The Role of HMGB1 in the Pathogenesis of Type 2 Diabetes.

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Term Occurence Count Dictionary
Insulin 4 endocrinologydiseasesdrugs
diabetes mellitus 6 endocrinologydiseases
hyperglycemia 4 endocrinologydiseases
metformin 3 endocrinologydiseasesdrugs
obesity 12 endocrinologydiseases
type 1 diabetes mellitus 1 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 2440 overnutrition, metabolic balance of body is broken and becomes an origination of insulin resistance. Insulin resistance leads to compensatory increase of insulin secretion and β-cell hypertrophy. Long-term overload
Insulin 4021 and pancreatic β-cell dysfunction, resulting from an unsettled hyperglycemia condition [[2], [3]]. Insulin resistance runs through the whole process of diabetes. The liver, muscle, and adipose tissue can act
Insulin 19892 have an important role in the initiation and development of adipose tissue inflammation.5.2. HMGB1 and Insulin ResistanceInsulin resistance refers to decreased capability of insulin to promote glucose uptake. In
Insulin 19910 role in the initiation and development of adipose tissue inflammation.5.2. HMGB1 and Insulin Resistance Insulin resistance refers to decreased capability of insulin to promote glucose uptake. In simple terms, insulin
metformin 15857 by infusion of glucose in a rat model, was associated with elevated serum HMGB1 levels. In addition, metformin , a first-line antidiabetic drug, was also known to have anti-inflammatory effects. Tsoyi et al. [[89]]
metformin 15985 antidiabetic drug, was also known to have anti-inflammatory effects. Tsoyi et al. [[89]] indicated that metformin significantly decreased HMGB1 expression in LPS-treated RAW264.7 cells. Another report by Zhang et al.
metformin 16123 HMGB1 expression in LPS-treated RAW264.7 cells. Another report by Zhang et al. [[90]] demonstrated that metformin protected against hyperglycemia-induced cardiomyocyte injury by inhibiting the expression of RAGE and
Select Disease Character Offset Disease Term Instance
diabetes mellitus 544 /2016Publication date (epub): 12/2016AbstractSignificance. With an alarming increase in recent years, diabetes mellitus has become a global challenge. Despite advances in treatment of diabetes mellitus, currently, medications
diabetes mellitus 626 in recent years, diabetes mellitus has become a global challenge. Despite advances in treatment of diabetes mellitus , currently, medications available are unable to control the progression of diabetes and its complications.
diabetes mellitus 853 Growing evidence suggests that inflammation is an important pathogenic mediator in the development of diabetes mellitus . The perspectives including suggestions for new therapies involving the shift from metabolic stress
diabetes mellitus 2074 percent of the adult population suffering from diabetes in the world. More importantly, the incidence of diabetes mellitus is increasing at an alarming rate [[1]]. T2D, a metabolic disorder formed after a long and complicate
diabetes mellitus 3863 anti-inflammatory therapeutic strategies for T2D.2. Type 2 DiabetesT2D, also called non-insulin-dependent diabetes mellitus , is characterized by insulin resistance and pancreatic β-cell dysfunction, resulting from an unsettled
diabetes mellitus 27464 cells and HMGB1 might signal through TLR4 to selectively damage β cells rather than α cells in type 1 diabetes mellitus . Another study in NOD mice indicated that HMGB1 could be passively released from damaged pancreatic
hyperglycemia 3985 characterized by insulin resistance and pancreatic β-cell dysfunction, resulting from an unsettled hyperglycemia condition [[2], [3]]. Insulin resistance runs through the whole process of diabetes. The liver, muscle,
hyperglycemia 15733 and the same phenomenon was observed by Škrha et al. [[87]] Hagiwara et al. [[88]] demonstrated that hyperglycemia , induced by infusion of glucose in a rat model, was associated with elevated serum HMGB1 levels. In
hyperglycemia 16151 RAW264.7 cells. Another report by Zhang et al. [[90]] demonstrated that metformin protected against hyperglycemia -induced cardiomyocyte injury by inhibiting the expression of RAGE and HMGB1.5.1. HMGB1 and Adipose Tissue
hyperglycemia 24265 immune cell infiltration. Recent studies on human islets with T2D demonstrated that the combination of hyperglycemia and elevated FFAs induced a more efficient proinflammatory phenotype, mainly via TLR, MyD88, and interleukin-1
obesity 2787 hypoxia, and lipotoxicity, are all involved in overnutrient-induced metabolic inflammation. Importantly, obesity and obesity-associated inflammation have long been proposed to be responsible for insulin resistance
obesity 2799 lipotoxicity, are all involved in overnutrient-induced metabolic inflammation. Importantly, obesity and obesity -associated inflammation have long been proposed to be responsible for insulin resistance and T2D [[4]].T2D
obesity 3635 responses in T2D.In this review we will focus on the pathophysiological connections between HMGB1 and obesity , insulin resistance, and islet dysfunction. The understanding of the role of HMGB1 may provide a new
obesity 4376 capability and results in β cells failure [[7]].Chronic, low-grade adipose tissue inflammation links obesity and insulin resistance, thereby playing a key role in the early phase of T2D. In recent years, the role
obesity 5568 (TNF-) α, was the first inflammatory maker that was been suggested to play a role in the development of obesity -induced insulin resistance in the 1990s [[10], [11]]. In 1993, Hotamisligil et al. [[12]] demonstrated
obesity 5999 can lead to decreased insulin sensitivity. Now, there are many lines of researches illustrating that obesity and obesity-induced insulin resistance are closely linked to inflammation. Recent studies have also
obesity 6011 decreased insulin sensitivity. Now, there are many lines of researches illustrating that obesity and obesity -induced insulin resistance are closely linked to inflammation. Recent studies have also identified a
obesity 16567 tissue (such as preadipocyte, adipocyte, T cell, dendritic cell, and macrophage) has a contribution to obesity -induced inflammation and insulin resistance [[92]], macrophage is the primary source of inflammatory
obesity 18049 such as activating proinflammatory macrophages. Recently, a study among obese children showed that obesity was positively correlated with increased HMGB1 serum levels and was related to a number of proinflammatory
obesity 20724 kinase complex (IKK)β/NF-κB [[109]]. The JNK is known to play a role in regulating the development of obesity -induced insulin resistance. The activation of the JNK decreased insulin sensitivity and this related
obesity 21139 and IRS-2, a process closely related to insulin resistance. Furthermore, knockout of JNKs ameliorated obesity -induced insulin resistance [[112], [113]]. However, there was no clear evidence showing that HMGB1 was
obesity 29093 functional association among HMGB1, RAGE, and TLRs augments the inflammation in the course of T2D including obesity -induced inflammation, insulin resistance, and islet inflammation. Therefore, blockade of HMGB1 and its
type 1 diabetes mellitus 27457 β cells and HMGB1 might signal through TLR4 to selectively damage β cells rather than α cells in type 1 diabetes mellitus . Another study in NOD mice indicated that HMGB1 could be passively released from damaged pancreatic

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