Pancreatic Beta Cell Death: Novel Potential Mechanisms in Diabetes Therapy.

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Annotation Summary

Term Occurence Count Dictionary
Insulin 2 endocrinologydiseasesdrugs
hyperglycemia 7 endocrinologydiseases
obesity 4 endocrinologydiseases
childhood obesity 1 endocrinologydiseases
diabetes mellitus 4 endocrinologydiseases
hyperinsulinemia 1 endocrinologydiseases
metabolic syndrome 1 endocrinologydiseases
type 1 diabetes mellitus 1 endocrinologydiseases
type 2 diabetes mellitus 1 endocrinologydiseases

Graph of close proximity drug and disease terms (within 200 characters).

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Select Drug Character Offset Drug Term Instance
Insulin 2733 synthesis, storage, and secretion of insulin, a key hormone in the regulation of human metabolism [[3], [4]]. Insulin is a polypeptide hormone formed by 51 amino acids [[5]] which once bound with its receptor, mainly expressed
Insulin 26377 vital proteins for the PBC towards the cytosol [[82], [89]] (Figure 2).7. Type 2 Diabetes Mellitus: Insulin Resistance MechanismsDM2 constitutes 90–95% of the DM cases, and it is considered as an ensemble of
Select Disease Character Offset Disease Term Instance
childhood obesity 8852 [[33]], vitamin D deficiency, viral infections, limited exposure to microorganisms during childhood, and childhood obesity [[34]]. These have all been associated with the development of DM, converging in the loss of immunologic
diabetes mellitus 931 (particularly immunological) involved in the death of the pancreatic beta cell in type 1 and type 2 diabetes mellitus . Recent FindingsBeta cell death is the final event in a series of mechanisms that, up to date, have
diabetes mellitus 1151 not been entirely clarified; it represents the pathophysiological mechanism in the natural history of diabetes mellitus . These mechanisms are not limited to an apoptotic process only, which is characteristic of the immune-mediated
diabetes mellitus 1300 limited to an apoptotic process only, which is characteristic of the immune-mediated insulitis in type 1 diabetes mellitus . They also include the action of proinflammatory cytokines, the production of reactive oxygen species,
diabetes mellitus 3487 both, will lead to a cluster of metabolic alterations characterized by chronic hyperglycemia known as diabetes mellitus (DM). This can be classified according to its etiology and pathology in type 1 DM (DM1) and type 2 DM
hyperglycemia 3464 secretion, action or both, will lead to a cluster of metabolic alterations characterized by chronic hyperglycemia known as diabetes mellitus (DM). This can be classified according to its etiology and pathology in type
hyperglycemia 4430 necroptosis [[13], [14]]. In contrast with DM1, DM2 is a metabolic disease characterized by chronic hyperglycemia secondary to insulin resistance (IR). This represents a decrease in tissue response to insulin action,
hyperglycemia 26541 cases, and it is considered as an ensemble of metabolic alterations. It is characterized by chronic hyperglycemia due to the progressive loss of insulin secretion associated to the presence of IR, representing an existing
hyperglycemia 45534 to ER stress and increased levels of cleaved caspase 3, activating apoptosis [[148]].During chronic hyperglycemia , the proteolytic activity of trypsin, caspases, and chymotrypsin is affected in vivo, associated with
hyperglycemia 48178 adipocyte, inducing obesity and IR [[161], [162]]. An increase of IL-1β expression as a response to chronic hyperglycemia has been observed in PBC [[163]]. However, the common mechanism of all of these events is the generation
hyperglycemia 49913 myocardium is one of the most analyzed tissues in experimental models. As it occurs in PBC, chronic hyperglycemia appears to increase ROS production on this tissue, which then promotes NF-κB translocation to the nucleus
hyperglycemia 52861 reported that glucotoxicity and lipotoxicity affect proinflammatory cytokine profiles. PBCs exposed to hyperglycemia in vitro generate increased expression of IL-1 β, activating NF-κB pathway and FAS signaling, which
hyperinsulinemia 34975 the onset and development of diseases like DM2, its production rises as a consequence of compensatory hyperinsulinemia , characteristic of the IR state [[114]]. Eventually, the greater protein expression by the PBC leads
metabolic syndrome 26943 hepatic tissues), constituting the main pathophysiological display of several diseases such as obesity, metabolic syndrome (MS), polycystic ovarian syndrome (PCOS), among others [[90]]. Resistance to the action of these hormones
obesity 8862 D deficiency, viral infections, limited exposure to microorganisms during childhood, and childhood obesity [[34]]. These have all been associated with the development of DM, converging in the loss of immunologic
obesity 26934 and hepatic tissues), constituting the main pathophysiological display of several diseases such as obesity , metabolic syndrome (MS), polycystic ovarian syndrome (PCOS), among others [[90]]. Resistance to the
obesity 42508 pancreatic mass and a lesser glucose tolerance [[133]]. These effects seem exaggerated by stressors like obesity [[140]], which predisposes for DM and complications like diabetic nephropathy. Furthermore, autophagy
obesity 48089 inflammasome could participate in the inflammatory response mediated by macrophage in the adipocyte, inducing obesity and IR [[161], [162]]. An increase of IL-1β expression as a response to chronic hyperglycemia has been
type 1 diabetes mellitus 1293 not limited to an apoptotic process only, which is characteristic of the immune-mediated insulitis in type 1 diabetes mellitus . They also include the action of proinflammatory cytokines, the production of reactive oxygen species,
type 2 diabetes mellitus 924 mechanisms (particularly immunological) involved in the death of the pancreatic beta cell in type 1 and type 2 diabetes mellitus . Recent FindingsBeta cell death is the final event in a series of mechanisms that, up to date, have

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