2022
DOI: 10.1093/jmcb/mjac046
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β-cell dynamics in type 2 diabetes and in dietary and exercise interventions

Abstract: Pancreatic β-cell dysfunction and insulin resistance are two of the major causes of type 2 diabetes (T2D). Recent clinical and experimental studies have suggested that the functional capacity of β-cells, particularly in the first phase of insulin secretion, is a primary contributor to the progression of T2D and its associated complications. Pancreatic β-cells undergo dynamic compensation and decompensation processes during the development of T2D, in which metabolic stresses such as endoplasmic reticulum (ER) s… Show more

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Cited by 20 publications
(17 citation statements)
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“…In pre-diabetes, blood glucose can still be maintained at normal levels due to the compensatory response of the beta cells [ 62 ]. As oxidative stress and inflammatory responses proceed in later stages, the compensatory mechanisms of the beta cells are continuously compromised, eventually leading to the development of type 2 diabetes [ 63 ].…”
Section: Hfd-induced Diabetes In Animal Models and Humansmentioning
confidence: 99%
“…In pre-diabetes, blood glucose can still be maintained at normal levels due to the compensatory response of the beta cells [ 62 ]. As oxidative stress and inflammatory responses proceed in later stages, the compensatory mechanisms of the beta cells are continuously compromised, eventually leading to the development of type 2 diabetes [ 63 ].…”
Section: Hfd-induced Diabetes In Animal Models and Humansmentioning
confidence: 99%
“…Type 2 diabetes (T2D) is a complex and chronic disease that affects the quality of life of patients and the incidence of other diseases [9]. The VDR gene is expressed in pancreatic cells and disrupting its signaling pathway may affect insulin secretion [10,11]. Previous studies provide evidence of the association of VDR polymorphisms as potential genetic factors that may increase the risk of developing T2D.…”
Section: Recent Findingsmentioning
confidence: 99%
“…IF, by reducing cellular glucose flux, decreases adenosine triphosphate (ATP) intracellular levels and increases adenosine monophosphate (AMP). The increase in AMP activates Adenosine monophosphate kinase (AMPK), a sensor of lower energy levels, that also activates PPARG Coactivator 1-α (PGC1-α), stimulating mitochondrial biogenesis and function 11,12 . Enhanced redox homeostasis helps to neutralize ROS, which prevents oxidative stress, cell dysfunction and, chronically, cell death 13 .…”
Section: Introductionmentioning
confidence: 99%