Insulin action in subjects with type 2 diabetes following biliopancreatic diversion

Author(s):  
Francesco Papadia ◽  
Flavia Carlini ◽  
Alice Rubartelli ◽  
Micaela Battistini ◽  
Renzo Cordera ◽  
...  
Diabetes ◽  
2013 ◽  
Vol 62 (8) ◽  
pp. 2978-2983 ◽  
Author(s):  
Anna Jonsson ◽  
Claes Ladenvall ◽  
Tarunveer Singh Ahluwalia ◽  
Jasmina Kravic ◽  
Ulrika Krus ◽  
...  

2009 ◽  
Vol 204 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Yi Lin ◽  
Zhongjie Sun

Type 2 diabetes mellitus (T2DM) affects a large population worldwide. T2DM is a complex heterogeneous group of metabolic disorders including hyperglycemia and impaired insulin action and/or insulin secretion. T2DM causes dysfunctions in multiple organs or tissues. Current theories of T2DM include a defect in insulin-mediated glucose uptake in muscle, a dysfunction of the pancreatic β-cells, a disruption of secretory function of adipocytes, and an impaired insulin action in liver. The etiology of human T2DM is multifactorial, with genetic background and physical inactivity as two critical components. The pathogenesis of T2DM is not fully understood. Animal models of T2DM have been proved to be useful to study the pathogenesis of, and to find a new therapy for, the disease. Although different animal models share similar characteristics, each mimics a specific aspect of genetic, endocrine, metabolic, and morphologic changes that occur in human T2DM. The purpose of this review is to provide the recent progress and current theories in T2DM and to summarize animal models for studying the pathogenesis of the disease.


1999 ◽  
Vol 58 (3) ◽  
pp. 647-653 ◽  
Author(s):  
Mark J. Holness

The goal of this review is to develop the hypothesis, and review the evidence, that protein restriction, through synergistic effects on multiple organ systems predisposes to loss of normal regulation of fuel homeostasis that plays the central role in the development of type 2 (non-insulin-dependent) diabetes mellitus. The ability of insulin to regulate glucose production and disposal varies between individuals. These differences, together with the various compensatory mechanisms that are invoked to attempt to normalize fuel homeostasis, are of fundamental importance in the development and clinical course of type 2 diabetes mellitus. Protein deprivation impacts on both insulin secretion and insulin action. These effects may persist even when a diet containing adequate protein is presented subsequently. Data are presented that suggest that protein restriction results in an impaired ability of pancreatic β-cells to compensate adequately for the defect in insulin action in insulin-resistant individuals. This persistent impairment of insulin secretion resulting from protein restriction predisposes to loss of glucoregulatory control and impaired insulin action after the subsequent imposition of a diabetogenic challenge. This inability to maintain the degree of compensatory hyperinsulinaemia necessary to prevent loss of glucose tolerance may have relevance to the increased incidence of diabetes on changing from a nutritionally-poor diet to a Western diet, and to the hypothesis that some cases of type 2 diabetes in adulthood may be related to poor early nutrition.


2016 ◽  
Vol 26 (10) ◽  
pp. 2442-2448 ◽  
Author(s):  
Gian Franco Adami ◽  
Raffaella Gradaschi ◽  
Gabriella Andraghetti ◽  
Nicola Scopinaro ◽  
Renzo Cordera

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