Association between insulin resistance and the development of cardiovascular disease

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Term Occurence Count Dictionary
obesity 12 endocrinologydiseases
polycystic ovary syndrome 1 endocrinologydiseases
Insulin 22 endocrinologydiseasesdrugs
glucose intolerance 1 endocrinologydiseases
hyperglycemia 15 endocrinologydiseases
hyperinsulinemia 6 endocrinologydiseases
hyperlipidemia 2 endocrinologydiseases
hypertriglyceridemia 3 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 529 associated with CVD are comorbidities such as obesity, abnormal lipid profiles and insulin resistance. Insulin is a key hormone that functions as a regulator of cellular metabolism in many tissues in the human body.
Insulin 642 key hormone that functions as a regulator of cellular metabolism in many tissues in the human body. Insulin resistance is defined as a decrease in tissue response to insulin stimulation thus insulin resistance
Insulin 1500 which in turn triggers oxidative stress and causes an inflammatory response that leads to cell damage. Insulin resistance can also alter systemic lipid metabolism which then leads to the development of dyslipidemia
Insulin 4240 changes in glucose and lipid metabolism induced by insulin and their impact on the CVD development. Insulin signalingInsulin is a potent anabolic hormone that exerts a variety of effects on many types of cells.
Insulin 4257 glucose and lipid metabolism induced by insulin and their impact on the CVD development.Insulin signaling Insulin is a potent anabolic hormone that exerts a variety of effects on many types of cells. Some of the main
Insulin 8150 activation of glycogen synthase, increased hepatic gluconeogenesis, and glucose delivery by the liver Insulin resistanceInsulin resistance is defined as an experimental or clinical condition in which insulin exerts
Insulin 8168 glycogen synthase, increased hepatic gluconeogenesis, and glucose delivery by the liverInsulin resistance Insulin resistance is defined as an experimental or clinical condition in which insulin exerts a biological
Insulin 8976 about 60–70% and 10% of insulin-stimulated glucose uptake respectively via the GLUT 4 receptors. Insulin resistance cause impaired glycogen synthesis and protein catabolism in skeletal muscles and inhibit
Insulin 9485 acid metabolism leading to increased triglyceride content and VLDL secretion from liver [[5], [21]]. Insulin resistance causes endothelial cell dysfunction by decreasing the production of nitric oxide from endothelial
Insulin 10428 maintain blood glucose levels and utilization by vital systems like the brain and red blood cells [[24]]. Insulin resistance is increased in pregnancy particularly from the second to third trimester. This ensures the
Insulin 11643 these lipotoxic effects and enhances rates of apoptosis [[32]].Cellular mechanisms of insulin resistance Insulin works on multiple processes, essentially providing an integrated set of signals that allows the correct
Insulin 18251 contractile dysfunction, apoptosis, fibrosis, and impaired left ventricular diastolic function [[66]–[68]]. Insulin resistance and cardiovascular diseaseElevated levels of LDL, smoking, elevated blood pressure and type
Insulin 18807 approximately 30% of subjects with a diagnosis of hypertension [[69]]. In 1996, investigators in the Insulin Resistance Atherosclerosis Study (IRAS), showed a direct relation between insulin resistance and atherosclerosis
Insulin 21824 objective for the development of a new generation drugs for the treatment of diabetic cardiomyopathy. Insulin resistance and dyslipidemiaThe dyslipidemia induced by insulin resistance and type 2 diabetes (diabetic
Insulin 23379 release of fatty acids into the circulation that consequences a proatherogenic phenotype [[19], [90]]. Insulin resistance and lipoproteins profile alterationsVLDL, very low-density lipoprotein, is assembled and
Insulin 24620 synthesis is produced, which explains the hypertriglyceridemia observed under insulin resistance [[95]]. Insulin resistance also decreases lipoprotein lipase activity, a major mediator of VLDL clearance. This effect
Insulin 26874 and triglyceride glucose index with insulin resistance and CVD has been demonstrated [[102], [103]]. Insulin resistance leads to increased release of FFA from adipocytes and the product of fasting plasma FFA by
Insulin 27203 as a risk factor for aortic valve calcification, thereby predicting cardiovascular outcomes [[104]]. Insulin resistance, hypertension and endothelial dysfunctionClinical studies have demonstrated that about 50%
Insulin 29795 cardiomyopathy. Normally, the insulin signaling regulates the glucose and lipids metabolism in heart. Insulin resistance produces a metabolic derangement that results in high lipid oxidation and low of glucose
Insulin 32189 It also leads to impaired myocardial glucose utilization and to a decrease in diastolic relaxation. Insulin resistance and endothelial dysfunctionThe integrity of the functional endothelium is a fundamental vascular
Insulin 37095 contributes to the progression of diabetic complications such as retinopathy, nephropathy and CVD [[134]]. Insulin resistance and changes in the cardiac metabolismThe thickest layer of the heart wall is the myocardium,
Insulin 45917 apoptosis. This also contributes to diabetic cardiomyopathy pathogenesis [[175], [176]].Conclusions Insulin essentially provides an integrated set of signals allowing the balance between nutrient demand and availability.
Select Disease Character Offset Disease Term Instance
glucose intolerance 27372 studies have demonstrated that about 50% of hypertensive subjects have comorbid hyperinsulinemia or glucose intolerance , whereas at least 80% of patients with type 2 diabetes have comorbid hypertension [[105]]. The coexistence
hyperglycemia 1382 For instance, insulin resistance can induce an imbalance in glucose metabolism that generates chronic hyperglycemia , which in turn triggers oxidative stress and causes an inflammatory response that leads to cell damage.
hyperglycemia 12142 the impairment of glucose uptake in muscle and an increased gluconeogenesis by the liver resulting in hyperglycemia , both in fasting and postprandial states [[35]]. A number of theories have been suggested to understand
hyperglycemia 14925 inflammatory cytokines that inhibit insulin signaling and expedites hepatic gluconeogenesis, and postprandial hyperglycemia [[47], [48]].Other mechanisms that explain insulin resistance are the activation of both mTOR and S6K1
hyperglycemia 20278 expression pattern associated with estrogen receptor, as reported in animal models [[78]]. Furthermore, hyperglycemia produces alterations in various metabolic and cellular functions [[7]–[9]] including dyslipidemia,
hyperglycemia 28960 and the myocardium, which can have pathophysiological consequences [[108]].Literature has shown that hyperglycemia increases transcription of angiotensinogen, ACE and Ang II [[105], [109]]. On a different matter, an
hyperglycemia 34151 by HOMA-IR is strongly correlated with endothelial dysfunction with prognostic value [[122]].Chronic hyperglycemia in cardiovascular diseaseThe increased CVD risk in patients with type 2 diabetes has been known for
hyperglycemia 34715 of deaths [[124]].To support the latter, epidemiological and pathophysiological studies suggest that hyperglycemia may be largely responsible for CVD. Blood glucose has been reported as an independent predictor of atherosclerosis
hyperglycemia 35034 artery [[125]]. Long-term follow up data from patients with type 1 and type 2 diabetes suggest that hyperglycemia is a risk factor for diabetes related diseases and CVDMoreover, it has been suggested by Salvin et al.
hyperglycemia 35467 cardiac autonomic function leading to high risk of cardiac diseases [[127]].The detrimental effects of hyperglycemia on cardiomyocytes can be explained by a phenomenon called hyperglycemic memory, which is known as a
hyperglycemia 35707 hyperglycemic stress even after blood glucose normalization [[128], [129]]. Glucose fluctuations and hyperglycemia trigger inflammatory responses via mitochondrial dysfunction and endoplasmic reticulum stress. This
hyperglycemia 36252 reason, inflammation leads to insulin resistance and β-cell dysfunction, which further aggravates hyperglycemia , the latter help perpetuate this deregulation. Moreover, changes produced by glucose fluctuations and
hyperglycemia 36368 the latter help perpetuate this deregulation. Moreover, changes produced by glucose fluctuations and hyperglycemia can induce long-lasting epigenetic modifications in the promoter of the NF-κB, which appears to be
hyperglycemia 36566 which appears to be mediated by increased oxidative stress [[132]].Another harmful effect of persistent hyperglycemia is the advanced glycation end products (AGEs) generation, which are non-enzymatic glycation products
hyperglycemia 46118 demand and availability. Impaired nutrition contributes to hyperlipidemia and insulin resistance causing hyperglycemia . This condition alters cellular metabolism and intracellular signaling that negatively impact cells.
hyperglycemia 46517 changes. All these effects induce cellular events including: (1) gene expression modifications, (2) hyperglycemia and dyslipidemia, (3) activation of oxidative stress and inflammatory response, (4) endothelial dysfunction,
hyperinsulinemia 3393 resistance, the pancreas attempts to compensate by secreting increasing amounts of insulin, resulting in hyperinsulinemia [[4]].During insulin resistance and/or hyperinsulinemia, normal glucose tolerance is maintained due
hyperinsulinemia 3449 increasing amounts of insulin, resulting in hyperinsulinemia [[4]].During insulin resistance and/or hyperinsulinemia , normal glucose tolerance is maintained due a series of physiological changes activated by these phenomenon
hyperinsulinemia 20032 associated with fasting plasma glucose levels [[77]]. In addition to insulin resistance, the compensatory hyperinsulinemia associated with insulin resistance can play a critical role in the formation of atherosclerotic plaques
hyperinsulinemia 27352 dysfunctionClinical studies have demonstrated that about 50% of hypertensive subjects have comorbid hyperinsulinemia or glucose intolerance, whereas at least 80% of patients with type 2 diabetes have comorbid hypertension
hyperinsulinemia 30276 endoplasmic reticulum, FFA free fatty acidsMoreover, it has been shown that the activation of RAAS and hyperinsulinemia may synergistically stimulate the MAPK pathway, which exerts an effect damaging to the vascular wall
hyperinsulinemia 33113 resistance state, the NO synthesis stimulated by insulin is selectively impaired and the compensatory hyperinsulinemia may activate the MAPK pathway, resulting in a vasoconstriction enhancement, inflammation, increased
hyperlipidemia 14736 macrophages). The inflammatory factors increase lipolysis and promote hepatic triglyceride synthesis, and hyperlipidemia due to increased fatty acid esterification. ATM also stimulates inflammatory cytokines that inhibit
hyperlipidemia 46072 signals allowing the balance between nutrient demand and availability. Impaired nutrition contributes to hyperlipidemia and insulin resistance causing hyperglycemia. This condition alters cellular metabolism and intracellular
hypertriglyceridemia 7553 Increased free fatty acids flux to the liver stimulates the assembly and secretion of VLDL resulting in hypertriglyceridemia . Triglycerides (TG) in VLDL are transferred to both HDL and LDL through the action of cholesteryl ester
hypertriglyceridemia 18607 predict adverse cardiovascular events. Furthermore, insulin resistance is related to disorders such as hypertriglyceridemia as well as low levels HDL. Additionally, insulin resistance has been found in approximately 30% of subjects
hypertriglyceridemia 24558 and (3) greater stabilization of apoB; an increase in VLDL synthesis is produced, which explains the hypertriglyceridemia observed under insulin resistance [[95]].Insulin resistance also decreases lipoprotein lipase activity,
obesity 472 been the leading cause of death around the world. Often associated with CVD are comorbidities such as obesity , abnormal lipid profiles and insulin resistance. Insulin is a key hormone that functions as a regulator
obesity 2692 pathological processes and risk factors associated with CVD begin as early as during childhood [[1]]. Notably, obesity associated with an abnormal lipid profile at younger age has been strongly correlated with insulin resistance
obesity 2881 correlated with insulin resistance [[2], [3]]. As highlighted in the literature, multiple factors such as obesity , abnormal lipid profiles and insulin resistance play key roles in the origin of CVD.Under physiological
obesity 12498 grouped into: genetic defects, fat derived signal (ectopic lipid accumulation), physical inactivity, obesity , and inflammation [[36]–[38]]. One approach to analyze the genetic defect is to define candidate genes
obesity 13981 type 2 diabetes.In relation to external factors, the increase in free fatty acids (FFA) induced by obesity can trigger insulin resistance through lipid accumulation (ectopic lipids). This may activate atypical
obesity 14509 direct activation of Toll-like Receptor 4 (TLR4) and the innate immune response [[46]].Furthermore, obesity is associated with inflammatory factors characterized by an increase in the accumulation of ATMs (adipose
obesity 15802 decline in insulin signaling strength along the metabolic pathway [[49], [52], [53]].The influence of obesity on insulin resistanceObesity, in patients with higher body mass index (BMI) levels (≥ 30 kg/m2),
obesity 16066 disease compared to patients with normal BMI (BMI = 18.8–24.9 kg/m2) [[54]]. Moreover, central obesity is linked to insulin resistance. However, the molecular mechanism by which fat causes insulin resistance
obesity 22812 associated with the development of type 2 diabetes and CVDs. Visceral and epicardial adiposity related to obesity are the major drivers for cardiac disease in these individuals [[60]]. Obesity has a major effect in
obesity 23261 or catabolism of lipoprotein particles. These changes may contribute to increased basal lipolysis in obesity and the release of fatty acids into the circulation that consequences a proatherogenic phenotype [[19],
obesity 44809 ketogenic diet may be associated with a decreased incidence of risk factors of cardiovascular disease such obesity , diabetes, arterial blood pressure and cholesterol levels, but these effects are usually limited in
obesity 46694 inflammatory response, (4) endothelial dysfunction, and (5) ectopic lipid accumulation, which, favored by obesity , perpetuates the metabolic deregulation.Overall, insulin resistance contributes to generate CVD via
polycystic ovary syndrome 10884 observed in several clinical conditions such as breast cancer [[27]], rheumatoid arthritis [[28]], polycystic ovary syndrome [[29]], non-alcoholic fatty liver disease [[30]], and CVD [[31]].The excess of lipids in the cardiomyocyte

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