Uncoupling protein-2 negatively regulates insulin secretion and is a major link between obesity, beta cell dysfunction, and type 2 diabetes.

By Chen-Yu Zhang, G. Baffy, P. Perret, S. Krauss, O. Peroni, D. Grujic, T. Hagen, Antonio Vidal-Puig, O. Boss, Young-Bum Kim and 5 more. Cell, 2001

964 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/43671c3f541ef3271185a16a2cc093fed192b8a6

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Citations in the corpus

Sirt1 Regulates Insulin Secretion by Repressing UCP2 in Pancreatic β Cells (2005, positive): “higher ATP levels in islets and increased insulin secretion upon glucose stimulation [36].”
Thermogenic mechanisms and their hormonal regulation. (2006, positive): “In addition to limiting the production of reactive oxygen species, a role that UCP3 and plant UCPs (224) may share with UCP2, UCP2 may modulate insulin secretion (55, 258) and, along with UCP3, may be important for fatty acid metabolism (reviewed in Ref.”
The mitochondrial uncoupling-protein homologues (2005, background): “In thymocytes and β-cells that are isolated from UCP2 -knockout mice, the mitochondrial membrane potential and total ATP concentration of the cell are mildly, but significantly, increase”
Mitochondrial proton and electron leaks (2010, background): “Upon observation that UCP2 ablation increased GSIS, UCP2 was implicated as a negative regulator of insulin secretion, presumably by lowering the ATP/ADP ratio [50].”
Reactive Oxygen Species in Health and Disease (2012, background): “Other emerging roles of UCP have been suggested, for example, UCP2 is thought to exert a negative regulatory effect on pancreatic insulin secretion, as well as an ROS buffering effect on hypothalamic neurons controlling eating behavior; this will be detailed later [46, 47].”
Regulation of Insulin Synthesis and Secretion and Pancreatic Beta-Cell Dysfunction in Diabetes (2012, positive): “Leptin also potently inhibits glucoincretin- or GLP-1-induced insulin secretion, which augments GSIS through activation of the cAMP signaling pathways [252, 262].”
Molecular and metabolic mechanisms of insulin resistance and β-cell failure in type 2 diabetes (2008, background): “Furthermore, UCP2 expression is increased in islets from ob/ob mice, and breeding of Ucp2 −/− mice with ob/ob mice results in the restoration of first-phase insulin secretion and normalization of blood glucose level”