Role of hormonal and inflammatory alterations in obesity-related reproductive dysfunction at the level of the hypothalamic-pituitary-ovarian axis.

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hyperinsulinemia 1 endocrinologydiseases
metabolic syndrome 2 endocrinologydiseases
Insulin 10 endocrinologydiseasesdrugs
diabetes mellitus 2 endocrinologydiseases
ovarian dysfunction 7 endocrinologydiseases
testosterone 1 endocrinologydiseasesdrugs
type 2 diabetes mellitus 1 endocrinologydiseases
hyperandrogenism 2 endocrinologydiseases
obesity 37 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 5536 associated with growth velocity, [[23]] possibly through the stimulation of the growth hormone – Insulin like growth factor 1 (IGF-1) axis [[24], [25]].Obesity and the HPO axisIt has been thought that obesity
Insulin 19668 every level of the reproductive axis making it a great therapeutic target for ovulatory dysfunction. Insulin Insulin is a 51 amino acid protein synthesized in the beta islet cells of the pancreas. Its release is
Insulin 19675 level of the reproductive axis making it a great therapeutic target for ovulatory dysfunction.Insulin Insulin is a 51 amino acid protein synthesized in the beta islet cells of the pancreas. Its release is stimulated
Insulin 19896 glucose in the gastrointestinal tract from ingestion, as well as various amino acids directly [[116]]. Insulin levels rise and its sensitivity decreases with obesity [[116]]. Insulin resistance, in conjunction with
Insulin 19968 amino acids directly [[116]]. Insulin levels rise and its sensitivity decreases with obesity [[116]]. Insulin resistance, in conjunction with obesity, impacts reproduction. While not a direct adipokine, adipose
Insulin 20332 in turn leads to increased free circulating steroid hormone levels, such as estrogens and androgens. Insulin increases androgen production by two independent pathways; first by up-regulating CYP17A1 enzymes, which
Insulin 20633 insulin augments LH action on the ovary to increase androgen production and secretion [[118], [119]]. Insulin resistance is associated with higher leptin levels [[38]]. As noted previously, higher circulating leptin
Insulin 20830 circulating leptin levels lead to leptin resistance which in turn leads to greater insulin resistance. Insulin acts on the pituitary to modulate the GnRH receptor and increases LH secretion after GnRH stimulation
Insulin 20949 pituitary to modulate the GnRH receptor and increases LH secretion after GnRH stimulation [[120]]. Insulin augments FSH activity by increasing ovarian steroidogenesis and inducing LH responsiveness [[121]].
Insulin 21161 Hyperinsulinemia is consequently associated with elevated basal LH levels and hyperandrogenism [[119]]. Insulin alone does not have an effect on ovarian response to gonadotropic hyperstimulation during IVF in women
testosterone 16651 effect on progesterone secretion [[97]], but it recently has been found to stimulate estradiol and testosterone secretion in catfish [[98]]. Data pertaining to the direct effect of NPY and AgRP on ovarian steroidogenesis
Select Disease Character Offset Disease Term Instance
diabetes mellitus 2229 health care expenditures by the year 2030 [[2]]. This is due to obesity-related comorbidities such as diabetes mellitus , hypertension, dyslipidemia, and cardiovascular disease [[3]]. Besides these chronic disorders, obesity
diabetes mellitus 17632 certain genetic polymorphisms, have been linked to insulin resistance, metabolic syndrome and type 2 diabetes mellitus [[103]–[105]]. Interestingly, the adiponectin gene is located at 3q27, near the diabetes susceptibility
hyperandrogenism 21135 responsiveness [[121]]. Hyperinsulinemia is consequently associated with elevated basal LH levels and hyperandrogenism [[119]]. Insulin alone does not have an effect on ovarian response to gonadotropic hyperstimulation
hyperandrogenism 21518 severe insulin resistance, as seen in some genetic disorders, is associated with enlarged ovaries and hyperandrogenism independent of gonadotropin levels. Elevated insulin levels over a long period of time can lead to increased
hyperinsulinemia 22129 pituitary is still sensitive to changes in insulin levels despite peripheral insulin resistance and basal hyperinsulinemia [[120]].Disruption of insulin signaling in diet-induced obesity improves reproductive cyclicity in mice,
metabolic syndrome 17602 adiponectin levels, as seen in certain genetic polymorphisms, have been linked to insulin resistance, metabolic syndrome and type 2 diabetes mellitus [[103]–[105]]. Interestingly, the adiponectin gene is located at 3q27,
metabolic syndrome 24088 through smoking [[132]]. AGE levels are elevated in chronic diseases such as type 2 Diabetes Mellitus, metabolic syndrome , cardiovascular disease, and neurodegenerative disorders [[133]–[135]]. AGEs have also been studied
obesity 101 Title: Reproductive Biology and Endocrinology : RB&ERole of hormonal and inflammatory alterations in obesity -related reproductive dysfunction at the level of the hypothalamic-pituitary-ovarian axisMichelle GoldsammlerZaher
obesity 424 (collection): /2018AbstractBackgroundBesides being a risk factor for multiple metabolic disorders, obesity could affect female reproduction. While increased adiposity is associated with hormonal changes that
obesity 628 that could disrupt the function of the hypothalamus and the pituitary, compelling data suggest that obesity -related hormonal and inflammatory changes could directly impact ovarian function.ObjectiveTo review
obesity 790 directly impact ovarian function.ObjectiveTo review the available data related to the mechanisms by which obesity , and its associated hormonal and inflammatory changes, could affect the female reproductive function
obesity 1061 axis.MethodsPubMed database search for publications in English language until October 2017 pertaining to obesity and female reproductive function was performed.ResultsThe obesity-related changes in hormone levels,
obesity 1127 until October 2017 pertaining to obesity and female reproductive function was performed.ResultsThe obesity -related changes in hormone levels, in particular leptin, adiponectin, ghrelin, neuropeptide Y and agouti-related
obesity 1539 monocyte chemotactic protein-1 (MCP-1) are emerging as relatively new players in the pathophysiology of obesity -related ovarian dysfunction.ConclusionThere is an intricate crosstalk between the adipose tissue and
obesity 1800 Understanding the mechanisms behind this crosstalk could lead to potential therapies for the common obesity -related reproductive dysfunction.BackgroundAccording to a recent population study, approximately 39%
obesity 2075 the ages of 2–19 are obese [[1]]. Obesity causes a huge economic burden where it is estimated that obesity will add 48–66 billion dollars in related health care expenditures by the year 2030 [[2]]. This is
obesity 2191 48–66 billion dollars in related health care expenditures by the year 2030 [[2]]. This is due to obesity -related comorbidities such as diabetes mellitus, hypertension, dyslipidemia, and cardiovascular disease
obesity 2343 mellitus, hypertension, dyslipidemia, and cardiovascular disease [[3]]. Besides these chronic disorders, obesity is also associated with reproductive and obstetric complications such as menstrual irregularities, subfertility,
obesity 2615 obstetrical and perinatal outcomes [[4]–[7]]. This review will focus on the relationship between obesity and female reproductive function with a focus on alterations in the hypothalamic pituitary ovarian (HPO)
obesity 2758 with a focus on alterations in the hypothalamic pituitary ovarian (HPO) axis and the direct effect of obesity -related inflammatory processes on ovarian function.Normal HPO AxisThe female reproductive physiology
obesity 5640 Insulin like growth factor 1 (IGF-1) axis [[24], [25]].Obesity and the HPO axisIt has been thought that obesity changes the expected time course of puberty and leads to earlier thelarche, adrenarche and menarche
obesity 6187 androgens to estrogens. Population studies have demonstrated a trend for earlier menarche, due to the obesity epidemic, over the past 30 years [[31]], highlighting the potential for significant increase in health
obesity 6790 mean LH release without changing its frequency, leading to impaired luteal phase [[35]]. Additionally, obesity may affect various components of the HPO axis, and may have direct effect on ovarian function independent
obesity 14682 decrease in corpus luteum number in a rat model [[84]]. Additionally, ghrelin, with its connection to obesity , is related to insulin regulation and insulin resistance where it decreases insulin secretion and sensitivity
obesity 18237 [[107]]. This inflammation in turn contributes to both insulin and leptin resistance, promoting further obesity and subsequently diabetes [[107]]. In fact, in obese women adiponectin levels are low and pro-inflammatory
obesity 19951 well as various amino acids directly [[116]]. Insulin levels rise and its sensitivity decreases with obesity [[116]]. Insulin resistance, in conjunction with obesity, impacts reproduction. While not a direct adipokine,
obesity 20008 levels rise and its sensitivity decreases with obesity [[116]]. Insulin resistance, in conjunction with obesity , impacts reproduction. While not a direct adipokine, adipose tissue stimulates pancreatic beta islet
obesity 22202 insulin resistance and basal hyperinsulinemia [[120]].Disruption of insulin signaling in diet-induced obesity improves reproductive cyclicity in mice, suggesting that insulin represents a mediator for pituitary
obesity 22331 cyclicity in mice, suggesting that insulin represents a mediator for pituitary LH dysregulation in obesity [[120]]. Further study of insulin at the level of the ovary, specifically in insulin receptor knockout
obesity 23661 with insulin resistance [[128]].The pro-inflammatory AGEs may be part of the link between diet-induced obesity and inflammation, with AGEs inducing MCP-1 gene expression [[129]] thus forming the AGEs/MCP-1 axis.
obesity 24818 reflected by prolonged diestrus phase (unpublished data). We have also shown that high-fat diet induced obesity leads to ovulatory dysfunction in mice, as demonstrated by fewer oocytes ovulated following superovulation
obesity 25183 ingestion of a high-fat diet, suggesting that lack of MCP-1 may be protective against high-fat- and obesity -induced ovarian dysfunction. Further supporting this hypothesis, we showed that elevated serum MCP-1
obesity 25692 fewer embryos and lower ongoing pregnancy rate [[137]]. Taken together, these observations suggest that obesity may have direct deleterious effects on the ovaries partly through activation of inflammatory AGE/MCP-1
obesity 25829 effects on the ovaries partly through activation of inflammatory AGE/MCP-1 axis.Relationship between obesity and assisted reproductive technology (ART) outcomePopulation studies on the clinical sequelae of obesity
obesity 25934 obesity and assisted reproductive technology (ART) outcomePopulation studies on the clinical sequelae of obesity provide a connection between obesity and subfertility. Several studies indicated that obesity is a risk
obesity 25971 technology (ART) outcomePopulation studies on the clinical sequelae of obesity provide a connection between obesity and subfertility. Several studies indicated that obesity is a risk factor for ovulatory dysfunction
obesity 26028 sequelae of obesity provide a connection between obesity and subfertility. Several studies indicated that obesity is a risk factor for ovulatory dysfunction [[141]–[143]]. For women who ovulate regularly, obesity
obesity 26129 obesity is a risk factor for ovulatory dysfunction [[141]–[143]]. For women who ovulate regularly, obesity increases the time to conception; for instance, a high waist- height ratio decreases fecundity by 30%
obesity 27000 ART interventions [[147]]. Obesity could also impact ovarian reserve markers. Studies have shown that obesity is negatively correlated with serum AMH [[148], [149]], FSH, LH and inhibin B levels [[150]]. These
obesity 28683 outcomes observed in obese patients are quite intriguing. These observations suggest that the effect of obesity on ovarian function is not solely dependent on the HPO axis, since gonadotropins are supplied exogenously
obesity 29726 given high-fat diet ovulated fewer oocytes following superovulation, further supporting the notion that obesity may have direct effect on ovaries, independent of HPO axis. Clearly the data to date demonstrates that
obesity 29837 have direct effect on ovaries, independent of HPO axis. Clearly the data to date demonstrates that obesity affects ART outcome in women undergoing IVF possibly via actions on all aspects: oocyte, embryo and
obesity 29985 IVF possibly via actions on all aspects: oocyte, embryo and endometrium.ConclusionWith the uncurbed obesity epidemic, more reproductive-aged women will face metabolic and reproductive complications. Body energy
obesity 30643 reproductive dysfunction associated with adiposity and may provide, along with MCP-1, a crucial link between obesity and ovarian macrophage infiltration. Each of these molecules and their prospective pathways may represent
ovarian dysfunction 1555 protein-1 (MCP-1) are emerging as relatively new players in the pathophysiology of obesity-related ovarian dysfunction .ConclusionThere is an intricate crosstalk between the adipose tissue and the inflammatory system with
ovarian dysfunction 7069 following sections the changes that occur in the metabolic and inflammatory systems that are related to ovarian dysfunction .LeptinLeptin is a 16-kDa adipokine secreted primarily by white adipose tissue, although it can be secreted
ovarian dysfunction 18926 upregulation of VEGF and COX-2 expression in the periovulatory ovary [[109]]. Adiponectin knockout mice show ovarian dysfunction reflected by fewer oocytes, more atretic follicles, prolonged diestrus cycles and decreased LH receptor
ovarian dysfunction 24995 oocytes ovulated following superovulation compared to mice on normal chow diet (controls) [[139]]. This ovarian dysfunction was not observed in MCP-1 knockout mice that became obese following ingestion of a high-fat diet, suggesting
ovarian dysfunction 25199 high-fat diet, suggesting that lack of MCP-1 may be protective against high-fat- and obesity-induced ovarian dysfunction . Further supporting this hypothesis, we showed that elevated serum MCP-1 levels were associated with
ovarian dysfunction 31356 problem, is an overwhelming condition that causes reproductive disturbances in women in part due to ovarian dysfunction . Losing weight is commonly challenging and often not sustainable. Thus there is a need to establish
ovarian dysfunction 31490 is commonly challenging and often not sustainable. Thus there is a need to establish therapies for ovarian dysfunction and to improve ovarian health in the obese patient population
type 2 diabetes mellitus 17625 seen in certain genetic polymorphisms, have been linked to insulin resistance, metabolic syndrome and type 2 diabetes mellitus [[103]–[105]]. Interestingly, the adiponectin gene is located at 3q27, near the diabetes susceptibility

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