The role of vascular endothelial growth factor-B in metabolic homoeostasis: current evidence.

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Term Occurence Count Dictionary
type 2 diabetes mellitus 1 endocrinologydiseases
diabetes mellitus 1 endocrinologydiseases
hyperinsulinemia 2 endocrinologydiseases
metabolic syndrome 14 endocrinologydiseases
metformin 4 endocrinologydiseasesdrugs
obesity 29 endocrinologydiseases
polycystic ovary syndrome 3 endocrinologydiseases
glucose intolerance 3 endocrinologydiseases
hyperlipidemia 1 endocrinologydiseases
hypertriglyceridemia 1 endocrinologydiseases

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metformin 31751 IR and β-cell function indices. Moreover, in patients with polycystic ovary syndrome treated with metformin , this drug treatment reduced VEGF-B levels and ameliorated IR [[61]].So, growing scientific evidence
metformin 34433 obese patients, finding that VEGF-B correlates with BMI and the level of IR [[61]]. They reported that metformin reduced VEGF-B levels and ameliorated IR. However, knowing that metformin stimulates FAs oxidation with
metformin 34507 [[61]]. They reported that metformin reduced VEGF-B levels and ameliorated IR. However, knowing that metformin stimulates FAs oxidation with inhibition of cholesterol and triglyceride synthesis in the liver, promote
metformin 34809 sensitivity itself, the question remains—does the regained metabolic balance reflex the effect of metformin , of decreased VEGF-B levels and subsequent impaired FAs uptake or something else?VEGF-B as a potential
Select Disease Character Offset Disease Term Instance
diabetes mellitus 4024 Postprandial increases in perfusion, however, were not observed either in obese [[12],[13]] and type 2 diabetes mellitus (T2DM) patients or in animal models of T2DM and IR [[11],[14],[15]]. Pathogenetically, adipose tissue
glucose intolerance 1562 2 (VEGFR2) pathway. While in some preclinical high-fat diet studies, VEGF-B overexpression reverted glucose intolerance and stimulated fat burning, in others it further promoted accumulation of lipids and lipotoxicity. Data
glucose intolerance 14954 skeletal muscle as biological buffers [[16],[17],[36]]. IR, an important feature of T2DM, obesity, glucose intolerance and dyslipidemia is also an important component of cardiovascular disorders, including hypertension
glucose intolerance 23507 other authors reported opposite findings. Robciuc et al. [[32]] found that Vegfb transduction reverted glucose intolerance in the preclinical mouse model of metabolic syndrome, stimulated fat burning, augmented basal oxygen
hyperinsulinemia 417 has been shown that adipose tissue and skeletal muscles in lean individuals respond to meal-induced hyperinsulinemia by increase in perfusion, the effect not observed in patients with metabolic syndrome. In conditions
hyperinsulinemia 3706 postprandial glucose and lipid homoeostasis [[8]–[10]]. In lean, healthy individuals, meal-induced hyperinsulinemia augments the resting blood volume of the skeletal muscle microvascular bed and this mechanism seems
hyperlipidemia 31225 led the authors to the conclusion that high serum VEGF-B levels might correlate with the presence of hyperlipidemia and target organ damage in T2DM patients [[51]].In a group of 103 women with polycystic ovary syndrome
hypertriglyceridemia 557 perfusion, the effect not observed in patients with metabolic syndrome. In conditions of hyperglycaemia and hypertriglyceridemia , this insufficient vascularization leads to the liberation of reactive oxygen species (ROS), and disruption
metabolic syndrome 501 to meal-induced hyperinsulinemia by increase in perfusion, the effect not observed in patients with metabolic syndrome . In conditions of hyperglycaemia and hypertriglyceridemia, this insufficient vascularization leads to
metabolic syndrome 1224 discoveries indicate that this growth factor may be a promising therapeutic agent in patients with metabolic syndrome . Preclinical studies agree over two crucial metabolic effects of VEGF-B: (i) regulation of FAs uptake
metabolic syndrome 19409 in inflammation has been found to diminish metabolic complications caused by high-fat diet and the metabolic syndrome [[50],[51]]. Accordingly, several authors have reported increased levels of VEGF-A in human obesity
metabolic syndrome 23561 [[32]] found that Vegfb transduction reverted glucose intolerance in the preclinical mouse model of metabolic syndrome , stimulated fat burning, augmented basal oxygen consumption and metabolic rate, acting protectively
metabolic syndrome 27261 humans [[32]]. Increased insulin delivery as a consequence of increased vascularity might alleviate metabolic syndrome s, but hypoxia markers as a formal proof of restored tissue oxygenation have not yet been investigated
metabolic syndrome 29202 signalling [[2]], clinical data related to the pathological roles of VEGF-B in obese patients and those with metabolic syndrome are very scarce.In 2009, Gomez-Ambrosi et al. [[27]] compared serum concentrations of VEGFs in 15 lean
metabolic syndrome 36371 needed to elucidate the expression and functional status of VEGF-B in obese patients and those with metabolic syndrome , and to verify whether these conditions in humans may potentially be associated with any functional
metabolic syndrome 38038 in clinical studies.It is reasonable to expect that pathological lipid accumulation in obesity and metabolic syndrome may be affected by VEGF-B, considering its critical role in FAs uptake regulation [[3]]. However, besides
metabolic syndrome 38899 clinical approach should determine the clinical relevance of the endothelial signalling in the context of metabolic syndrome , thus providing greater insights that may ultimately lead to therapeutic advances against the increasing
metabolic syndrome 39249 perfusion – inflammation – IR’ has been widely accepted as a basis of IR development in patients with metabolic syndrome , the exact signalling pathways responsible for it are still open to many questions. The angiogenic role
metabolic syndrome 39492 counterpart, VEGF-A, is clearly reflected through its increased circulating concentrations in obesity and metabolic syndrome , but VEGF-B seems to have a more complex role in metabolic homoeostasis.ResultsPreclinical studies agree
metabolic syndrome 40417 Elucidating blood levels of this growth factor in healthy, non-obese patients, obese patients without metabolic syndrome and obese patients with metabolic syndrome may represent a promising first step towards better understanding
metabolic syndrome 40460 factor in healthy, non-obese patients, obese patients without metabolic syndrome and obese patients with metabolic syndrome may represent a promising first step towards better understanding of a complex VEGF-B’s role in humans.Potential
metabolic syndrome 40990 for human use. Hence, the expression and functional status of VEGF-B in obese patients and those with metabolic syndrome require the immediate attention of the scientific community
obesity 1011 insulin signalling. While the angiogenic role of VEGF-A and its increased circulating concentrations in obesity have been widely confirmed, the data related to the metabolic role of VEGF-B are diverse. However, recent
obesity 2191 remain to be clarified through future translational research.IntroductionThe worldwide pandemic of obesity associated with net positive energy balance, sedentary lifestyle and increased consumption of animal
obesity 3024 resistance (IR), lead to the abnormal behaviour of endothelial cells (ECs) [[6]]. It has been shown that obesity -related accumulation of neutral lipids in locations other than adipose tissue, especially in skeletal
obesity 5516 inhibition of VEGFR tyrosine kinases impairs the development of adipose tissue in murine models of obesity [[23]–[25]]. Several authors have reported increased levels of circulating VEGF-A in human obesity
obesity 5617 obesity [[23]–[25]]. Several authors have reported increased levels of circulating VEGF-A in human obesity [[26],[27]]. Similarly, a significant decrease in VEGF-A concentrations was observed in patients with
obesity 6052 ECs which takes place mostly through the VEGF/VEGFR system plays a key role in the pathogenesis of obesity and metabolic disturbances [[29]].Because of its high sequence homology and similar receptor binding
obesity 14122 NRP1, neuropilin 1.The role of endothelial dysfunction and VEGF-B in pathogenesis of IRThe effect of obesity to increase the risk of cardiovascular morbidity and mortality is strongly associated with IR in peripheral
obesity 14473 in models of both genetic (e.g. the Fatty Zucker rat) [[37],[38]] and acquired (e.g. diet-induced) obesity [[39]] involves activation of some key transcriptional mediators of cellular inflammation in response
obesity 14945 liver and skeletal muscle as biological buffers [[16],[17],[36]]. IR, an important feature of T2DM, obesity , glucose intolerance and dyslipidemia is also an important component of cardiovascular disorders, including
obesity 15242 characterized by endothelial malfunction [[16]]. In turn, endothelial malfunction is present in T2DM, obesity and dyslipidemias [[16]]. In a proinflammatory milieu of excess FAs and/or glucose, the most obvious
obesity 16448 aetiopathogenetic factors: glucotoxicity in T2DM, lipotoxicity caused by elevated levels of FAs in T2DM, obesity and dyslipidemias, and proinflammatory states associated with metabolic and cardiovascular diseases
obesity 19014 independently from each other. However, it has been shown that one of the key roles in the pathogenesis of obesity and metabolic disorders belongs to a perturbed cross-talk between adipocytes and ECs that as already
obesity 19520 syndrome [[50],[51]]. Accordingly, several authors have reported increased levels of VEGF-A in human obesity [[26],[27]]. Similarly, a significant decrease in VEGF-A concentrations was observed in patients with
obesity 22615 can function as an efficient barrier to excess muscle lipid uptake even under conditions of severe obesity and T2DM, and that this barrier can be maintained by inhibition of VEGF-B signalling [[4]]. In experimental
obesity 23701 burning, augmented basal oxygen consumption and metabolic rate, acting protectively against diet-induced obesity and metabolic complications. Nonetheless, when Robciuc et al. [[32]] experimentally limited VEGF-B expression
obesity 24575 and Fatp4, initiating transendothelial transport of FAs into the muscle fibres in high-fat diets and obesity , it would be reasonable to expect that decreased VEGF-B expression prevents lipid accumulation in skeletal
obesity 25707 [[30],[33],[39]].Recently, Robciuc et al. [[32]] reported that Vegfb gene transduction into mice inhibits obesity -associated inflammation and improves metabolic health without changes in body weight or ectopic lipid
obesity 26348 subcutaneous adipose tissue, which increased the basal metabolic rate, thus preventing diet-induced obesity and related metabolic complications. In obese and IR mice, Vegfb gene transfer, together with endothelial
obesity 27438 oxygenation have not yet been investigated [[32]]. However, since metabolic events associated with obesity and IR occur in adipose tissue earlier than in any other tissue in humans, adipose tissue should be
obesity 29053 can function as an efficient barrier to excess muscle lipid uptake even under conditions of severe obesity and T2DM by antagonizing VEGF-B signalling [[2]], clinical data related to the pathological roles of
obesity 29791 of VEGF-B were in agreement with the previous results. However, increased VEGF-B concentrations in obesity were not confirmed by other authors. Aiming to establish the relationship between adipose tissue angiogenic
obesity 29917 by other authors. Aiming to establish the relationship between adipose tissue angiogenic capacity, obesity and IR, in 2012 Tinahones et al. [[60]] compared angiogenic factor expression levels in subcutaneous
obesity 31960 evidence indicates that angiogenesis is a process involved in adipose tissue expansion that takes place in obesity [[50],[51]]. Suboptimal fat tissue perfusion can limit its expansion capacity and provoke inflammation,
obesity 34094 and would in these pathological conditions inhibition of VEGF-B signalling have any effect? Or, is obesity in human potentially associated with some functional defect of VEGF-B? In the study where patients with
obesity 34967 impaired FAs uptake or something else?VEGF-B as a potential therapeutic agent for metabolic disorder and obesity As mentioned earlier, the binding of VEGF-B to VEGFR1 activates the VEGF-A/VEGFR2 pathway leading to
obesity 35687 well established that adipose tissue inflammation is a major contributor to systemic IR in T2DM and obesity [[63]]. Suboptimal vascularization and perfusion of adipose tissue can limit its expansion capacity
obesity 38026 be confirmed in clinical studies.It is reasonable to expect that pathological lipid accumulation in obesity and metabolic syndrome may be affected by VEGF-B, considering its critical role in FAs uptake regulation
obesity 39037 greater insights that may ultimately lead to therapeutic advances against the increasing burden of the obesity pandemic and associated metabolic derangements.PerspectivesBackgroundWhile the axes ‘impaired perfusion
obesity 39480 VEGF-B’s counterpart, VEGF-A, is clearly reflected through its increased circulating concentrations in obesity and metabolic syndrome, but VEGF-B seems to have a more complex role in metabolic homoeostasis.ResultsPreclinical
polycystic ovary syndrome 31317 presence of hyperlipidemia and target organ damage in T2DM patients [[51]].In a group of 103 women with polycystic ovary syndrome and 96 age-matched healthy controls, Cheng et al. [[61]] found that both lean and overweight/obese patients
polycystic ovary syndrome 31456 age-matched healthy controls, Cheng et al. [[61]] found that both lean and overweight/obese patients with polycystic ovary syndrome had higher plasma VEGF-B levels than the healthy controls (P<0.05) and that VEGF-B levels were correlated
polycystic ovary syndrome 31712 percentage, homoeostasis model assessment of IR and β-cell function indices. Moreover, in patients with polycystic ovary syndrome treated with metformin, this drug treatment reduced VEGF-B levels and ameliorated IR [[61]].So, growing
type 2 diabetes mellitus 4017 [[10],[11]]. Postprandial increases in perfusion, however, were not observed either in obese [[12],[13]] and type 2 diabetes mellitus (T2DM) patients or in animal models of T2DM and IR [[11],[14],[15]]. Pathogenetically, adipose tissue

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