Localization of fat depots and cardiovascular risk

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Term Occurence Count Dictionary
hyperinsulinemia 2 endocrinologydiseases
metabolic syndrome 1 endocrinologydiseases
obesity 20 endocrinologydiseases
type 2 diabetes mellitus 2 endocrinologydiseases
vascular calcification 1 endocrinologydiseases
Insulin 3 endocrinologydiseasesdrugs
diabetes mellitus 2 endocrinologydiseases

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

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Select Drug Character Offset Drug Term Instance
Insulin 6073 obesity)+–– Interleukin-1β+++++ (morbid obesity)+–– EffectsProtective production of adiponectin• Gluconeogenesis• Insulin resistance• Dyslipidemia• Systemic inflammation• Protecting cardiomyocytes from hyperthermia•
Insulin 6617 involvement in the regulation of renal vessel tone• Synthesis of inflammation markers• Gluconeogenesis• Insulin resistance• Dyslipidemia• Insulin resistance• DyslipidemiaSAT subcutaneous adipose tissue, VAT
Insulin 6655 tone• Synthesis of inflammation markers• Gluconeogenesis• Insulin resistance• Dyslipidemia• Insulin resistance• DyslipidemiaSAT subcutaneous adipose tissue, VAT visceral adipose tissue, EAT epicardial
Select Disease Character Offset Disease Term Instance
diabetes mellitus 2197 the current consumption of high-calorie foods and decreasing activity have made obesity and type 2 diabetes mellitus the leading risk factors for CAD progression and mortality [[7]]. Moreover, the large Framingham and
diabetes mellitus 19887 around the thoracic aorta was significantly correlated with BMI, VO, arterial hypertension, and type 2 diabetes mellitus [[61]].The data presented above reveal variability in the effects of local fat depots on the risk of
hyperinsulinemia 8231 leads to decreased insulin sensitivity and the development of insulin resistance (IR) and systemic hyperinsulinemia , which subsequently contributes to the development of peripheral IR [[23]]. Moreover, both IR and excess
hyperinsulinemia 23533 FFA leads to decreased sensitivity to insulin and the development of insulin resistance and systemic hyperinsulinemia , which increase the production of “hepatic” glucose. In hypertrophied adipocytes, the insulin-dependent
metabolic syndrome 3553 of metabolic and cardiovascular complications [[13]].A number of studies have examined the topic of metabolic syndrome (MS), which includes hypertension, hyperglycaemia, and dyslipidaemia in the absence of obesity, and
obesity 2178 [[6]]. Nevertheless, the current consumption of high-calorie foods and decreasing activity have made obesity and type 2 diabetes mellitus the leading risk factors for CAD progression and mortality [[7]]. Moreover,
obesity 3659 metabolic syndrome (MS), which includes hypertension, hyperglycaemia, and dyslipidaemia in the absence of obesity , and their results led to the proposal of the term “metabolically healthy obesity” [[14]]. This
obesity 3743 the absence of obesity, and their results led to the proposal of the term “metabolically healthy obesity ” [[14]]. This term describes the marked metabolic heterogeneity of obesity, which is related to the
obesity 3820 “metabolically healthy obesity” [[14]]. This term describes the marked metabolic heterogeneity of obesity , which is related to the distribution of fat in different ectopic depots, and highlights the importance
obesity 5475 spectroscopy–––––++Factors expressed Peroxisomal proliferator+++––– Activated receptor-γ (PPAR-γ)+++ ( obesity )+/−–– Uncoupling protein-1–––++–– Uncoupling protein-2++++–––Secretory activity Lipoprotein
obesity 5648 protein-2++++–––Secretory activity Lipoprotein lipase++–+++ Free fatty acids+++ (morbid obesity )++++VLDL+ Plasminogen activator inhibitor-1++++++ (morbid obesity)+–– Leptin++++++ (morbid obesity)+–– Resistin–++
obesity 5716 lipase++–+++ Free fatty acids+++ (morbid obesity)++++VLDL+ Plasminogen activator inhibitor-1++++++ (morbid obesity )+–– Leptin++++++ (morbid obesity)+–– Resistin–++ (morbid obesity)––– Angiotensinogen+++–++–– Adiponectin+++–+–– Tumor
obesity 5755 obesity)++++VLDL+ Plasminogen activator inhibitor-1++++++ (morbid obesity)+–– Leptin++++++ (morbid obesity )+–– Resistin–++ (morbid obesity)––– Angiotensinogen+++–++–– Adiponectin+++–+–– Tumor
obesity 5795 inhibitor-1++++++ (morbid obesity)+–– Leptin++++++ (morbid obesity)+–– Resistin–++ (morbid obesity )––– Angiotensinogen+++–++–– Adiponectin+++–+–– Tumor necrosis factor-α+++–+–– Interleukin-6++++++
obesity 5942 obesity)––– Angiotensinogen+++–++–– Adiponectin+++–+–– Tumor necrosis factor-α+++–+–– Interleukin-6++++++ (morbid obesity )+–– Interleukin-1β+++++ (morbid obesity)+–– EffectsProtective production of adiponectin•
obesity 5989 factor-α+++–+–– Interleukin-6++++++ (morbid obesity)+–– Interleukin-1β+++++ (morbid obesity )+–– EffectsProtective production of adiponectin• Gluconeogenesis• Insulin resistance• Dyslipidemia•
obesity 7352 transition towards adipose tissue deposition in the visceral depots. The development of abdominal-visceral obesity is combined with unfavourable metabolic activity and an increased risk of cardiovascular complications.
obesity 7569 this context, the metabolic activity of visceral fat is considered a key factor in the development of obesity -related complications, [[21]] with much higher lipolytic activity observed in visceral adipose tissue
obesity 9336 leptin, which in turn helps maintain a chronic inflammatory condition in obese patients. When visceral obesity (VO) is combined with leptin resistance, leptin may induce vascular calcification, cholesterol accumulation
obesity 14877 mechanic, and textural (synthesizing adiponectin and adrenomedullin) [[47]]. However, in the context of obesity , the positive functions are replaced by negative functions, with the increased epicardial fat being
obesity 16010 lysophospholipids. Nevertheless, it is unclear whether these changes are a cause of FFA hyperproduction during obesity , and further studies are needed to evaluate the participation of EAT in the pathogenesis of cardiovascular
obesity 17197 with MS, [[52]] with EAT volume being directly correlated with some MS components, such as visceral obesity , fasting hyperglycaemia, myocardial infarction, hypertension, increased triglyceride concentrations,
obesity 17466 measuring EAT thickness is practically useful, as thickness or volume are directly correlated with visceral obesity , CAD, MS, and NASH, which indicates that EAT may accurately reflect cardiovascular risk and be useful
obesity 21137 functions, which allows them to play important roles in human metabolism, especially in relation to obesity and its associated diseases, such as CVD.An example of a phenotypic difference within a single depot
obesity 24010 strengthens peripheral insulin resistance. Excess FFA and insulin resistance, combined with visceral obesity , lead to disruption of lipid metabolism and the development of atherogenic dyslipidaemia. Thus, disruption
type 2 diabetes mellitus 2190 Nevertheless, the current consumption of high-calorie foods and decreasing activity have made obesity and type 2 diabetes mellitus the leading risk factors for CAD progression and mortality [[7]]. Moreover, the large Framingham and
type 2 diabetes mellitus 19880 thickness around the thoracic aorta was significantly correlated with BMI, VO, arterial hypertension, and type 2 diabetes mellitus [[61]].The data presented above reveal variability in the effects of local fat depots on the risk of
vascular calcification 9403 in obese patients. When visceral obesity (VO) is combined with leptin resistance, leptin may induce vascular calcification , cholesterol accumulation by macrophages, oxidative stress, an increased tone of the sympathetic nervous

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