INSULIN AND C-PEPTIDE RESPONSE TO A STAND ARDIZED MEAL IN NON-INSULIN-DEPENDENT DIABETICS UNDER INSULIN AND CHLOROPROPAMIDE TREATMENT

Glucose control in NIDDM is prone to progressive deterioration due to secondary failure to oral hypoglycemic therapy. Insulin may subsequent ly be required for optimal control in spite of peripheral hyperinsulin emia. In Mexico, diabetes associated with obesity is common. We theref ore designed a prospective study combining insulin and chloropropamide in order to evaluate any improvement in insulin response to a standar dized meal load and a consequent amelioration of glucose control. Meth ods. Twenty diabetic patients with secondary failure to full doses of hypoglycemic drugs and moderate hyperglycemia were recruited. Therapy was initiated with human insulin 20 IU/day and 500 mg cholopropamide, titrating insulin dosage in order to achieve euglycemia. Before treatm ent and at the end of the study period, a glucose/insulin/C peptide re sponse curve to a mixed standardized meal was performed. Blood glucose , serum lipids fructosamine and glycosylated hemoglobin levels were al so determined. All patients were followed by capillary glucose measure ments three times a week and glucose and fructosamine concentrations e very two weeks during the study period. Results. All patients required less insulin, and glucose control improved significantly. Glucose, fr uctosamine and glycosylated hemoglobin levels decreased from 262 mg/dL , 369 mmol/L and 14% to 111 mg/dL, 252 mmol/L, and 8% respectively; al l differences were statistically significant. Insulin and C peptide le vels increased significantly from 22.2 mU/mL and 1.65 ng/mL to 29.8 mU /mL and 1.97 ng/mL, respectively. When we measured the area under the curve, total values improved from 110 and 7.69 to 127 and 9.37, respec tively; this was also statistically significant. Lipids levels decreas ed significantly, including triglicerides, total and LDL cholesterol w hereas HDL cholesterol levels increased. Conclusions. Glucose control improved in our patient cohort the pancreatic insulin response probabl y due to a more adequate glycemic microenvironment and a possible enha nced exogenous and endogenous insulin function.