Different post-pancreatectomy glucagon responses to a meal test between surgical approaches.

Residual pancreatic endocrine function is important for maintaining metabolic status after pancreatectomy and is closely related to patient nutritional status and prognosis. In contrast to insulin secretion, the significance of glucagon secretion following pancreatectomy remains unclear. In this study, we assessed the changes in pancreatic glucagon secretion during pancreatectomy to determine their pathophysiological significance. We evaluated glucagon and insulin secretion using a liquid meal tolerance test before and after pancreatectomy in patients scheduled to undergo pancreaticoduodenectomy (PD) or distal pancreatectomy (DP). After pancreatectomy, fasting plasma glucagon levels were significantly decreased in both the PD (n = 10) and DP (n = 5) groups (PD: from 18.4 to 10.5 pg/mL, p = 0.037; DP: from 21.0 to 12.1 pg/mL, p = 0.043), whereas postprandial plasma glucagon levels were not changed. In the liquid meal tolerance test after pancreatectomy, 60-min plasma glucagon levels and the area under the curve (AUC) for 0-120 min of PD were significantly higher than those for DP (60-min plasma glucagon: PD 49.0 vs. DP 21.7 pg/mL, p = 0.040; AUC0-120min: PD 4,749 vs. DP 3,564 µg min/mL, p = 0.028). Postoperative plasma glucose, serum insulin, and serum C-peptide levels during the liquid meal tolerance test were not significantly different between the two groups. Although fasting plasma glucagon levels decreased, postprandial glucagon responses were maintained after both PD and DP. The difference in residual meal-stimulated glucagon response between PD and DP suggests that a relative excess of postprandial glucagon is involved in the postoperative nutritional status after PD through its impact on systemic metabolic status.

Changes in glucagon secretion induced by food intake in fulminant type 1 diabetes mellitus: a case report.

Fulminant type 1 diabetes mellitus (FT1DM) is a subtype of type 1 diabetes mellitus and is characterized by a remarkably abrupt onset and almost complete destruction of ß-cells within a few days. Here, we report a case of diabetic ketoacidosis in a 63-year-old man with no history of hyperglycemia. The patient was diagnosed with FT1DM and had almost no insulin secretion. We examined his insulin and glucagon secretions induced by a liquid meal test at the onset of FT1DM and 1 year later. The results suggested severely attenuated insulin secretion and an undetectable level of serum insulin 1 year after onset. In contrast, glucagon secretion, which was highly impaired at onset, increased in response to food intake. Although previous reports have suggested that both ß- and α-cells of pancreatic islets are damaged in patients with FT1DM, the number of α-cells may increase over time after the onset of FT1DM.