Regulation of visceral and epicardial adipose tissue for preventing cardiovascular injuries associated to obesity and diabetes.

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Term Occurence Count Dictionary
hyperlipidemia 1 endocrinologydiseases
metformin 2 endocrinologydiseasesdrugs
phentermine 1 endocrinologydiseasesdrugs
sitagliptin 2 endocrinologydiseasesdrugs
Liraglutide 1 endocrinologydiseasesdrugs
diabetes mellitus 2 endocrinologydiseases
metabolic syndrome 4 endocrinologydiseases
amphetamine 2 endocrinologydiseasesdrugs
atorvastatin 1 endocrinologydiseasesdrugs
orlistat 1 endocrinologydiseasesdrugs
pioglitazone 1 endocrinologydiseasesdrugs
rosiglitazone 1 endocrinologydiseasesdrugs
hyperglycemia 2 endocrinologydiseases
hypertriglyceridemia 1 endocrinologydiseases
obesity 30 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Liraglutide 31679 not metformin, reduced 29 and 36% EAT at 3 and 6 months, respectively, after administration [[111]]. Liraglutide also stimulated WAT browning and thermogenesis in mice independently of nutrient intake [[112]] (Fig. 2).
amphetamine 30306 decreases adverse effects and increases tolerability. Thus, naltrexone + bupropion (opioid antagonist/ amphetamine ) demonstrated a reduction of body weight and VAT, and improved cardiovascular and metabolic parameters,
amphetamine 30548 lipids and glycaemia [[104]]. In overweight and obese/T2DM subjects, phentermine + topiramate (meta- amphetamine /monosaccharide) ameliorated body weight and obesity-associated cardio-metabolic conditions, such as
atorvastatin 31030 thickness and inflammation were reduced in T2DM subjects and hyperlipidemic post-menopausal women after atorvastatin administration, independently of lipid lowering or CAD progression [[106], [107]].Remarkably, agonists
metformin 28447 against obesity.Pharmacological reduction of the WAT/BAT ratioThe most noteworthy treatment for T2DM, metformin , decreased VAT volume, activated BAT and selectively enhanced clearance of VLDL lipoproteins into BAT
metformin 31581 subjects after 12 weeks of treatment [[110]] (Table 2). In obese/T2DM individuals, liraglutide, but not metformin , reduced 29 and 36% EAT at 3 and 6 months, respectively, after administration [[111]]. Liraglutide
orlistat 29872 [[101]], but their role in VAT, and overall EAT, is rather unknown. An inhibitor of pancreatic lipase, orlistat , shrink 24% VAT volume in parallel to total cholesterol, LDL-C, TAG, and fasting blood glucose [[102]].
phentermine 30515 parameters, such as blood pressure, lipids and glycaemia [[104]]. In overweight and obese/T2DM subjects, phentermine + topiramate (meta-amphetamine/monosaccharide) ameliorated body weight and obesity-associated cardio-metabolic
pioglitazone 29201 been withdrawn from market because of cardiotoxic side effects [[98]] Similarly, a PPARγ activator ( pioglitazone ) was associated with a reduction of pro-inflammatory genes as IL-1β in EAT from T2DM patients with
rosiglitazone 29332 with a reduction of pro-inflammatory genes as IL-1β in EAT from T2DM patients with CAD [[29]]. Also, rosiglitazone triggered lipid turnover and hypolipidemic actions by rapid browning of WAT in EAT depots of obese/T2DM
sitagliptin 32126 plasma clearance of triacylglycerol and glucose, following BAT activation [[112], [113]]. In this line, sitagliptin , a DPP-4 inhibitor that avoid GLP-1 degradation, reduced also EAT (15%) in parallel to VAT and more
sitagliptin 32323 to VAT and more intensively than BMI and waist circumference, in T2DM individuals [[114]]. Moreover, sitagliptin enhanced energy expenditure in obese mice by UCP-1 up-regulation in BAT repositories [[115]]. Thus,
Select Disease Character Offset Disease Term Instance
diabetes mellitus 524 world, and is associated with the development and progression of high-mortality diseases such as type-2 diabetes mellitus (T2DM) and its subsequent cardiovascular pathologies. Recent data suggest that both body fat distribution
diabetes mellitus 2878 care problems, being largely associated with multiple pathologies such as insulin resistance, type-2 diabetes mellitus (T2DM), metabolic dysfunction, and several cardiovascular injuries (i.e., acute myocardial infarct,
hyperglycemia 8554 peripheral insulin sensitivity [[15]], which associated with components of the metabolic syndrome (i.e., hyperglycemia , hypertriglyceridemia, and low HDL-C) [[16]]. Importantly, several clinical studies have linked VAT
hyperglycemia 18611 triacylglycerol-clearing organ, and such function could potentially be used to alleviate dyslipidaemias, hyperglycemia , and insulin resistance [[57]]. Furthermore, BAT influences cardiovascular physiology by releasing factors
hyperlipidemia 19846 in experimental cardiac hypertrophy and ischemia. Also, administration of FGF21 in humans improved hyperlipidemia by lowering plasma TAG and LDL-C levels, while increasing HDL-C levels [[61]]. Neuregulin-4, a BATokine
hypertriglyceridemia 8569 sensitivity [[15]], which associated with components of the metabolic syndrome (i.e., hyperglycemia, hypertriglyceridemia , and low HDL-C) [[16]]. Importantly, several clinical studies have linked VAT deposition with HF. The
metabolic syndrome 8528 independent negative marker of peripheral insulin sensitivity [[15]], which associated with components of the metabolic syndrome (i.e., hyperglycemia, hypertriglyceridemia, and low HDL-C) [[16]]. Importantly, several clinical studies
metabolic syndrome 13582 several meta-analysis studies showed that EAT was correlated with plasma TAG, fasting glucose, and metabolic syndrome , and it was linked to high systolic blood pressure and CAD [[33]].Adipocyte tissue in EAT undergoes
metabolic syndrome 13920 to FFA accumulation through expansion of adipocytes. EAT reached 7.5 mm in thickness in the human metabolic syndrome compared to 4.0 mm in control patients, and this accumulation disturbed insulin resistance in a similar
metabolic syndrome 14300 [[36]]. Also, rheumatic patients treated with steroids, which are known to imitate some effects of metabolic syndrome , develop thickening of EAT [[37]]. Thus, threshold values for high-risk echocardiographic EAT measures
obesity 139 DiabetologyRegulation of visceral and epicardial adipose tissue for preventing cardiovascular injuries associated to obesity and diabetesN. GonzálezZ. Moreno-VillegasA. González-BrisJ. EgidoÓ. LorenzoPublication date (epub):
obesity 348 (epub): 4/2017Publication date (pmc-release): 4/2017Publication date (collection): /2017AbstractNowadays, obesity is seriously increasing in most of the populations all over the world, and is associated with the development
obesity 2371 billion of overweight individuals and more than 700 million of obese adults (http://www.who.int/topics/ obesity /en/). In high-income countries, the overall rates are more than four times than those detected in lower
obesity 2525 rates are more than four times than those detected in lower and lower-middle income countries, though obesity is dangerously growing in Southeast Asia and Latin America. In addition, this dread is not restricted
obesity 6163 distinguished by their location, size, mitochondria content, and function, playing diverse roles in obesity and T2D. Importantly, WAT could be browned to bAT and BAT by several approaches. LD stands for lipid
obesity 10474 associated with noteworthy reduction in the EAT volume [[25]].Fig. 1VAT and EAT alterations under obesity and T2DM. In non-obese and non-T2DM subjects, WAT and BAT deposits in both VAT and EAT serve as storages
obesity 13099 1-α (PGC1α), and UCP-1, are more expressed in EAT than in other fat locations [[32]]. However, in obesity and T2DM, EAT becomes thicker and dysfunctional, promoting cardiovascular injuries, such as coronary
obesity 13351 dysfunction and cardiovascular riskAs VAT, EAT is also subjected to the maladaptive adipocyte biology of obesity , which is characterized by hypertrophy, failure to store TAG, increased lipolysis, and inflammation.
obesity 16544 anti-inflammatory/-atherogenic adipokines released from EAT (i.e., adiponectin) are also decreased under obesity , contributing to metabolic diseases, and HF [[46]] (Fig. 1). Particularly, omentin-1, a novel EAT-derived
obesity 18374 pathophysiologyRemarkably, fat accumulation as BAT may be considered an alternative mean to reduce cardiometabolic risk in obesity and T2DM. Despite its small relative size, BAT is highly vascularized and constitutes an important glucose,
obesity 20260 ischemic cardiomyocytes and diabetic isolated hearts [[63]].However, a negative correlation between obesity and levels of BAT volume and activity has been recently stated [[64]] (Fig. 1). In some South Asians
obesity 20481 populations, the lower amount of BAT can explain their frequent metabolic and cardiovascular disorders such as obesity , insulin resistance, T2DM, and dyslipidemia [[65]]. A reduced activity of BAT may predispose subjects
obesity 20622 dyslipidemia [[65]]. A reduced activity of BAT may predispose subjects to T2DM not only by increasing obesity , but also through a direct pro-diabetic mechanisms, such as by reduction of glucose uptake [[59], [64]].
obesity 20935 larger, unilocular, and mostly UCP1-negative [[66]]. Thus, conservation of BAT depots with an anti- obesity phenotype may be suggested for therapeutic interventions against cardiovascular pathologies in obese
obesity 21067 suggested for therapeutic interventions against cardiovascular pathologies in obese and T2DM patients.Anti- obesity strategies and reduction of cardiovascular riskA major goal in the therapeutic field of obesity and
obesity 21163 patients.Anti-obesity strategies and reduction of cardiovascular riskA major goal in the therapeutic field of obesity and related cardiovascular disorders is the development of effective treatments to balance the volume
obesity 23272 BAT, and bariatric surgery, the WAT/BAT ratio can be decreased. Metformin, PPARγ activators, anti- obesity drugs, statins, and more safely, incretins (stabilized by GLP-1R agonists and DPP-4 inhibitors), could
obesity 23495 reduce this ratioFig. 2Prospective fat-modulating interventions for cardiovascular dysfunction in obesity and T2DM. In addition to lifestyle modifications on diet and exercise, cardiovascular complications
obesity 24136 insulin sensitivityNon-pharmacological stimulation of BATSupraclavicular BAT was associated with less obesity and a more favourable metabolic profile in patients with cardiovascular diseases [[77]], meanwhile severe
obesity 24440 [[78]]. Consequently, increasing BAT formation and activity may account for novel strategies against obesity and its related cardiometabolic pathologies. In this regard, activation of BAT by β3-adrenergic receptor
obesity 25628 stimulatory factor 1 (USF1) activated BAT in obese/T2DM mice, and promoted protection against dyslipidaemia, obesity , insulin resistance, and atherosclerosis. These data were also confirmed in subjects carrying a mutation
obesity 26051 browning [[83]]. Transgenic overexpression of PRDM-16 in subcutaneous WAT protected mice from diet-induced obesity and insulin resistance [[84]]. In addition, injections of an miR-125b-5p inhibitor directly into WAT
obesity 27739 than in lean subjects [[93]].Therefore, we know that WAT accumulation in VAT and EAT is harmful for obesity and related-cardiovascular diseases, and that reduction of these stores or their browning to BAT by
obesity 28090 glucose/lipid metabolism could be exclusive for each patient, and unknown (epi)genetic predisposition to obesity and microbiome, may also individually disturb fat storing [[94]]. Hence, until research progresses on
obesity 28353 improves, specific pharmacological approaches could be used to modulate WAT and BAT activity against obesity .Pharmacological reduction of the WAT/BAT ratioThe most noteworthy treatment for T2DM, metformin, decreased
obesity 28885 liver and markers of inflammation and thrombosis were not alleviated [[97]]. On the other hand, anti- obesity drugs usually work by suppressing appetite, inhibiting fat absorption, or increasing energy consumption
obesity 29700 ben related with cardio-pathological secondary effects in T2DM patients [[100]].Thus, only five anti- obesity drugs have been approved by the FDA for long-term treatments [[101]], but their role in VAT, and overall
obesity 30604 subjects, phentermine + topiramate (meta-amphetamine/monosaccharide) ameliorated body weight and obesity -associated cardio-metabolic conditions, such as blood pressure, total cholesterol and glycated haemoglobin
obesity 33386 and T2DM patients.ConclusionsAdipose tissue may shift from being protective to being detrimental for obesity and cardiovascular homeostasis. WAT in VAT and EAT can hypertrophy and saturate in obese and T2DM subjects,
obesity 33733 additional interventions to life-style change, such as bariatric surgery, BAT transplantation or anti- obesity drugs have exhibited promising outcomes on diminishing the WAT/BAT ratio. Nevertheless, further investigations

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