Beta Cell Function in Long Term NIDDM (Type 2) Patients and its Relation to Treatment

Abstract

Pancreatic beta cell function was assessed by estimation of fasting and post prandial plasma C-peptide in 183 non-insulin dependent diabetic patients, who were treated with oral hypoglycaemic drugs, for more than 10 years. One-hundred-and-forty-one patients, continued to respond to oral hypoglycaemic agents (Group I) and in 42 the control was not satisfactory and had to be changed over to insulin (secondary failure, Group II). Significant beta cell reserve (PP CP greater than or equal to 0.6 pmol/ml) was present in 89 out of 183 patients (48%) and 83 (93%) of them responded to oral hypoglycaemic agents. Among the 94 patients with low beta cell reserve, 58 (62%) were on oral hypoglycaemic agents and the other 36 (38%) were on insulin. Of the 42 patients with secondary failure to the oral drugs, 36 (86%) had low C-peptide while 6 (14%) had significant C-peptide values. Secondary failure to oral hypoglycaemic agents can also occur in spite of good beta cell reserve. Beta cell reserve was not correlated either to the duration of diabetes or the age at diagnosis of the patients.

Residual B Cell Function in Patients with Long-Standing NIDDM and its Relation to Metabolic Control and Diabetic Complications.

“…Serum C-peptide response to glucagon in patients treated with sulfonylurea or insulin in the present study was substantially the same as the reported values (Matsuda et al, 1985) and it was suggested that the residual B cell function was not lowered in long-standing NIDDM, being consistent with previous studies (Lev-Ran et al, 1986;Snehalatha et al, 1986). Some reports on IDDM indicated that the more active the residual B cell function, the better the metabolic control (Gonen et al, 1979;Clarson et al, 1987;Sjoberg et al, 1987).…”

The Beta Cell Function in NIDDM Patients with Secondary Failure:

“…Groop et al (1986) classified these patients as pseudo-type II/or latent type I; this suggests that many of these patients were IDDM. In a study of 183 NIDDM patients treated with OHAs for more than 10 years, Snehalatha, Ramachandran, Mohan, Timothy and Viswanathan (1986) found no evidence of beta-cell exhaustion. Gutniak, Karlander and Efendic (1987) observed that in OHA failure patients, insulin increased beta-cell response and thus reactivated beta-cell sensitivity to OHA treatment.…”