Interorgan Crosstalk Contributing to β-Cell Dysfunction.

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Term Occurence Count Dictionary
glucose intolerance 2 endocrinologydiseases
hyperglycemia 5 endocrinologydiseases
obesity 10 endocrinologydiseases
Insulin 3 endocrinologydiseasesdrugs
diabetes mellitus 2 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 3310 both the function and mass of β-cells.2. Adipocyte to β-Cell Crosstalk Mediated by the Adipokines Insulin resistance resulting from obesity is associated with a particular milieu of circulating factors in the
Insulin 11560 operating at the molecular level, has been proposed to underlie insulin-mediated osteocalcin activation. Insulin signaling in osteoblasts facilitates osteoclastic bone resorption via the inhibition of osteoblast expression
Insulin 17559 myotube-derived cytokines (“myokines”) with different profiles depending on insulin sensitivities. Insulin -resistant muscle contributes to proinflammatory milieu associated with impaired β-cell function. Recent
Select Disease Character Offset Disease Term Instance
diabetes mellitus 381 Medicine, Ube, Yamaguchi, JapanPublication date (ppub): /2017Publication date (epub): 1/2017AbstractType 2 diabetes mellitus (T2DM) results from pancreatic β-cell failure in the setting of insulin resistance. In the early stages
diabetes mellitus 1269 interorgan communications underlying β-cell failure during the progression of T2DM.1. IntroductionType 2 diabetes mellitus (T2DM) is a complex multifactorial disorder characterized by both insulin resistance and defects in
glucose intolerance 9727 allowing it to reach target tissues and exert its endocrine functions. Mice lacking osteocalcin exhibit glucose intolerance resulting from the coexistence of impaired insulin secretion and insulin resistance [[38], [40]]. Conversely,
glucose intolerance 11350 specifically in osteoblasts exhibited a decrease in circulating levels of the active form of osteocalcin, glucose intolerance , impaired insulin secretion, and insulin resistance [[40]]. A complicated mechanism, operating at the
hyperglycemia 1807 chronically increased workload on remaining β-cells results in their failure, ultimately leading to hyperglycemia [[3]]. Based on numerous experiments in rodent models and human subjects, it is believed that the failure
hyperglycemia 6706 adipocyte-brain-bone-β cell axis). On the other hand, the leptin administration in animal models of T1DM prevents hyperglycemia and ketoacidosis without the restoration of insulin deficiency. The suppression of the glucagon actions
hyperglycemia 18860 β-Cells are capable of producing chemokines (e.g., MCP1/CCL2) in the presence of high FFA levels, and hyperglycemia forces β-cells to produce islet amyloid polypeptide (IAPP) [[35], [75]–[77]]. In response to chemokines
hyperglycemia 22621 bypass surgery such as Roux-Y gastric bypass, which provides significant weight loss and ameliorates hyperglycemia and insulin resistance. The increasing evidences of elevated postprandial GLP-1 levels after Roux-Y
hyperglycemia 26226 production of chemokines in β-cells, recruiting M1 macrophages into islets. In the diabetic milieu, hyperglycemia and IAPP derived from β-cells synergistically promote inflammatory responses through the promotion
obesity 2901 adipocytes, the skeletal system, and various immune cells, not only constitute a significant link between obesity and insulin resistance but also adversely affect β-cells by impairing their functions and limiting
obesity 3344 β-cells.2. Adipocyte to β-Cell Crosstalk Mediated by the AdipokinesInsulin resistance resulting from obesity is associated with a particular milieu of circulating factors in the plasma, any of which could signal
obesity 3994 release of FFAs, which have been shown to activate inflammatory signaling, may also be increased in obesity as a result of activated lipolysis. Although modified adipokines were initially recognized as exerting
obesity 4185 recognized as exerting effects on the hypothalamus and peripheral tissues as an important link between obesity and insulin resistance, a more detailed understanding of the interactions between these factors and
obesity 5556 documented, suggesting that leptin negatively affects β-cell mass. In the setting of high fat diet-induced obesity , however, β-cell specific loss of the leptin receptor worsened glucose tolerance, impairing both insulin
obesity 6022 increased adiposity could play a role in β-cell adaptation in the setting of high fat diet-induced obesity in mice [[20]]. However, the precise in vivo mechanisms of leptin action on β-cells have yet to be
obesity 7088 [25]].Adiponectin, another adipocyte-derived hormone, of which the circulating level correlates negatively with obesity and T2D, facilitates β-cell regeneration in mice with STZ-induced β-cell ablation [[26]]. Additionally,
obesity 17965 10 (CXCL-10) [[64], [65]] (Figure 1).7. Interplay between Immune Cells and β-CellsAs noted so far, obesity and T2DM are associated with chronic inflammation [[66]–[68]]. Islet inflammation has increasingly
obesity 18417 β-cell failure. Although inflammation can be triggered by metabolic signals, how overnutrition and obesity initiate and sustain inflammation in islets has yet to be fully characterized. In response to a glucolipotoxic
obesity 22501 licensed for the treatment of T2DM [[90]]. On the other hand, one of the options offered for extreme obesity is gastric bypass surgery such as Roux-Y gastric bypass, which provides significant weight loss and

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