Glucose intolerance in uremic patients: the relative contributions of impaired beta-cell function and insulin resistance.

A Alvestrand, M Mujagic, A Wajngot, S Efendic - Clinical nephrology, 1989 - europepmc.org
A Alvestrand, M Mujagic, A Wajngot, S Efendic
Clinical nephrology, 1989europepmc.org
Glucose tolerance and tissue sensitivity to insulin were examined in 19 renal failure patients
on chronic regular hemodialysis (group U) and in 6 matched control subjects with normal
renal function (group A). Based on glucose tolerance as assessed by an oral glucose
tolerance test (OGTT), glucose tolerance was normal in 5 (group U: N), borderline in 5
(group U: BL) and decreased in 9 uremic subjects (group U: D). Compared with group A the
uremics demonstrated significantly (p less than 0.01) impaired insulin sensitivity as …
Glucose tolerance and tissue sensitivity to insulin were examined in 19 renal failure patients on chronic regular hemodialysis (group U) and in 6 matched control subjects with normal renal function (group A). Based on glucose tolerance as assessed by an oral glucose tolerance test (OGTT), glucose tolerance was normal in 5 (group U: N), borderline in 5 (group U: BL) and decreased in 9 uremic subjects (group U: D). Compared with group A the uremics demonstrated significantly (p less than 0.01) impaired insulin sensitivity as assessed by a continuous mixed infusion of somatostatin, insulin and glucose (SIGIT). In addition 19 non-diabetic subjects with normal fasting blood glucose and normal renal function, matching the uremic patients with respect to glucose tolerance as assessed by OGTT, were studied (group B). In group B impairments in both insulin secretion and insulin sensitivity tended to be more pronounced in subjects with decreased OGTT as compared with those with borderline OGTT. In contrast, insulin resistance was present to a similar degree in uremic subjects of group U: N, U: BL and U: D. During SIGIT endogenous insulin, glucagon and growth hormone (GH) were suppressed in both uremic and control subjects. This implies that insulin resistance in uremia is most likely not due to hyperglucagonemia or abnormal GH metabolism. During OGTT subjects of group U: N had significantly higher insulin response than subjects of group U: BL (p less than 0.02) and group U: D (p less than 0.01). Insulinogenic index was significantly higher in group U: N than in group U: BL (p less than 0.02) and group U: D (p= 0.01) and was higher in group U: BL than in group U: D (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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