Role of Omentin, Vaspin, Cardiotrophin-1, TWEAK and NOV/CCN3 in Obesity and Diabetes Development

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17β-estradiol 1 endocrinologydiseasesdrugs
hyperlipidemia 2 endocrinologydiseases
lipodystrophy 1 endocrinologydiseases
metabolic syndrome 12 endocrinologydiseases
obesity 56 endocrinologydiseases
amphetamine 2 endocrinologydiseasesdrugs
hyperinsulinemia 1 endocrinologydiseases
pioglitazone 1 endocrinologydiseasesdrugs
diabetes mellitus 3 endocrinologydiseases
glucose intolerance 1 endocrinologydiseases
hyperglycemia 3 endocrinologydiseases
metformin 2 endocrinologydiseasesdrugs
rosiglitazone 1 endocrinologydiseasesdrugs
type 2 diabetes mellitus 1 endocrinologydiseases

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17β-estradiol 7305 of mRNA for omentin-1 in adipose tissue and omentin-1 serum concentration correlated negatively with 17β-estradiol [[14]]. Moreover, in such study significant negative correlations, based on variance components analysis
amphetamine 18903 the hypothalamic gene expression of agouti-related protein (AgRP), neuropeptide Y (NPY), orexin-A, amphetamine -regulated transcript (CART), corticotropin-releasing hormone (CRH) and pro-opiomelanocortin (POMC) [[34]].
amphetamine 72048 studies) suggesting increased food intake. Akt: protein kinase b, IRS: insulin receptor substrate, CART: amphetamine -regulated transcript, CRH: corticotropin-releasing hormone.Figure 2Schematic representation of the metabolic
metformin 37257 Also, Kadoglou et al. (2011) observed in patients with type 2 diabetes that 6 months of treatment with metformin monotherapy and the combination of rosiglitazone and metformin decreased serum vaspin [[69]]. Finally,
metformin 37320 diabetes that 6 months of treatment with metformin monotherapy and the combination of rosiglitazone and metformin decreased serum vaspin [[69]]. Finally, Jian et al. reported that low circulating vaspin level can be
pioglitazone 41291 inflammatory adipokines and this effect may be beneficial for improvement in insulin resistance. Since pioglitazone treatment up-regulates vaspin mRNA expression in rodents, vaspin may be one of the effector molecules
rosiglitazone 37302 patients with type 2 diabetes that 6 months of treatment with metformin monotherapy and the combination of rosiglitazone and metformin decreased serum vaspin [[69]]. Finally, Jian et al. reported that low circulating vaspin
Select Disease Character Offset Disease Term Instance
diabetes mellitus 35754 in the study only newly diagnosed diabetic patients, they concluded that, at the beginning of type 2 diabetes mellitus , vaspin might have a compensatory role [[61]]. The authors also declared that after diabetes treatment,
diabetes mellitus 38589 confers a state of insulin resistance and hyperinsulinemia that may predispose some women to gestational diabetes mellitus when their pancreatic function is not sufficient to overcome the diabetogenic environment of pregnancy.
diabetes mellitus 38835 vaspin level, mRNA and protein levels of vaspin in adipose tissue obtained from women with gestational diabetes mellitus (GDM) with those from women with normal glucose tolerance, Mm et al. reported higher vaspin plasma levels
glucose intolerance 66884 described in this review, the authors observed that NOV−/− mice were protected against diet-induced glucose intolerance and insulin resistance [[166]]. Finally, Shimoyama et al. [[168]] demonstrated that NOV/CCN3 expression
hyperglycemia 8507 with chronic inflammation. Finally, they reported that two of the main modulating factors seemed to be hyperglycemia and BMI [[16]].The relationship found between omentin-1 and obesity has also been found in adolescents
hyperglycemia 52086 inhibitors) that mediate intestinal glucose absorption or increase glucose excretion, could help to control hyperglycemia through an insulin-independent mechanism, introducing a new concept to the diabetes treatment [[101]].Another
hyperglycemia 72262 metabolic actions of cardiotrophin-1. This adipokine promotes body weight and fat mass losses, reduces hyperglycemia and increases insulin sensitivity by coordinately acting on key metabolic tissues (hypothalamus, adipose
hyperinsulinemia 38526 reported by Tonjes et al. [[71]].Finally, human pregnancy often confers a state of insulin resistance and hyperinsulinemia that may predispose some women to gestational diabetes mellitus when their pancreatic function is not
hyperlipidemia 64966 (PGC1-α). In humans, Pakradouni et al. [[155]] studied plasma concentration of NOV/CCN3 in adults showing hyperlipidemia with or without lipid-lowering therapy. They showed, for the first time, a strong correlation between
hyperlipidemia 67274 to human beings, in the study reported by Pakradouni et al. [[155]], carried out in adults showing hyperlipidemia with or without lipid-lowering therapy, HbA1c which is an important blood marker that gives a good indication
lipodystrophy 57385 obesity [[132]]. On the other hand, in a situation of a huge adipose tissue loss, such as occurs in the lipodystrophy associated to the HIV infection, TWEAK levels were lower compared with their controls counterparts [[133]].
metabolic syndrome 14874 glycemic control are concerned, several authors have documented lower levels of serum omentin-1 in nascent metabolic syndrome ; even after correction for obesity [[26]]. Shang et al. (2011) also reported lower serum omentin-1 concentration
metabolic syndrome 15023 obesity [[26]]. Shang et al. (2011) also reported lower serum omentin-1 concentration in patients with metabolic syndrome , however they did not correct data for the increased BMI and waist circumference, and thus they were
metabolic syndrome 15201 and waist circumference, and thus they were unable to conclude that this correlation was a feature of metabolic syndrome per se [[27]].Vu et al. (2014) carried out a study to determine the relationship between circulating
metabolic syndrome 15367 study to determine the relationship between circulating omentin-1 concentration and components of the metabolic syndrome in adults without type 2 diabetes. They also evaluated whether sexual dimorphism existed for such relationships.
metabolic syndrome 15569 existed for such relationships. Unlike other studies, no differences between subjects with or without metabolic syndrome were found [[28]]. The authors considered that this discrepancy with other studies was likely to be
metabolic syndrome 16061 differences between men and women were observed when the entire study cohort was analyzed; however, men with metabolic syndrome had lower plasma omentin-1 concentrations than women did.Moreover, studies in subjects showing type
metabolic syndrome 27912 group of subjects with >20% body fat [[43]]. This association has also been found in subjects with metabolic syndrome . Tan et al. observed that serum vaspin concentration correlated positively with BMI, waist circumference
metabolic syndrome 34307 with fasting insulin and HOMA-IR [[10]].Significant correlations were also found in subjects showing metabolic syndrome . Tan et al. observed that serum vaspin concentration was significantly higher in men with metabolic
metabolic syndrome 34416 syndrome. Tan et al. observed that serum vaspin concentration was significantly higher in men with metabolic syndrome than in men without the syndrome. By contrast, no differences were observed in women. Moreover, among
metabolic syndrome 44147 great influence on metabolic disturbances and vice versa [[83]]. Although the exact mechanisms linking metabolic syndrome with chronodisruption are still unknown, most hypotheses point to an internal desynchronization of circadian
metabolic syndrome 46102 mice [[88],[89]]. Moreover, plasma levels of this cytokine are elevated in patients with obesity and metabolic syndrome , suggesting that CT-1 could be considered as a marker and a link between adipose tissue, insulin resistance
metabolic syndrome 70579 alterations in glycemic control, several authors have documented lower levels of serum omentin-1 in nascent metabolic syndrome , type 2 diabetes or even type 1 diabetes. It has been proposed that omentin-1 improves insulin sensitivity.
obesity 1402 necrosis factor-like Weak Inducer of Apoptosis (TWEAK) and nephroblastoma overexpressed (NOV/CCN3) on obesity and diabetes. Omentin is produced by the stromal-vascular fraction of visceral adipose tissue. Obesity
obesity 2211 cardiotrophin-1 are down-regulated in white adipose tissue from diet-induced obese mice. It also shows anti- obesity and hypoglycemic properties. TWEAK is a potential regulator of the low-grade chronic inflammation characteristic
obesity 2335 properties. TWEAK is a potential regulator of the low-grade chronic inflammation characteristic of obesity . TWEAK levels seem not to be directly related to adiposity, and metabolic factors play a critical role
obesity 3842 vaspin, cardiotrophin-1, TWEAK and NOV/CCN3. More specifically, it focuses on their relationship with obesity , insulin resistance and diabetes. In the case of omentin-1 and vaspin, the review mainly describes those
obesity 6304 is known that its expression and production are modified in several pathological situations, such as obesity and insulin resistance. Omentin-1 expression is also altered in inflammatory states [[12]]. Thus, taking
obesity 6435 Omentin-1 expression is also altered in inflammatory states [[12]]. Thus, taking into account that obesity itself is associated with low levels of chronic inflammation, this may contribute to the increase in
obesity 6634 increase in omentin-1 concentration observed in obese subjects.2.1. Omentin and ObesityWith regard to obesity , De Souza Batista et al. (2007) reported that serum omentin-1 concentration, as well as visceral adipose
obesity 7806 positively correlated with plasma omentin-1 values. They proposed that an inverse relationship between obesity and both omentin-1 and adiponectin may suggest similar regulation. Similarly, Auguet et al. (2011) reported
obesity 8581 modulating factors seemed to be hyperglycemia and BMI [[16]].The relationship found between omentin-1 and obesity has also been found in adolescents and children. Oświęcimska et al. (2015) measured plasma omentin-1
obesity 9773 omentin-1 attenuates these metabolic abnormalities [[19]].Taken together these results clearly show that obesity reduces serum omentin-1 concentration and adipose tissue secretion in adults and adolescents. In the
obesity 10202 induces increased omentin-1 serum concentrations. As far as energy restriction, the main tool used in obesity treatment, is concerned, Moreno-Navarrete et al. (2010) reported a significant increase in serum omentin-1
obesity 11791 due to the short-term dietary intervention [[21]].Another important strategy used in the treatment of obesity and glucose homeostasis alterations (insulin resistance and diabetes) is to increase physical activity.
obesity 14686 effective in correcting the alterations induced in omentin-1 serum concentration induced by overweight and obesity .2.2. Omentin and Alterations in Glycemic ControlAs far as alterations in glycemic control are concerned,
obesity 14920 documented lower levels of serum omentin-1 in nascent metabolic syndrome; even after correction for obesity [[26]]. Shang et al. (2011) also reported lower serum omentin-1 concentration in patients with metabolic
obesity 18460 Actions of OmentinGiven the above studies, scientific evidence clearly supports the role of omentin in obesity and glucose metabolism regulation. However, knowledge concerning the mechanisms involved are scarce
obesity 20842 identified for the first time by Hida et al. in 2000 in the visceral adipose tissue of a rat model of obesity and type 2 diabetes (Otsuka Long-Evans Tokushima fatty rat; OLETF) [[38]]. The authors observed that
obesity 21053 the expression of this adipokine reached its highest values at the age when plasma insulin levels and obesity peaked. As the diabetes worsened, the expression of vaspin decreased [[39]]. Human vaspin protein is
obesity 26299 and ObesityWith regard to this issue, while several studies showed an association between vaspin and obesity [[43],[52],[59],[60],[61]], others did not find it [[15],[54]]. Auguet et al. (2011) reported that serum
obesity 28096 positively with BMI, waist circumference and percentage of body fat, which all reflect the degree of obesity . Among these variables, the percentage of body fat was associated most strongly with vaspin concentration
obesity 29811 post-menopausal women) or administered drugs [[63]]. Studies concerning the association between vaspin and obesity are not restricted to adults. Younger subjects have also been analyzed by other authors, although data
obesity 30336 reported by other authors. Thus, Ko et al. found that elevated vaspin concentrations were related to obesity in pre-pubertal Korean children, after adjustment for sex, blood pressure, biochemical parameters, and
obesity 30612 discrepancy may be partly explained by different population origins of subjects, or different definitions of obesity in children. In addition, the study reported by Ko et al. had a larger sample size and all children
obesity 30947 concentrations of vaspin have been found, reinforcing the idea that there is an association between obesity and this adipokine. Thus, Chang et al. reported decreased concentrations of serum vaspin after a modest
obesity 31573 concentration was concomitant with reductions in waist circumference, which is a useful index of central obesity . A limitation of this study was that abdominal fat distribution was not measured. Nevertheless, taking
obesity 33983 vaspin mRNA expression in human adipose tissue could represent a compensatory mechanism associated with obesity , severe insulin resistance, and type 2 diabetes [[42]]. In another study, carried out in normal weight
obesity 44838 [[80],[86],[87]]. In this sense, it has been described that CT-1 deficiency brings on late-onset adult obesity in mice, accompanied by insulin resistance and hypercholesterolemia [[86]]. It is important to highlight
obesity 45036 important to highlight that CT-1−/− mice, by contrast with other deficiencies in gp130 ligands, develop obesity despite reduced food intake probably as a consequence of decreased energy expenditure. Hence, CT-1 deficient
obesity 45190 consequence of decreased energy expenditure. Hence, CT-1 deficient mice represent a hypophagic model of obesity [[86]]. Moreover, oxygen consumption rate (VO2) circadian rhythmicity was disrupted in aged obese CT-1-deficient
obesity 45816 genes in mice.However, there is still some controversy regarding the regulation of CT-1 levels during obesity both in rodents and humans. Indeed, studies performed in mice have shown that gene expression levels
obesity 46090 diet-induced obese mice [[88],[89]]. Moreover, plasma levels of this cytokine are elevated in patients with obesity and metabolic syndrome, suggesting that CT-1 could be considered as a marker and a link between adipose
obesity 46867 subjects when compared to overweight/obese individuals, suggesting that other factors associated to obesity , and not the increased adiposity directly, could be determining the levels of this cytokine. So, the
obesity 46992 increased adiposity directly, could be determining the levels of this cytokine. So, the role of CT-1 in obesity in humans remains to be further elucidated.4.2. Cardiotrophin-1 and Alterations in Glycemic ControlConcerning
obesity 49025 factor κB (NF-κB) system [[82]]. Figure 2 summarizes the main metabolic actions underlying the anti- obesity and anti-diabetic properties of CT-1. In this context, activation of hypothalamic pathways involved
obesity 51885 [[100]]. The inhibition of intestinal sugar uptake could also account for the hypoglycemic and anti- obesity properties of CT-1. In this sense, agents that inhibit glucose co-transporters (SGLT inhibitors) that
obesity 54178 research community as a potential regulator of the low-grade chronic inflammation characteristic of obesity (extensively reviewed in Burkly [[105]]).TWEAK gene is located at chromosomal position 17p13.1, encoding
obesity 55549 deciphered TWEAK as a component of the network that contributes to the inflammatory imbalance observed in obesity [[111],[122],[123],[124]].5.1. TWEAK, Obesity and Alterations in Glycemic ControlSome studies have focused
obesity 55719 in Glycemic ControlSome studies have focused on the potential relationship between TWEAK levels and obesity , but overall on understanding the relevance of TWEAK in morbid obesity. Nevertheless, the data reported
obesity 55790 relationship between TWEAK levels and obesity, but overall on understanding the relevance of TWEAK in morbid obesity . Nevertheless, the data reported are sometimes controversial. In morbidly obese patients TWEAK and Fn14
obesity 56418 [[112]].Interestingly, TWEAK knock-out mice fed on a high fat diet showed more susceptibility to develop adult obesity than the wild-type mice [[128]]. However, these TWEAK knock-out mice were protected from dyslipidemia
obesity 57115 Moreover, lower TWEAK levels have been associated with higher levels of glucose, HOMA-IR index and visceral obesity [[129],[130]] and higher TWEAK levels have been positively related to triglycerides [[131]]. Finally,
obesity 57281 related to triglycerides [[131]]. Finally, other studies reported no association between TWEAK and obesity [[132]]. On the other hand, in a situation of a huge adipose tissue loss, such as occurs in the lipodystrophy
obesity 57587 counterparts [[133]]. Increased levels of TWEAK in skeletal muscle favors the development of visceral obesity , accompanied with insulin resistance, and metabolic dysfunction, suggesting that TWEAK inhibition could
obesity 58005 metabolic factors are playing a critical role in TWEAK levels regulation. Moreover, the role of TWEAK in obesity and in the risk of metabolic complications seem to be tissue-dependent. Consequently, further studies
obesity 58188 Consequently, further studies with larger cohorts are needed to better characterize TWEAK/Fn14 role in obesity -associated metabolic disturbances.5.2. TWEAK Aeceptors and Signaling Pathways Involved in the Metabolic
obesity 64405 observed. By contrast, NOV−/− mice, but not wild-type mice, were protected against diet-induced obesity and adipose tissue inflammation. This different behavior of knock-out and wild type mice occurred without
obesity 66667 insulin secretion [[166]]. These authors also reported that NOV/CCN3 contributed to the development of obesity -induced insulin resistance, based on their studies in knock-out mice. Thus, in the experiment previously
obesity 67609 correlation was found between plasma NOV/CCN3 concentration and blood glucose.7. Concluding RemarksAs far as obesity is concerned, it has been reported that this pathology reduces serum omentin-1 concentration and adipose
obesity 68133 effective in correcting the alterations induced in omentin-1 serum concentration induced by overweight and obesity . Animal studies suggest that omentin could be involved in the regulation of appetite due to the neuromodulatory
obesity 68786 in serum concentrations of vaspin have been found, reinforcing the idea that an association between obesity and this adipokine exists. Vaspin reduces food intake and may inhibit inflammatory processes by reducing
obesity 69724 research community as a potential regulator of the low-grade chronic inflammation characteristic of obesity . TWEAK levels are not directly related to adiposity, and other tissues or metabolic factors are playing
obesity 69911 metabolic factors are playing a critical role in TWEAK levels regulation. Moreover, the role of TWEAK in obesity and risk of metabolic complications seem to be tissue-dependent. Consequently, further studies with
obesity 70087 Consequently, further studies with larger cohorts are needed to better characterize TWEAK/Fn14 role in obesity -associated metabolic pathologies.Finally, a strong correlation has been observed between NOV/CC3 plasma
obesity 71243 addition, lower TWEAK levels have been associated with higher levels of glucose, HOMA-IR index and visceral obesity . Finally, there is just a study addressing the effects of NOV/CCN3 on glycemic control in humans where
obesity 71706 involved in the effects of omentin, vaspin, cardiotrophin-1, TWEAK and NOV/CCN3 on insulin resistance or obesity .Figure 1Schematic representation of the metabolic actions of omentin-1 in adipose tissue (data obtained
obesity 73150 involved in the effects of omentin, vaspin, cardiotrophin-1, TWEAK and NOV/CCN3 on insulin resistance and obesity . On the left side of the figure, target tissues and organs involved in the effects of adipokines on
obesity 73358 insulin resistance. On the right side of the figure, target tissues and organs involved in the anti- obesity action of adipokines
type 2 diabetes mellitus 35747 included in the study only newly diagnosed diabetic patients, they concluded that, at the beginning of type 2 diabetes mellitus , vaspin might have a compensatory role [[61]]. The authors also declared that after diabetes treatment,

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