory blood glucose concentration and the plasma C-peptide responses to stimulation with 1 mg of glucagon iv or a standard mixed meal were studied in 8 C-peptide positive patients with insulin-dependent diabetes mellitus. Hyperglycemia was maintained for 90 min before stimulation using a hyperglycemic clamp technique. Each test was performed at the steady state blood glucose levels ~5, ~12, and ~20 mmol/l. The glucose potentiation of the incremental plasma C-peptide area under the curve at the two levels of hyperglycemia in percent of the area at normoglycemia (median and range) was 343% (53-1053) (p<0.05) and 341% (267-1027) (p<0.05) after glucagon and 140% (76-227) (NS) and 251% (95-1700) (p<0.05) after the meal. The corresponding relative glucose potentiation of plasma C-peptide 6 min after stimulation with glucagon was 124% (100-427) (p<0.02) and 144% (100-209) (p<0.05). There was no significant difference in the degree of glucose potentiation at ~12 or ~20 mmol/l. Furthermore, there was no significant difference in the degree of glucose potentiation of the different estimated values of B-cell function. In conclusion, the plasma C-peptide responses to iv glucagon or to a standard test meal were markedly potentiated by acute hyperglycemia in insulin-dependent diabetes mellitus. No further potentiation was, however, obtained when the prestimulatory blood glucose concentration was raised above 12 mmol/l. These findings contrast those reported in non-insulin-dependent diabetes, where endogenous insulin secretion is potentiated further when the blood glucose concentration is raised to ~20 mmol/l.

DEPARTMENT OF CORRECTIONS

1990 ◽  
Vol 12 (1) ◽  
pp. 21-21
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Children And Adolescents ◽  
Glucose Concentration ◽  
Blood Concentration ◽  
Blood Glucose Concentration ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Insulin Dependent

In the article by Ginsberg-Fellner in the February 1990 issue of Pediatrics in Review, "Insulin-Dependent Diabetes Mellitus," the blood concentration at which the kidneys excrete glucose was stated incorrectly. On page 242, the 22nd line of the section on the management of children and adolescents with diabetes should indicate that this occurs only when the blood glucose concentration is greater than 180 mg/dL.

Oral hypoglycaemics for diabetes: when and which?

1991 ◽  
Vol 29 (4) ◽  
pp. 13-16
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Regular Exercise ◽  
Control Blood Glucose ◽  
District Policy ◽  
Insulin Dependent ◽  
Market Leader

People with non-insulin-dependent diabetes mellitus should modify their diet, avoid obesity and take regular exercise. An oral hypoglycaemic drug may be needed if these measures fail to control blood glucose, but it is now clear that they commonly cause hypoglycaemia. More than 3 million prescriptions were issued in 1988 for the sulphonylureas (eight currently available) and the biguanide, metformin. Glibenclamide is the market leader (1.4 million prescriptions in 1988), followed by metformin (950,000), chlorpropamide (280,000), tolbutamide (260,000) and gliclazide (200,000). Instituting a district policy to restrict the choice of sulphonylureas can improve care and save money.1 No new oral hypoglycaemics have been marketed since we last reviewed them2 but their place in overall management has been clarified.

scholarly journals Lack of physiological suppression of circulating IGFBP-1 in puberty in patients with insulin-dependent diabetes mellitus

2002 ◽  
pp. 235-241 ◽  
Author(s):  
PH Riihimaa ◽  
M Knip ◽  
A Ruokonen ◽  
P Tapanainen
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Body Fat ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Free Insulin ◽  
Total Body Fat ◽  
Insulin Dependent ◽  
Total Body

OBJECTIVE: To evaluate the interaction between serum free insulin, insulin-like binding protein (IGFBP)-1 and leptin concentrations during puberty in insulin-dependent diabetes mellitus (IDDM). DESIGN: Adolescent patients with IDDM (n=101, age >9 years, duration >2 years) from the Outpatient Clinic of the Department of Pediatrics at Oulu University Hospital, and non-diabetic controls, were recruited to the study. Free insulin, IGFBP-1, leptin and insulin antibody concentrations were measured from a fasting serum sample. RESULTS: Free insulin concentrations were lower in the patients than in the controls (4.3+/-2.3 mU/l compared with 6.5+/-3.1 mU/l, P<0.001), and there was an inverse correlation between free insulin and fasting blood glucose in the boys with diabetes (r=-0.53, P<0.001), whereas a positive correlation was observed between free insulin and leptin concentrations in the girls with diabetes (r=0.30, P=0.020). The IGFBP-1 concentrations were greater in the patients than in the controls (16.5+/-10.6 microg/l compared with 4.0+/-3.3, P<0.001), and they correlated significantly with blood glucose (r=0.63, P<0.001) and free insulin (r=-0.35, P<0.001). No significant difference was observed in the leptin concentrations between the patients and controls overall, despite greater total body fat in the girls with diabetes compared with the control girls. CONCLUSIONS: Adolescents with IDDM are characterised by morning hypoinsulinaemia and high circulating IGFBP-1 concentrations, which may contribute to insulin resistance and impaired metabolic control during puberty. The mechanism behind the increased total body fat in the postpubertal female patients remains to be determined.

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