Beta-cell deficit and increased beta-cell apoptosis in humans with type 2 diabetes.

By A. Butler, J. Janson, S. Bonner-Weir, R. Ritzel, Robert A. Rizza, P. Butler. Diabetes, 2003

2,025 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/0d1154fcef96951a829f4d631d7d6da19a5363c4

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Citations in the corpus

Glucagon-like peptide 1 (GLP-1) (2019, background): “The replication rate of human bcells is greatest in young childhood and puberty but declines with increasing age [526,531,533,536].”
Beta Cell Dysfunction and Insulin Resistance (2013, background): “In human adult beta cells, replication is estimated at 10-fold less than in adult mice (Butler et al., 2003, 2007) with the most replication in <5 year old children (Meier et al., 2008).”
Regulation of Insulin Synthesis and Secretion and Pancreatic Beta-Cell Dysfunction in Diabetes (2012, unknown): “Obese non-diabetic humans show increased relative β-cell volume in islets while obese and non-obese patients with impaired fasting glucose and T2D show at least a 40 % reduction in β-cell volume compared with respective non-diabetic patients [404].”
Role of incretin hormones in the regulation of insulin secretion in diabetic and nondiabetic humans. (2004, background): “Given that the extent of adaptive changes in the -cell mass in humans is much lower than that observed in, for example, mice (5), it seems likely that such changes will be much more difficult to demonstrate, or that therapy must be maintained for a long time, before significant effects might be appa”
Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol (2011, background): “The underlying changes in beta cell function have been well described [3, 4], and beta-cell mass decreases steadily during the course of type 2 diabetes [5, 6].”
The Pathophysiology of Gestational Diabetes Mellitus (2018, background): “Pancreatic samples from T2DM patients can show a reduction of β-cell mass by 40–60% [81], but less than 24% loss after five years of disease has also been reported [82].”
The physiology of glucagon-like peptide 1. (2007, background): “However, in a subsequent reanalysis of the pancreatic sections on which this hypothesis was based, the existence of nesidioblastosis could not be confirmed (179), and the most likely explanation for the hypoglycemic attacks is probably exaggerated GLP-1-stimulated insulin secretion in combination wi”
β-Cell Replication Is the Primary Mechanism Subserving the Postnatal Expansion of β-Cell Mass in Humans (2008, methodology): “The ratio of the -cell area/exocrine area was digitally quantified as previously described (8) using Image Pro Plus software.”
CONSENSUS STATEMENT BY THE AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND AMERICAN COLLEGE OF ENDOCRINOLOGY ON THE COMPREHENSIVE TYPE 2 DIABETES MANAGEMENT ALGORITHM--2016 EXECUTIVE SUMMARY. (2016, background): “It is now clear that the progressive pancreatic beta-cell defect that drives the deterioration of metabolic control over time begins early and may be present before the diagnosis of diabetes (1).”
Endoplasmic reticulum stress contributes to beta cell apoptosis in type 2 diabetes (2007, background): “This not only supports the presence of ER stress but also provides a potential mechanistic explanation for the apoptosis that appears to underlie the reductions in beta cell mass that contribute to type 2 diabetes in humans [2].”
RNA Sequencing of Single Human Islet Cells Reveals Type 2 Diabetes Genes. (2016, background): “This is of interest since reduced b cell mass in patients with T2D contributes to onset and progression of the disease (Butler et al., 2003; Rahier et al., 2008).”
Autophagy is important in islet homeostasis and compensatory increase of beta cell mass in response to high-fat diet. (2008, unknown): “Recent studies have shown that progressively decreased pancreatic b cell function and b cell mass are common features of subjects with type 2 diabetes mellitus (Butler et al., 2003; Rhodes, 2005).”
Thioredoxin-interacting protein mediates ER stress-induced β cell death through initiation of the inflammasome (2012, background): “In contrast, type 2 diabetes is a state of relative insulin deficiency as a result of b cell dysfunction and death caused by a combination of increased circulating glucose and saturated fatty acids and development of inflammation (Butler et al., 2003; Donath and Halban, 2004).”
Why Does Obesity Cause Diabetes? (2022, background): “Greaterweight losscanachieve diabetes remission, but the rate of remission depends primarily on the duration of diabetes, the ability of weight loss to improve b cell function, and the criteria used to define remission (Camastra et al., 2011; Taylor et al., 2018).”