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Del Prato, S., Vigili de Kreutzenberg, S., Riccio, A., Maifreni, L., Duner, E., Lisato, G., Iavicoli, M. and Tiengo, A. (1990) Partial Recovery of Insulin Secretion and Action after Combined Insulin-Sulfonylurea Treatment in Type 2 (Non-Insulin-Dependent) Diabetic Patients with Secondary Failure to Oral Agents. Diabetologia, 33, 688-695. http://dx.doi.org/10.1007/BF00400571

has been cited by the following article:

• TITLE: Progressive β Cell Failure in Type 2 Diabetes Mellitus: Microvascular Pancreatic Isletopathy?

  AUTHORS: Udaya M. Kabadi, Mary U. Kabadi, Sommany Weber, Aaron Bubolz, Edward Finnerty

  KEYWORDS: Type 2 Diabetes, Beta Cell Failure, Pancreatic Isletopathy

  JOURNAL NAME: Journal of Diabetes Mellitus, Vol.5 No.1, January 13, 2015

  ABSTRACT: Background: UKPDS suggested relentless deterioration of β cell function as a part of natural course of type 2 diabetes mellitus. However, the course was apparently not universal since many patients maintained glycemic goal (HbA1c β cell failure occurred around the same time as the time of onset of microvascular complications. Finally, the exact mechanism of progressive β cell failure remains to be defined. It is plausible that β cell failure may be due to fibrosis of pancreatic islets secondary to microangiopathy since no organ or tissue is exempt from this complication. Objective: To assess epidemiologic correlation between presence of b cell failure and microvascular complications by determining the prevalence of β cell failure in subjects with type 2 diabetes with increasing number of known microvascular complications. Methods: 650 Subjects with ages 40-75 years and duration of DM 4-23 years were divided into 4 groups according to number of microvascular complications, e.g. retinopathy, nephropathy, and neuropathy. β cell failure (β -ve ) is defined as HbA1c > 7.0% with any therapy or HbA1c β cell function is deemed “preserved” (β + ve) with HbA1c b cell failure progressively rose with increasing number of microvascular complications from 0 to 2 with no further significant rise with 3 complications whereas subjects with preserved β cell function declined with increasing number of microvascular complications (p β cell failure (p β cell failure/β cell preserved with increasing number of microvascular complications as well as the greater duration of Diabetes. However, a significantly (p β cell failure persisted for rising number of microvascular complications even after eliminating the influence of age and duration of diabetes. Conclusion: β cell failure may be a manifestation of microvascular pancreatic isletopathy similar to other microvascular complications.