From Placenta to Polycystic Ovarian Syndrome: The Role of Adipokines

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Term Occurence Count Dictionary
Precocious puberty 1 endocrinologydiseases
cortisol 1 endocrinologydiseasesdrugs
diabetes mellitus 3 endocrinologydiseases
hyperandrogenism 5 endocrinologydiseases
metabolic syndrome 6 endocrinologydiseases
testosterone 8 endocrinologydiseasesdrugs
type 2 diabetes mellitus 1 endocrinologydiseases
Insulin 4 endocrinologydiseasesdrugs
obesity 13 endocrinologydiseases
ovarian dysfunction 2 endocrinologydiseases
polycystic ovary syndrome 1 endocrinologydiseases
hyperglycemia 1 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 2152 and have been related mainly to insulin sensitivity, inflammation, and other functions [[5]–[7]]. Insulin sensitivity and inflammation have been shown to influence both growth [[8]–[10]] and ovarian function;
Insulin 45111 functionAdiponectinAdipocytesPlacentaOsteoblastsCardiomyocytesAnti-inflammatory functions [[30]–[33]]Fatty acid oxidation [[22]] Insulin sensitivity [[24]] Glucose metabolism [[24]–[29]]Pubertal onset and regulation [[104], [105]]Leptin
Insulin 45504 [[39]–[41]]Resistin Peripheral-blood mononuclear cellsPlacentaRegulation of inflammatory response [[43], [48], [50]] Insulin resistance [[44]–[46]]Ovarian function and PCOS [[55]]VisfatinAdipose tissueLiverMuscleKidneyHeartBone
Insulin 45674 [[55]]VisfatinAdipose tissueLiverMuscleKidneyHeartBone marrowPlacentaRegulation of inflammatory responses [[51]] Insulin resistanceGlucose metabolism [[52]]Ovarian function and PCOS [[55]]Table 2Role of adipokines in fetal
cortisol 7164 evening and early morning and shows relationships with other hormones having a circadian rhythm such as cortisol . The relationship between these two hormones is explained by the direct stimulatory action that leptin
testosterone 31250 The authors of this study further showed a negative correlation between adiponectin concentrations, testosterone , and dehydroepiandrosterone sulfate serum levels; however, pubertal stage was shown to be the strongest
testosterone 31452 the strongest independent predictor of adiponectin concentrations, followed by body mass index and testosterone . This model did not seem to fit for female pubertal development. Experimental data have shown for testosterone,
testosterone 31563 testosterone. This model did not seem to fit for female pubertal development. Experimental data have shown for testosterone , but not for estrogens, an inhibitory action on adiponectin secretion from adipocytes, confirming a
testosterone 32654 puberty in healthy boys leptin concentrations rise by approximately 50% even before the increase in testosterone , LH, and FSH and then subsequently decline to baseline values [[107]–[110]].In addition, nocturnal
testosterone 35887 Leptin also has a similar action in male gonadal tissue, with a dose-dependent inhibitory effect on testosterone production from Leydig cells as demonstrated in rats [[119]]. Therefore, leptin would have a bimodal
testosterone 39044 further described a positive correlation between leptin, BMI, bone age, testicular volume, FSH, LH, and testosterone concentrations confirming previous findings.Therefore, sexual immaturity in adolescents with CDGP seems
testosterone 46257 describedControversial [[88]]Table 3Role of adipokines in puberty.AdipokineGnRH, LH, and FSHEstradiol (E2) and testosterone (T)Adiponectin AdipoR2 is regulated by the LH receptor function via a cAMP dependent mechanism [[132]].T
testosterone 47589 non-PCOS controls.Low levels of adiponectin in PCOS are probably related to insulin resistance but not to testosterone levels. Total adiponectin should not be used as a biomarker of PCOS severity.Further investigations
Select Disease Character Offset Disease Term Instance
Precocious puberty 26609 have explored the relationship between precocious puberty and pubertal growth in children born SGA. Precocious puberty causes advanced bone maturation, accelerated closing of epiphysis, and may compromise adult height.
diabetes mellitus 9487 [[43]].Resistin was first described as a factor contributing to the development of insulin resistance and diabetes mellitus in humans; a debate is still ongoing regarding its exact role in obesity, in insulin sensitivity, and
diabetes mellitus 9636 ongoing regarding its exact role in obesity, in insulin sensitivity, and in the development of type 2 diabetes mellitus (DM2) [[44]]. Resistin may represent a link between inflammatory processes and metabolic signals. Circulating
diabetes mellitus 20275 hyperglycaemic pregnant women [[80]]. These mechanisms could further confirm why newborns exposed to gestational diabetes mellitus have an increased risk of developing obesity and T2DM [[58], [81]].3.3. ResistinYura et al. [[82]] and
hyperandrogenism 27249 have been described to have more frequently than the general population idiopathic functional ovarian hyperandrogenism and hyperinsulinism at 18 years of age [[95]].Neville and Walker [[96]], in a retrospective Australian
hyperandrogenism 39506 women during reproductive age [[125]]. It is classically characterized by three distinctive features: hyperandrogenism , ovarian dysfunction, and polycystic morphology pattern of ovaries on ultrasound scan [[126]]. A pivotal
hyperandrogenism 39935 hypothalamic-pituitary-gonadal axis, many authors have suggested a central role for adipokines in the development of hyperandrogenism and infertility in PCOS. Obese women are more prone to developing PCOS, and considering that these subjects
hyperandrogenism 41078 secretion and that disruption of adiponectin and its pathway may play an important part in the onset of hyperandrogenism in PCOS.In addition, several authors have reported a correlation between lower adiponectin concentrations
hyperandrogenism 47330 suggesting that disruption of adiponectin and/or its receptors plays a key role in pathogenesis of hyperandrogenism in PCOS.Toulis et al. [[129]]AdiponectinMeta analysisIn vivo/humansAdiponectin levels seem to be lower
hyperglycemia 16314 [[64]].Interestingly, adiponectin gene DNA methylation has been shown to be influenced by maternal hyperglycemia [[58], [69]]. Bouchard et al. described lower methylation in the promoter of the adiponectin gene on
metabolic syndrome 695 mononuclear cells, liver, muscle, kidney, heart, and bone marrow. Adipokines play a significant role in the metabolic syndrome and in cardiovascular diseases, have implications in regulating insulin sensitivity and inflammation,
metabolic syndrome 2760 as being born small for gestational age are associated with an increased risk of insulin resistance, metabolic syndrome , and poor growth [[15], [16]]. Since Barker's theory on the fetal origin of adult disease, it has become
metabolic syndrome 5314 reduction in adiponectin levels plays a causal role in the development of insulin resistance (IR), metabolic syndrome , type 2 diabetes, and atherosclerosis. Plasma adiponectin levels are decreased in obesity. In the skeletal
metabolic syndrome 5874 levels are commonly observed in a variety of states frequently associated with insulin resistance and metabolic syndrome as shown by von Frankenberg et al. who demonstrated that adiponectin levels decrease by increasing the
metabolic syndrome 6006 von Frankenberg et al. who demonstrated that adiponectin levels decrease by increasing the number of metabolic syndrome criteria [[5]].Obesity is well known to be characterized by a state of low grade chronic inflammation.
metabolic syndrome 37501 association between premature pubarche and later development of insulin resistance, dyslipidemia, PCOS, and metabolic syndrome (especially in patients born small for gestational age); however, in most cases, it represents a variant
obesity 4715 knockout AdipoRs mice exhibit insulin resistance [[24]].In addition, AdipoRs are also decreased in obesity ; several authors have demonstrated that expression of both AdipoR1 and AdipoR2 are significantly decreased
obesity 5415 metabolic syndrome, type 2 diabetes, and atherosclerosis. Plasma adiponectin levels are decreased in obesity . In the skeletal muscle, adipokines increase expression of fatty-acid transport and, by activation of
obesity 6224 inflammation. Interestingly, adiponectin has been shown to have an anti-inflammatory action and is reduced in obesity . Adiponectin primarily acts modulating macrophage function suppressing TNF-alpha secretion by inhibiting
obesity 6719 inhibit production of many proinflammatory cytokines [[32], [33]]. Summarizing, low adiponectin in obesity may contribute to explaining inflammation in these patients.2.2. LeptinLeptin is the 167-amino acid
obesity 8480 levels present during these hours [[39], [40]].The absence of leptin or mutations in its receptor induce obesity and hyperphagia. Leptin deficient humans are obese, diabetic, and infertile [[41]]. This adipokine may
obesity 9570 insulin resistance and diabetes mellitus in humans; a debate is still ongoing regarding its exact role in obesity , in insulin sensitivity, and in the development of type 2 diabetes mellitus (DM2) [[44]]. Resistin may
obesity 9800 between inflammatory processes and metabolic signals. Circulating levels of resistin are increased in obesity . Many authors indicate a solid association between this adipokine and insulin resistance [[45], [46]].
obesity 16207 fetal growth, is the inverse correlation described between its serum levels and gestational diabetes or obesity [[64]].Interestingly, adiponectin gene DNA methylation has been shown to be influenced by maternal hyperglycemia
obesity 16596 hyperglycaemia, suggesting that this could contribute to the increased risk of reduced insulin sensitivity, obesity , and diabetes in the offspring in postnatal life [[69]].3.2. LeptinExpression of leptin is widespread
obesity 20330 confirm why newborns exposed to gestational diabetes mellitus have an increased risk of developing obesity and T2DM [[58], [81]].3.3. ResistinYura et al. [[82]] and Lappas et al. [[83]] showed that resistin
obesity 24376 still remain unknown. Many authors report a relationship between increasing rates of overweight and obesity in childhood and a trend towards an anticipation of pubertal onset, especially in girls. These observations
obesity 26034 presenting a final height below their midparental height, as well as developing cardiovascular disease, obesity , diabetes, and other metabolic disorders [[89]].Postnatal growth of SGA children has been analyzed in
obesity 32489 congenital leptin deficiency, due to mutations in leptin gene or leptin receptor gene, cause early-onset obesity and absence of pubertal development [[106]]. At onset of puberty in healthy boys leptin concentrations
ovarian dysfunction 39524 reproductive age [[125]]. It is classically characterized by three distinctive features: hyperandrogenism, ovarian dysfunction , and polycystic morphology pattern of ovaries on ultrasound scan [[126]]. A pivotal role in the pathophysiology
ovarian dysfunction 41345 women with PCOS compared with controls [[129]].Leptin has been thought to play a role in the onset of ovarian dysfunction in obese subjects, as previously mentioned; hyperleptinemia might interfere with estrogen production
polycystic ovary syndrome 40374 summarize the role of several adipokines in the pathogenesis of PCOS [[127]].The role of adiponectin in polycystic ovary syndrome is still debated. Several studies have reported that adiponectin levels in women with PCOS are lower
type 2 diabetes mellitus 9629 still ongoing regarding its exact role in obesity, in insulin sensitivity, and in the development of type 2 diabetes mellitus (DM2) [[44]]. Resistin may represent a link between inflammatory processes and metabolic signals. Circulating

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