Minireview: Secondary β-Cell Failure in Type 2 Diabetes-A Convergence of Glucotoxicity and Lipotoxicity.

By Vincent Poitout, R. Robertson. Endocrinology, 2002

706 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/531a3a8c7087583a2a14dfc1dff6988056b44b8e

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Citations in the corpus

Endothelial Dysfunction and Diabetes: Effects on Angiogenesis, Vascular Remodeling, and Wound Healing (2012, background): “ROS causes loss of insulin type 1 diabetes by destructing the β cells but it causes insulin resistance in type 2 diabetes by β cell dysfunction of [49, 55, 56].”
The role of FoxO in the regulation of metabolism (2008, background): “Both glucotoxicity and lipotoxicity increase the level of reactive oxygen species in beta cells (Poitout and Robertson, 2002; Robertson et al., 2004).”
The mitochondrial uncoupling-protein homologues (2005, result): “Such a proposition might seem to be in conflict with other studies that show that oxidative stress causes β-cell dysfunction, increased apoptosis and consequent loss of β-cell mass (see Ref”
Oxidative stress and stress-activated signaling pathways: a unifying hypothesis of type 2 diabetes. (2002, background): “Data from Poitout, Robertson, and colleagues (355, 386, 387) have indicated that -cell lipotoxicity is an amplifying effect that is manifested only in the context of concurrent hyperglycemia.”
The role for endoplasmic reticulum stress in diabetes mellitus. (2008, background): “The loss of -cell mass in type 2 diabetes may be due to chronic exposure to high glucose and free fatty acid (FFA) levels (gluco- and lipotoxicity) (5, 23, 24).”
beta-cell failure in diabetes and preservation by clinical treatment. (2007, background): “␤-Cell exhaustion, according to Robertson et al. (47), refers to a physical depletion of ␤-cell insulin stores secondary to prolonged chronic stimulation with glucose or nonglucose secretagogues, so that insulin secretion is not possible, even if the ␤-cell were to become resensitized to glucose.”
Molecular and metabolic mechanisms of insulin resistance and β-cell failure in type 2 diabetes (2008, background): “Similarly, exposure of islets to elevated levels of fatty acids does not impair GSIS unless the islets are cultured at or above a threshold concentration of glucose (usually ∼8 mM”