Similar defects ID'd for T2DM, chronic pancreatitis and diabetes

(HealthDay)—Patients with type 2 diabetes and those with diabetes secondary to chronic pancreatitis have similarly impaired α-cell responses to oral glucose ingestion and hypoglycemia, according to a study published online July 27 in Diabetes Care.

Lena Mumme, from St. Josef Hospital in Bochum, Germany, and colleagues compared 10 patients with diabetes secondary to chronic pancreatitis with 13 patients with type 2 diabetes and 10 healthy controls. Participants underwent stepwise hypoglycemic clamp and an oral glucose tolerance test (OGTT).

The researchers found that patients with diabetes and chronic pancreatitis had higher glucose levels during the OGTT, while levels were lower in controls (P < 0.0001). In both groups with diabetes, insulin and C-peptide levels were reduced, and glucose-induced suppression of glucagon was impaired (all P < 0.0001 versus controls). In patients with chronic pancreatitis and with type 2 diabetes, glucagon concentrations were reduced during hypoglycemia (P < 0.05). There was an inverse relationship between the increase in glucagon during the clamp and the glucose-induced glucagon suppression, and a positive relationship with β-cell function. In patients with type 2 diabetes, but not those with chronic pancreatitis, growth hormone responses to hypoglycemia were lower (P = 0.0002).

"α-cell responses to oral glucose ingestion and to hypoglycemia are disturbed in patients with diabetes and chronic pancreatitis and in patients with type 2 diabetes," the authors write. "The similarities between these defects suggest a common etiology."

Several authors disclosed financial ties to the pharmaceutical industry.

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