Role of hyperglycemia and insulin resistance in determining sodium retention in non-insulin-dependent diabetes

Role of hyperglycemia and insulin resistance in determining sodium retention in non-insulin-dependent diabetes. Sodium retention has been advocated to give rise to hypertension in humans. Increases in blood glucose and insulin concentrations ensue in the stimulation of sodium reabsorption by the kid...

Full description

Saved in:
Bibliographic Details
Published in:Kidney international 1993-07, Vol.44 (1), p.139-146
Main Authors: Nosadini, Romano, Sambataro, Maria, Thomaseth, Karl, Pacini, Giovanni, Cipollina, Maria Rita, Brocco, Enrico, Solini, Anna, Carraro, Andrea, Velussi, Mario, Frigato, Francesco, Crepaldi, Gaetano
Format: Article
Language:English
Subjects:
Adult
Biological and medical sciences
Blood Glucose - metabolism
Diabetes Mellitus, Type 2 - metabolism
Diabetes. Impaired glucose tolerance
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Female
Humans
Hyperglycemia - metabolism
Insulin - blood
Insulin Resistance - physiology
Male
Medical sciences
Middle Aged
Natriuresis - physiology
Sodium - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Role of hyperglycemia and insulin resistance in determining sodium retention in non-insulin-dependent diabetes. Sodium retention has been advocated to give rise to hypertension in humans. Increases in blood glucose and insulin concentrations ensue in the stimulation of sodium reabsorption by the kidney. Although the combined occurrence of hyperglycemia and hyperinsulinemia, frequently secondary to insulin resistance with regard to carbohydrate metabolism, is a hallmark of non-insulin dependent diabetes (NIDDM), the role of these abnormalities in determining an impaired natriuresis in NIDDM is not yet fully understood. We studied sodium homeostasis in 14 control subjects and 59 NIDDM normotensive, normoalbuminuric patients who were divided into two groups with markedly impaired (Group 2 NIDDM: 30) and less severely impaired (Group 1 NIDDM: 29) insulin sensitivity during euglycemic-hyperinsulinemic (80 to 90 µU/ml plasma insulin) clamp. A hyperglycemic (9 mmol/liter plasma glucose)—nearly euinsulinemic (20 to 40 µU/ml plasma insulin) clamp was also performed in the same 14 controls and in two cohorts of 22 Group 2 and 17 Group 1 NIDDM patients. The two groups of patients had similar overnight fasting glucose levels (Group 1 NIDDM vs. Group 2 NIDDM: 176 ± 13 vs. 185 ± 15 mg/dl, mean ± SE). Conversely, overnight fasting plasma insulin was significantly higher in Group 2 NIDDM than in Group 1 NIDDM patients (Group 1 NIDDM vs. Group 2 NIDDM: 12 ± 3 vs. 18 ± 3 µU/ml, P < 0.05). Both NIDDM Groups had higher plasma glucose and insulin than controls (75 ± 4 mg/dl and 6 ± 3 µU/ml). Blood pressure levels and albumin excretion rates were slightly but significantly higher in Group 2 NIDDM, but not in Group 1 NIDDM patients, than in controls. Insulin administration during the euglycemic-hyperinsulinemic clamp decreased in a similar manner the sodium excretion rate in controls and in both NIDDM groups. Conversely, the sodium excretion rate was always significantly lower in Group 2 than in Group 1 NIDDM patients and in controls during the hyperglycemic, near euinsulinemic clamp (euglycemia and hyperglycemia; Controls vs. Group 1 vs. Group 2: 156 ± 14 and 123 ± 15 vs. 138 ± 17 and 111 ± 10, NS; vs. 101 ± 8 and 74 ± 9, P < 0.01 vs. both, µmol · min-1 · 1.73 m-2). The sodium excretion rate was lower during hyperglycemia than euglycemia both in controls and NIDDM patients. An inverse relationship was observed between daily sodium excretion rate and glucose filtered load in bot
ISSN:0085-2538
1523-1755
DOI:10.1038/ki.1993.224