Diabetic autonomic neuropathy and impaired human pancreatic polypeptide secretion in response to food.

In normal subjects, the early human pancreatic polypeptide (hPP) increase induced by food is mainly dependent on vagal activity. Parasympathetic function and plasma hPP response to a standard mixed meal were evaluated in 10 long term insulin-dependent (type I) diabetic patients (group A), 6 age-matched newly diagnosed type I diabetic patients (group B), and 8 normal subjects. The indices of vagal function (beat to beat heart rate variation during deep breathing and the Valsalva maneuver) were uniformly altered in group A, while they were in the normal range in group B, thus excluding in these latter patients the presence of vagal damage. Plasma hPP in response to standard mixed meal was measured at 5, 15, 30, 60, and 120 min. Fasting plasma hPP concentrations (determined by RIA) in groups A and B (mean +/- SEM, 113 +/- 21 and 83 +/- 21 pg/ml, respectively) did not significantly differ from normal (59 +/- 12 pg/ml). In group A, the initial meal-induced hPP increase was significantly lower than normal (5 min, 139 +/- 12; 15 min, 173 +/- 24; 30 min, 137 +/- 17 pg/ml; P less than 0.01 vs. 5 min, 412 +/- 76; 15 min, 446 +/- 57; 30 min, 325 +/- 56 pg/ml). All group B patients had a marked early increase in the peptide, similar to that in the normal subjects. These results suggest that diabetic autonomic neuropathy is associated with dysfunction of hPP secretion, and the evaluation of hPP in response to SMM may be considered a sensitive and nonstressful method for the assessment of parasympathetic impairment in diabetes.

Plasma and skeletal muscle free amino acids in type I, insulin-treated diabetic subjects.

Insulin-dependent diabetes mellitus (IDDM) induces plasma amino acid (AA) abnormalities, including low alanine and high branched-chain (BCAA). While insulin treatment restores plasma AA pattern, proline, methionine, valine, isoleucine, and total BCAA remain elevated in skeletal muscle intracellular water. This suggests that the restoration of plasma AA concentrations is not a satisfactory index of recovered AA metabolism in IDDM.

Human pancreatic polypeptide and somatostatin in chronic renal failure.

Human pancreatic polypeptide is the only hormone so far reported which clearly suppresses somatostatin release, suggesting that this peptide may have a role in controlling somatostatin secretion from the gut and pancreas. In this study endogenous high circulating human pancreatic polypeptide concentrations in patients with chronic renal failure do not decrease somatostatin circulating levels. The reduced clearance rate of somatostatin in chronic renal failure may partially account for the normal circulating levels of somatostatin observed in our patients with respect to controls. Renal insufficiency may, itself, induce an increase in some gastrointestinal peptides capable of stimulating somatostatin secretion.