-transparent.png){kind=logo}
OBJECTIVE In eight glucokinase (GCK)-deficient subjects, we have investigated insulin secretion rates (ISRs) in response to intravenous arginine. Impairment in the enzymatic activity of mutant GCK leads to a reduced glycolytic flux in beta-cells. This defect translates in vivo as a right shift in the glucose/SR dose-response curve. Insulin secretion in response to other secretagogues has not been reported. METHODS The arginine test was performed immediately after a 2-h hyperglycemic (10 mM) clamp. ISR was computed by deconvolution of peripheral C-peptide levels. Linear regression analyses were performed to assess correlations between the beta-cell secretory responses to the arginine test, an intravenous glucose tolerance test (IVGTT), and a hyperglycemic clamp (areas under the C-peptide curves), and between these parameters and the glucose tolerance status (area under the glucose curve during an oral glucose tolerance test). RESULTS Two minutes after the injection of arginine, the increment in ISR was 30.17 +/- 10.01 pmol insulin.kg-1.min-1 in patients and 36.25 +/- 15.46 pmol insulin.kg-1.min-1 in control subjects (P = 0.38). Throughout the experiment, increments in ISR were comparable in both groups. The amount of insulin secreted in response to arginine (0-5 min) was similar in patients and control subjects: 81 +/- 28 vs. 119 +/- 55 pmol/kg (P = 0.16), respectively. The arginine test C-peptide response was not correlated with the IVGTT or hyperglycemic clamp responses. The arginine test and hyperglycemic clamp responses were not correlated to the glucose tolerance status. The best predictor of the glucose tolerance was the C-peptide response to the IVGTT (r2 = 0.78; P = 0.002). CONCLUSIONS beta-cell secretory increment in response to arginine was found to be in the normal range in GCK-deficient subjects. The arginine test does not seem to reflect either the beta-cell secretory defect or the glucose tolerance status of these subjects. IVGTT seems to be the best predictor of the latter parameter in this population.
M E Pueyo, and
K Clement, and
M Vaxillaire, and
P Passa, and
P Froguel, and
J J Robert, and
G Velho
January 1996,
Diabetologia,
M E Pueyo, and
K Clement, and
M Vaxillaire, and
P Passa, and
P Froguel, and
J J Robert, and
G Velho
December 1994,
Diabetes,
M E Pueyo, and
K Clement, and
M Vaxillaire, and
P Passa, and
P Froguel, and
J J Robert, and
G Velho
April 1992,
Diabetologia,
M E Pueyo, and
K Clement, and
M Vaxillaire, and
P Passa, and
P Froguel, and
J J Robert, and
G Velho
September 1996,
Diabetic medicine : a journal of the British Diabetic Association,
M E Pueyo, and
K Clement, and
M Vaxillaire, and
P Passa, and
P Froguel, and
J J Robert, and
G Velho
July 1990,
Endocrinology,
M E Pueyo, and
K Clement, and
M Vaxillaire, and
P Passa, and
P Froguel, and
J J Robert, and
G Velho
January 1978,
Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme,
M E Pueyo, and
K Clement, and
M Vaxillaire, and
P Passa, and
P Froguel, and
J J Robert, and
G Velho
April 1999,
Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas,
M E Pueyo, and
K Clement, and
M Vaxillaire, and
P Passa, and
P Froguel, and
J J Robert, and
G Velho
October 1996,
The Journal of clinical investigation,
M E Pueyo, and
K Clement, and
M Vaxillaire, and
P Passa, and
P Froguel, and
J J Robert, and
G Velho
December 1988,
Cardiovascular drugs and therapy,
M E Pueyo, and
K Clement, and
M Vaxillaire, and
P Passa, and
P Froguel, and
J J Robert, and
G Velho
June 1971,
Metabolism: clinical and experimental,
