Dietary Flavonoids in the Prevention of T2D: An Overview.

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Term Occurence Count Dictionary
hyperglycemia 14 endocrinologydiseases
hyperinsulinemia 1 endocrinologydiseases
hypoglycemia 2 endocrinologydiseases
metabolic syndrome 1 endocrinologydiseases
obesity 14 endocrinologydiseases
Insulin 4 endocrinologydiseasesdrugs
acarbose 1 endocrinologydiseasesdrugs
dexamethasone 1 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
Insulin 8753 precursors such as amino acids and glycerol, pathways that are blocked in the presence of insulin [[47]]. Insulin acts on target tissues such as muscle, liver, and adipose tissues [[9]]. It binds to its plasma membrane
Insulin 15293 evidence suggesting that such hepatic metabolic abnormalities in T2D are caused primarily by IR [[94]]. Insulin is involved in the direct and indirect suppression of hepatic glucose production, which is impaired
Insulin 25971 upregulated hepatic IRS-2 expression independent of adiponectin known receptors [[157]]. 2.2. Impaired Insulin Secretion and Development of T2DIt is well known that T2D is characterized by impaired insulin secretion
Insulin 46096 transporter in both skeletal muscle and adipose tissue, is primarily regulated by insulin [[286]]. Insulin stimulation of glucose entry into cells is executed via inducing the translocation of GLUT4 to the plasma
acarbose 42931 from raspberry and rowanberry inhibited α-amylase activity and acted synergistically with the drug acarbose to inhibit α-amylase activity in vitro [[275]]. Also, anthocyanins-rich extract from raspberry, blueberry,
dexamethasone 48104 increasing GLUT4 membrane translocation in L6 myotubes. In addition, treatment with EGCG inhibited dexamethasone -induced IR via activating AMPK and Akt [[296]]. Similarly, the isoflavone genistein stimulated glucose
Select Disease Character Offset Disease Term Instance
hyperglycemia 2111 2007 and 2012 [[4]]. Type 2 diabetes (T2D) is a progressive metabolic disorder with a characteristic hyperglycemia accompanied by abnormalities in carbohydrate [[5]], lipid [[6]], and protein metabolism [[7]]. The cascade
hyperglycemia 2742 β-cell failure plays a central role in the development T2D. There is a strong evidence suggesting that hyperglycemia plays a major role in the pathogenesis of diabetic complications that affects various organs in the
hyperglycemia 3049 reactive oxygen species (ROS) production that will impair cell function and survival [[14]]. Moreover, hyperglycemia , in turn, aggravates IR, thereby forming a vicious circle [[15]]. Improved glucose control was shown
hyperglycemia 9381 gluconeogenesis and glycogenolysis, which make a significant contribution to fasting and postprandial hyperglycemia , the hallmarks of T2D [[50],[51],[52]]. Likewise, IR may impair the function of the kidneys [[53]],
hyperglycemia 9538 Likewise, IR may impair the function of the kidneys [[53]], thereby contributing to the development of hyperglycemia in T2D, as kidneys also play a role in regulating glucose homeostasis [[54]]. In normal subjects, kidneys
hyperglycemia 10266 that the increased activity of glucose transporters in kidneys might make substantial contribution to hyperglycemia in T2D [[61]].2.1. IR and T2DThe underlying mechanisms that lead to the development of IR are still
hyperglycemia 16111 hepatic glucose production through gluconeogenesis and glycogenolysis, thereby contributing to fasting hyperglycemia [[50],[51],[52]]. Increased hepatic gluconeogenesis, in particular, is considered one of the early pathological
hyperglycemia 16631 In one report, gene expression of PEPCK and G6Pase was not changed nor was associated with fasting hyperglycemia in T2D subjects [[103]]. However, morbidly obese patients with T2D had an increase in hepatic glucose
hyperglycemia 20169 IRS and subsequently its initiated signaling, thereby leading to the development of hepatic IR and hyperglycemia [[111],[115]]. The accumulation of lipids in the liver and the promotion of fatty acid oxidation may
hyperglycemia 23760 robustly elevated in obesity [[139]]. In T2D individuals, IL-6 was independently associated with IR and hyperglycemia [[140]]. It can induce hepatic production of the inflammatory marker C-reactive protein (CRP) [[141]],
hyperglycemia 43430 obese and hyperglycemic mice delayed carbohydrate absorption and subsequently ameliorated postprandial hyperglycemia at least partially through inhibiting intestinal α-glucosidase activity [[277]]. However, in clinical
hyperglycemia 45747 subjects are needed.4.1.3. Effects of Flavonoids on Glucose DisposalAnother approach to preventing IR, hyperglycemia , T2D, and subsequent diabetic complications is to enhance glucose uptake by peripheral tissues. Various
hyperglycemia 49562 administration of naringin, a bioflavonoid from grapefruit, ameliorated dyslipidemia, hyperinsulinemia, hyperglycemia , hepatic steatosis, and IR in T2D rats, which were associated with reduced oxidative stress, upregulated
hyperglycemia 52564 diabetes have been extensively studied [[320],[321]]. Dietary supplementation of genistein improved hyperglycemia , glucose tolerance, and blood insulin levels in various diabetic mouse models, including non-obese diabetic
hyperinsulinemia 49544 [[301]]. Oral administration of naringin, a bioflavonoid from grapefruit, ameliorated dyslipidemia, hyperinsulinemia , hyperglycemia, hepatic steatosis, and IR in T2D rats, which were associated with reduced oxidative
hypoglycemia 17437 transcription of genes encoding PEPCK and G6Pase [[106]]. Liver-specific FoxO1 knockout mice displayed fasting hypoglycemia associated with reduced expression of gluconeogenic genes [[107]]. In addition, FoxO3 and FoxO4 enhance
hypoglycemia 18529 blood glucose levels, whereas FoxO6 deletion in the liver reduced gluconeogenesis, resulting in fasting hypoglycemia . However, unlike FoxO1, the transcriptional activity of FoxO6 is largely inhibited by insulin through
metabolic syndrome 10645 investigating IR is the accompanying metabolic abnormalities referred to as IR syndrome (IRS), or more commonly metabolic syndrome (MetS) [[63]], which also increases the risk of developing T2D [[64]]. Elevated plasma free fatty acids
obesity 10791 increases the risk of developing T2D [[64]]. Elevated plasma free fatty acids (FFAs) associated with obesity [[65]] or independent of obesity, i.e., consumption of a large amount of dietary fat, may impair the
obesity 10824 T2D [[64]]. Elevated plasma free fatty acids (FFAs) associated with obesity [[65]] or independent of obesity , i.e., consumption of a large amount of dietary fat, may impair the insulin signaling pathway leading
obesity 11945 [[73]].Obesity is a major risk factor for developing T2D, particularly once associated with IR [[74]]. In obesity , plasma FFAs are chronically elevated [[65]], which in muscle, can directly inhibit insulin activation
obesity 12975 IR [[78],[79]]. Increased activity of these PKC isoforms in muscle was observed in animal models of obesity and T2D [[80],[81]].Mitochondria generate energy via oxidative phosphorylation of nutrients such as
obesity 20765 strongly associated with the development of IR, dyslipidemia, and T2D [[118]]. It is well recognized that obesity is partly a chronic inflammatory disease. Indeed, studies have suggested a direct connection between
obesity 20874 is partly a chronic inflammatory disease. Indeed, studies have suggested a direct connection between obesity and systematic inflammation due to the upregulation of key genes associated with inflammation [[119]],
obesity 21088 the increased secretion of inflammatory markers from white adipose tissue (WAT) [[120]]. Abdominal obesity , in particular, is associated with many chronic diseases where visceral fat is responsible for the abnormally
obesity 21524 other types of immune cells such as dendritic cells, T-lymphocytes, B-cells, and neutrophils during obesity , increased number of macrophages infiltrated into adipose tissue attracted by adipocyte-released chemokines
obesity 21859 necrosis, and increased lipotoxicity play a major role in initiating a low-grade systematic inflammation in obesity , which has been reviewed elsewhere [[123]]. Accumulating evidence shows that inflammation initiated
obesity 22226 from the infiltrated macrophages in adipose tissue [[125]] may play an important role in developing obesity -associated IR. TNF-α expression levels are elevated in obese and diabetic rodent models [[126]]. Adipocytes
obesity 22620 insulin-mediated peripheral glucose uptake [[126]]. Consistently, deletion of TNF-α gene in rodent models of obesity protected them from developing IR [[128]]. One of the proposed mechanisms by which TNF-α induces IR
obesity 23677 secreted from adipose tissue and may be associated with IR. IL-6 plasma levels were robustly elevated in obesity [[139]]. In T2D individuals, IL-6 was independently associated with IR and hyperglycemia [[140]]. It
obesity 24528 associated with markers of IR and development of T2D [[147],[148]]. Low levels of adiponectin found in obesity were associated with inflammation, whereas a loss in weight increased circulating adiponectin [[149]].
obesity 24698 increased circulating adiponectin [[149]]. Adiponectin administration reversed IR in rodent models of obesity [[150],[151]]. Adiponectin binds to its receptors adiponectin receptor protein 1(AdipoR1) and adiponectin

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