scholarly journals B-cell function and blood glucose control in insulin dependent diabetics within the first month of insulin treatment

Diabetologia ◽  
1977 ◽  
Vol 13 (3) ◽  
pp. 263-268 ◽  
Author(s):  
O. K. Faber ◽  
C. Binder
Diabetologia ◽  
1981 ◽  
Vol 20 (5) ◽  
Author(s):  
S. Madsbad ◽  
T. Krarup ◽  
L. Regeur ◽  
O.K. Faber ◽  
C. Binder

1984 ◽  
Vol 105 (2) ◽  
pp. 221-225 ◽  
Author(s):  
Thure Krarup ◽  
Sten Madsbad ◽  
Lisbeth Regeur ◽  
Ole K. Faber ◽  
Bente Tronier

Abstract. The effect of strict glycaemic control on plasma immunoreactive gastric inhibitory polypeptide IR-GIP) concentrations and pancreatic B cell function as estimated by plasma C-peptide was evaluated in 14 Type 1 (insulin-dependent) diabetics. The effect was estimated by giving a test meal before (test 1) and after (test 2) 1 week with near normal blood glucose control (mean blood glucose 6.7 ± 0.2 mmol/l) and again 3 weeks later (test 3) in the outpatient clinic. The glycaemic control was significantly improved at test 2 and test 3 compared with that of test 1. The IR-GIP concentrations before and after the meals were similar at all three tests and not different from those found in 21 normal controls. In 8 patients with a significant B cell response at test 1, B cell function was significantly improved both at test 2 and test 3 but no change in fasting or post-prandial IR-GIP concentrations was found and no correlation between B cell function and IR-GIP existed. We conclude that strict glycaemic control improves B cell function but does not modulate plasma IR-GIP concentrations. Factors other than GIP seem to be of greater importance in determining the magnitude of B cell function in Type 1 diabetes.


1988 ◽  
Vol 118 (3) ◽  
pp. 365-373 ◽  
Author(s):  
Benjamin Glaser ◽  
Gil Leibovich ◽  
Rafael Nesher ◽  
Svend Hartling ◽  
Christian Binder ◽  
...  

Abstract. In Type II, non-insulin-dependent diabetes, insulin secretion is often reduced to the point where oral hypoglycaemic agents fail to control the plasma glucose level. We studied 12 patients (age 41–66 years; 4 lean, 8 obese) with Type II diabetes mellitus for 1–25 years who were uncontrolled despite maximal dose glibenclamide and metformin. After withdrawal of medication, blood glucose control was determined by measuring glucose before and 2 h after each meal for 48 h, and beta-cell function by insulin or C-peptide response to glucagon and to iv glucose. Following these tests, intensive insulin treatment (CSII) was initiated, and near-euglycaemia (mean of 7 daily glucose determinations < 7.7 mmol/l) was maintained for 16.6 ± 1.5 days, at which time the tests were repeated. Mean daily insulin requirement was 61 ± 9 IU (0.81 ± 0.09 IU/kg). Glucose control was improved after cessation of CSII (mean glucose 12.7 ± 0.6 mmol/l after vs 20 ± 1.5 mmol/l before, P <0.005). Maximum incremental C-peptide response improved both to glucagon (214 ± 32 after vs 134 ± 48 pmol/l before, P = 0.05) and to glucose iv bolus injection (284 ± 53 vs 113 ± 32 pmol/l, P < 0.05). Peak insulin response, measured after iv glucose infusion, also tended to be higher in the post-CSII test (42 ± 18 vs 22 ± 5.6 mU/l). Basal and stimulated proinsulin concentrations were high relative to C-peptide levels during the pre-treatment period, but returned to normal after CSII. Thus: 1) adequate blood glucose control could be obtained in most of our patients using moderate doses of insulin even in those who were obese; 2) short-term euglycaemia resulted in improved insulin response to both glucagon and glucose, and reduction of the relative proinsulin secretion; 3) although beta-cell function improved in most patients, only 6 could be adequately controlled with oral agents after hospital discharge. In those patients who do not respond well to conventional treatment, CSII is an attractive alternative.


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