β-Cell Glucose Sensitivity Is Linked to Insulin/Glucagon Bihormonal Cells in Nondiabetic Humans.

Context: Insulin resistance impacts virtually all tissues, including pancreatic β cells. Individuals with insulin resistance, but without diabetes, exhibit an increased islet size because of an elevated number of both β and α cells. Neogenesis from duct cells and transdifferentiation of α cells have been postulated to contribute to the β-cell compensatory response to insulin resistance. Objective: Our objective was to explore parameters that could potentially predict altered islet morphology. Methods: We investigated 16 nondiabetic subjects by a 2-hour hyperglycemic clamp to evaluate β-cell secretory function. We analyzed pancreas samples obtained during pancreatoduodenectomy in the same patients to examine glucagon and insulin double+ cells to assess islet morphology. Results: Among all the functional in vivo parameters of insulin secretion that were explored (basal, first phase and total secretion, glucose sensitivity, arginine-stimulated insulin secretion), β-cell glucose sensitivity was unique in exhibiting a significant correlation with both islet size and α-β double+ islet cells. Conclusions: Our data suggest that poor β-cell glucose sensitivity is linked to islet transdifferentiation, possibly from α cells to β cells, in an attempt to cope with higher demands for insulin secretion. Understanding the mechanism(s) that underlies the adaptive response of the islet cells to insulin resistance is a potential approach to design tools to enhance functional β-cell mass for diabetes therapy

METABOLIC SYNDROME IN TRANSPLANT PATIENTS: AN UPDATING POINT OF VIEW

Metabolic Syndrome is a cluster of risk factors that predispose individuals to major cardiovascular diseases and its complications, determining liver and kidney impairment. In the last decade, the indications to transplantation are increasing, with a linear incidence of the complications of the procedure. Metabolic syndrome represents one of the most common, being in turn the consequence of the underlying disease that required the transplantation, or the result of the medical treatment, as well as one of the most important factor influencing the morbidity and mortality of the transplanted patients. Due to the growing incidence of the metabolic syndrome in these patients, it is crucial to focus and clarify the leading causes determining the onset of the metabolic disarrangement, its outcome and the hypothetical mechanism through which the clinicians could reduce the impact of the disease. In fact, prevention, early recognition and treatment of the factor that could predict the onset or progression of the metabolic syndrome after the transplantation may impact long term survival of patients again, the scope of the same transplant. This review will update the different mechanisms of the pathogenesis of metabolic syndrome in this population, the clinical effects of the presence of the metabolic syndrome, observing the risk factors to be treated before and after the transplantation and suggesting the management of the follow-up

Metabolic consequences of the occlusion of the main pancreatic duct with acrylic glue after pancreaticoduodenectomy

Pancreaticoduodenectomy represents the major treatment for pancreatic and periampullary neoplasms. Complications related to pancreaticojejunostomy are still the leading cause of morbidity and mortality. A solution proposed by some surgeons is the occlusion of main pancreatic duct by acrylic glue, avoiding pancreaticojejunostomy. Nevertheless, the consequences of this procedure on glucose metabolism are not well-defined