Obesity as disruptor of the female fertility.

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Term Occurence Count Dictionary
polycystic ovary syndrome 3 endocrinologydiseases
rosiglitazone 1 endocrinologydiseasesdrugs
Insulin 4 endocrinologydiseasesdrugs
hyperandrogenism 11 endocrinologydiseases
metabolic syndrome 2 endocrinologydiseases
obesity 49 endocrinologydiseases
osteoporosis 2 endocrinologydiseases
ovarian dysfunction 1 endocrinologydiseases
Laron syndrome 1 endocrinologydiseases
diabetes mellitus 2 endocrinologydiseases
estrogen excess 1 endocrinologydiseases
hyperinsulinemia 11 endocrinologydiseases
hyperlipidemia 1 endocrinologydiseases
hyperthyroidism 1 endocrinologydiseases
hypothyroidism 1 endocrinologydiseases
metformin 4 endocrinologydiseasesdrugs
testosterone 5 endocrinologydiseasesdrugs
type 2 diabetes mellitus 2 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 26439 resistance. This figure illustrates the complex interactions underlying the pathophysiology of PCOS. Insulin resistance and the resulting hyperinsulinemia are responsible for the majority of the changes found
Insulin 26556 resistance and the resulting hyperinsulinemia are responsible for the majority of the changes found in PCOS. Insulin resistance in PCOS does not occur in all tissues, but rather appears to be tissue-specific. Skeletal-muscle
Insulin 27536 serum. Therefore, insuline resistance whith compensatory hyperinsulinemia results in hyperandrogenemia Insulin can bind IGF-I receptors (IGF-IR) as well as its own receptors and activates the tyrosine kinase of
Insulin 28214 final effect of enhancing the androgen production by theca interstitial and stromal cells Fig. 3.Fig. 3 Insulin receptor tyrosine kinases. The α subunit binds insulin and the β transmits a signal from bound insulin
metformin 46020 ameliorate the reproductive, and metabolic disorders, typical of the obese patient [[74]]. The action of metformin is widely discussed in the literature, which is considered as the first-line medication for the treatment
metformin 46182 considered as the first-line medication for the treatment of type 2 diabetes. Women with PCOS receiving metformin improved pregnancy outcomes, and this has been attributed to its ability to reduce the insulin resistance
metformin 46501 in improvement of oocyte quality and folliculogenesis for amelioration of PCOS.The major effects of metformin include its property to decrease the liver glucose production by suppressing hepatic gluconeogenesis
metformin 46724 the increase of insulin sensitivity and peripheral glucose uptake [[75]]. The molecular mechanism of metformin is incompletely understood. Multiple potential mechanisms of action have been proposed, including; inhibition
rosiglitazone 22271 PCOS. A randomized placebo-controlled study recently showed that treatment with the insulin sensitizer rosiglitazone significantly reduces the serum resistin levels in overweight women with PCOS, thus implying the contribution
testosterone 11019 resistance as well as in regulating the menstrual cyclicity, ovulation and fertility due to the lowered testosterone levels and increase of sex hormone binding globulin (SHBG), the intensively exerted agonistic sports
testosterone 27414 suppress hepatic production of sex hormone-binding globulin (SHBG), the primary binding protein for testosterone in the serum. Therefore, insuline resistance whith compensatory hyperinsulinemia results in hyperandrogenemiaInsulin
testosterone 32318 follicles does not seem to be influenced by insulin and body mass in these patients 46].Lastly, free testosterone (FT) levels are usually higher in obese premenopausal women without hyrsutism and normal/lower circulating
testosterone 32707 concentrations of FT may have a negative effect on fertility. DHEA is a hormone intermediary in the testosterone - and estrogen-pathway. Its plasma levels are significantly lower in morbid obesity [[47]], and are inversely
testosterone 47917 of weight loss results in significant improvement of endocrine parameters, such as decrease of free testosterone , and LH and insulin levels, with the improvement of ovulation frequency [[78]].Sim and collaborators
Select Disease Character Offset Disease Term Instance
Laron syndrome 29692 anovulation in these patients.A nature-experiment of the association obesity/infertility is related to the Laron syndrome (LS), a rare autosomal recessively inherited disease described in consanguineous families originating
diabetes mellitus 18011 these factors have been shown to be strongly associated with both insulin resistance (IR) and type 2 diabetes mellitus (T2DM) and in patients with the PCOS, a severe dysfunction of adipose tissue has been observed leading
diabetes mellitus 24060 omentin-2 are located as adjacent to each other at 1q22-q23, exactly in the region linked to type 2 diabetes mellitus . Both omentin homologues as circulating forms correlate with expression in visceral fat tissue [[37]].
estrogen excess 29529 estrogen production, due to peripheral conversion, impairs the function of HPG axis and renders both estrogen excess and hyperandrogenism as major causes of anovulation in these patients.A nature-experiment of the association
hyperandrogenism 24541 reproduction’s physiology is unclear.Dysendocrine effects of obesity: hyper- and hypo-androgenismObesity, hyperandrogenism and anovulation - Obesity, body fat location as upper versus lower body disposition, and muscle mass
hyperandrogenism 24830 majority of obese women have normal ovulatory menstrual cycles, remain fertile and have no apparent hyperandrogenism thus suggesting that obesity per se is not the only factor involved in the genesis of hyperandrogenism
hyperandrogenism 24933 hyperandrogenism thus suggesting that obesity per se is not the only factor involved in the genesis of hyperandrogenism and ovulatory dysfunction. However, elevated androgen levels in obese women appear to be a common finding
hyperandrogenism 25159 the presence of amenorrhea. The mechanism by which the excess adipose tissue can be associated with hyperandrogenism remains controversial although the hyperinsulinemia plays a primary role in influencing obesity in hyperandrogenism.Hyperinsulinemia
hyperandrogenism 25275 remains controversial although the hyperinsulinemia plays a primary role in influencing obesity in hyperandrogenism .Hyperinsulinemia and insulin resistance are the underlying causes that lead to obesity, accompanied
hyperandrogenism 25395 hyperandrogenism.Hyperinsulinemia and insulin resistance are the underlying causes that lead to obesity, accompanied by hyperandrogenism and alterations in steroidogenesis, in those patients with stromal hyperplasia of the ovaries. Both
hyperandrogenism 25533 steroidogenesis, in those patients with stromal hyperplasia of the ovaries. Both hyperinsulinemia and hyperandrogenism affect the ovarian function in both obese and non-obese women although the mechanism by which how hyperandrogenism
hyperandrogenism 25648 hyperandrogenism affect the ovarian function in both obese and non-obese women although the mechanism by which how hyperandrogenism and/or hyperinsulinemia inhibit the regular ovulation has not been fully understood. It has been experimentally
hyperandrogenism 26061 stromal cells, thus priming the production of extradiol [[38]] Fig. 2. Another proposed mechanism of hyperandrogenism induced by hyperinsulinemia, which can be found in the PCOS patient obese or not, occurs through the
hyperandrogenism 29549 due to peripheral conversion, impairs the function of HPG axis and renders both estrogen excess and hyperandrogenism as major causes of anovulation in these patients.A nature-experiment of the association obesity/infertility
hyperandrogenism 31125 fertility in obesity have been completed in hyperandrogenic women, very few studies examined women without hyperandrogenism and/or with normal menstrual cycle.One cross-sectional study performed in more than 250 overweight and
hyperinsulinemia 14300 of the increased peripheral aromatization of androgens to estrogens while the insulin resistance and hyperinsulinemia lead to hyperandrogenemia. Furthermore, the sex hormone-binding globulin (SHBG), growth hormone (GH),
hyperinsulinemia 25211 the excess adipose tissue can be associated with hyperandrogenism remains controversial although the hyperinsulinemia plays a primary role in influencing obesity in hyperandrogenism.Hyperinsulinemia and insulin resistance
hyperinsulinemia 25512 and alterations in steroidogenesis, in those patients with stromal hyperplasia of the ovaries. Both hyperinsulinemia and hyperandrogenism affect the ovarian function in both obese and non-obese women although the mechanism
hyperinsulinemia 25672 function in both obese and non-obese women although the mechanism by which how hyperandrogenism and/or hyperinsulinemia inhibit the regular ovulation has not been fully understood. It has been experimentally shown that insulin
hyperinsulinemia 26089 the production of extradiol [[38]] Fig. 2. Another proposed mechanism of hyperandrogenism induced by hyperinsulinemia , which can be found in the PCOS patient obese or not, occurs through the insulin-like growth factor-I
hyperinsulinemia 26476 the complex interactions underlying the pathophysiology of PCOS. Insulin resistance and the resulting hyperinsulinemia are responsible for the majority of the changes found in PCOS. Insulin resistance in PCOS does not occur
hyperinsulinemia 26865 increased lipolysis, respectively, whereas the ovary, adrenal and liver remain insulin sensitive. In PCOS, hyperinsulinemia occurs as a compensatory response to insulin resistance. This resulting hyperinsulinemia has a stimulatory
hyperinsulinemia 26954 sensitive. In PCOS, hyperinsulinemia occurs as a compensatory response to insulin resistance. This resulting hyperinsulinemia has a stimulatory effect on the ovaries and adrenal glands that leads to enhanced androgen production
hyperinsulinemia 27289 to luteinizing hormone (LH) stimulation, resulting in follicular arrest and anovulation. In contrast hyperinsulinemia acts to suppress hepatic production of sex hormone-binding globulin (SHBG), the primary binding protein
hyperinsulinemia 27491 primary binding protein for testosterone in the serum. Therefore, insuline resistance whith compensatory hyperinsulinemia results in hyperandrogenemiaInsulin can bind IGF-I receptors (IGF-IR) as well as its own receptors and
hyperinsulinemia 31821 is the most predictive parameter of oligomenorrhea in apparently fertile women, independently from hyperinsulinemia , insulin resistance or other parameters. However, obese non-hyperandrogenic women, even with normal
hyperlipidemia 30435 visceral fat, the majority of patients with LS progressively develop signs of metabolic syndrome as hyperlipidemia and non-alcoholic fatty liver disease. Based on this deeply altered metabolism of lipids, the women
hyperthyroidism 4521 well as ovulatory disorders dependent on extraovarian pathologies including either hypothyroidism or hyperthyroidism .Tubal infections– The factors responsible for tubal disease are different and derive from post-infection
hypothyroidism 4503 ovarian cysts as well as ovulatory disorders dependent on extraovarian pathologies including either hypothyroidism or hyperthyroidism.Tubal infections– The factors responsible for tubal disease are different and derive
metabolic syndrome 23095 visfatin is significantly increased in both overweight and obese subjects, or in patients with T2DM and metabolic syndrome [[35]]. It has been also reported that the gene expression and the circulating levels of visfatin are
metabolic syndrome 30413 both subcutaneous and visceral fat, the majority of patients with LS progressively develop signs of metabolic syndrome as hyperlipidemia and non-alcoholic fatty liver disease. Based on this deeply altered metabolism of
obesity 281 (epub): 3/2018Publication date (pmc-release): 3/2018Publication date (collection): /2018AbstractBoth obesity and overweight are increasing worldwide and have detrimental influences on several human body functions
obesity 721 the hormone disorders and subfertility that are common in the polycystic ovary syndrome (PCOS), in obesity the adipocytes act as endocrine organ. The adipose tissue indeed, releases a number of bioactive molecules,
obesity 3165 influence of the altered metabolic state on the reproductive health of women, focusing the effects of obesity on fertility, and the management of infertility in obese and overweight women.Pathophysiology of the
obesity 3656 hypercaloric nutrition usually resulting in metabolic derangements and increase in the body weight promoting obesity .Below are listed the major causes of infertility belonging to both of these pathogenic conditions as
obesity 9514 to conceive is longer in women with BMI over 25 kg/m2 or, vice versa, less than 19 kg/m2, and that obesity and overweight are significantly associated with decreased pregnancy rates, increased requirements for
obesity 12073 this field emphasize the role of lifestyle factors in affecting the woman fertility and particularly obesity may represent a major condition in which both alteration of metabolic pathways and inflammatory factors
obesity 12306 oocyte viability leading to subfertility or infertility.Molecular and endocrinological influence of obesity on woman fertilityIn female mammals, a number of evolutionary mechanisms are enrolled to integrate environmental,
obesity 13460 greater than 25 kg/m2, it is considered overweight, whereas the BMI higher than 30 kg/m2 defines obesity [[19]]. The WHO reports that 60% of women are overweight in the United States and in most European countries
obesity 13724 Moreover, 6% of all women are morbidly obese (BMI ≥ 35 kg/m2) [[20]]. The negative effects of obesity on the reproductive physiology are known, since obese women frequently undergo menstrual irregularity
obesity 13913 menstrual irregularity with ovulatory disorders, endometrial pathology, and infertility.The impact of obesity on reproductive function, especially ovulatory disorders, are mainly attributable to endocrine mechanisms
obesity 15667 fertility in obese women seems to be impaired also in assisted conception programs. In fact, overweight and obesity are also associated with negative outcomes for patients undergoing in vitro fertilization (IVF) due
obesity 16034 loss in order to improve the fertility functions [[26]].The molecular and endocrinological aspects of obesity , its effects and consequences on the reproductive system as well as benefits from modifying lifestyles
obesity 19282 energy expenditure mainly via its direct effects on hypothalamic neurons, and is thus considered an anti- obesity hormone. Its levels decrease with fasting and increase after food intake [[27]].Fig. 1Functional properties
obesity 20068 both estrogen and progesterone production in a dose-dependent manner [[28]]. This negative effect of obesity on the oocyte physiology could have downstream effects on endometrial receptivity and embryo implantation.Adiponectin-
obesity 20864 role in modulating the central reproductive endocrine axis [[30]].Circulating APN levels decrease with obesity and increase with weight loss and major effects of APN are devoted to increase the insulin sensitivity
obesity 21584 contribution to implantation failures and pregnancy loss in women with maternal metabolic conditions such as obesity and PCOS [[32]].Resistin- Resistin is a small cysteine-rich 94-amino acid polypeptide. This adipokine
obesity 21733 small cysteine-rich 94-amino acid polypeptide. This adipokine is considered a potential link between obesity and T2DM as result of its inhibitory effect on adipocyte differentiation and its association with IR.
obesity 22553 during treatment [[34]]. In summary, resistin seems to be an important adipokine that is involved in obesity , IR, PCOS and endocrine dysfunction.Visfatin- Visfatin is a protein expressed by a variety of tissues
obesity 24496 metabolism. Its role, however, in the reproduction’s physiology is unclear.Dysendocrine effects of obesity : hyper- and hypo-androgenismObesity, hyperandrogenism and anovulation - Obesity, body fat location as
obesity 24868 ovulatory menstrual cycles, remain fertile and have no apparent hyperandrogenism thus suggesting that obesity per se is not the only factor involved in the genesis of hyperandrogenism and ovulatory dysfunction.
obesity 25264 hyperandrogenism remains controversial although the hyperinsulinemia plays a primary role in influencing obesity in hyperandrogenism.Hyperinsulinemia and insulin resistance are the underlying causes that lead to obesity,
obesity 25371 in hyperandrogenism.Hyperinsulinemia and insulin resistance are the underlying causes that lead to obesity , accompanied by hyperandrogenism and alterations in steroidogenesis, in those patients with stromal
obesity 29398 arrest result in menstrual cycle disorders and oligo-anovulation which appears strictly related to the obesity [[40]]. The increased estrogen production, due to peripheral conversion, impairs the function of HPG
obesity 29654 hyperandrogenism as major causes of anovulation in these patients.A nature-experiment of the association obesity /infertility is related to the Laron syndrome (LS), a rare autosomal recessively inherited disease described
obesity 30177 [[42]]. However, one of the intriguing characteristics of LS, in addition to dwarfism, is the chronic obesity which occurs in early childhood and does not decrease with long-term IGF-I treatment. In parallel with
obesity 30791 Therefore, given the tight interconnection between energy metabolism and reproduction, the impact that obesity induces on fertility in these women can be considered an aggravating factor in this clinical condition.Obesity,
obesity 31031 fertility in hypoandrogenic women - Whether most of the studies on menstrual cycle and fertility in obesity have been completed in hyperandrogenic women, very few studies examined women without hyperandrogenism
obesity 32125 gonadotropins, estradiol and inhibin during the follicular phase, thus suggesting an inhibitory effect of obesity per se on the production of these hormones [[45]]. By contrast, the number of ovary follicles does not
obesity 32795 intermediary in the testosterone- and estrogen-pathway. Its plasma levels are significantly lower in morbid obesity [[47]], and are inversely correlated with total body fat. These relationships might be the expression
obesity 33611 decrease of DHEA levels may furtherly enhance the fat accumulation, thus generating a vicious circle in obesity and contributing to higher insulin concentrations and lower fertility in obese women.Obesity effects
obesity 34275 low-grade inflammatory state. To this regard, several mechanisms have been postulated to explain why obesity and/or the overweight affect the quality of female gametes and several hypotheses are related to plasmatic
obesity 34682 disarrayed meiotic spindles with misaligned metaphase chromosomes [[50]]. Independently from aneuploidy, obesity also appears to alter the mitochondrial function in the oocyte. One potential mechanism for oocyte organelle
obesity 34809 alter the mitochondrial function in the oocyte. One potential mechanism for oocyte organelle damage in obesity is the lipotoxicity. In fact, the excess fatty acids obtained from the diet can be stored as triglycerides
obesity 35558 including oocytes [[52]]. This effect is related to the chronic low grade inflammatory state related to obesity which is proven by the increased circulating levels of C-reactive protein (CRP), as well as lactate
obesity 36189 in a similar fashion as described for the oocyte. However, there are conflicting data as to whether obesity has a significant effect on the endometrium. Although many factors contribute to restrain reproductive
obesity 36953 maturing oocytes usually declines with aging. For this reason, the impact of maternal environment and obesity on the differentiation of these cells is particularly consequential and negative environmental exposures
obesity 37287 support the embryo development [[56]]. Thus, based on the systemic inflammatory state associated to the obesity , the oocyte maturation is variably affected by the altered balance of driver hormones as SHBG with other
obesity 37790 whereas leptin deficient mice (ob/ob) are the animal experimental model to investigate the effects of obesity , and female ob/ob mice develop low numbers of antral follicules resulting in impaired folliculogenesis,
obesity 40319 ERK, p38 and JNK.Adiponectin is primarily secreted by adipocytes, but its serum levels drop down in obesity and in insulin resistance while increasing with weight loss [[62]]. It has been demonstrated that in
obesity 42073 AMP-activated protein kinase. These results suggested that since adiponectin synthesis is reduced in obesity , this defect may play a substantial role in obesity-related ovarian dysfunction [[64]].Other adipokines
obesity 42125 that since adiponectin synthesis is reduced in obesity, this defect may play a substantial role in obesity -related ovarian dysfunction [[64]].Other adipokines such as interluekin-6 (IL6), plasminogen activator
obesity 42551 adipokines impact the oocyte quality have not been elucidated yet, their altered concentrations due to obesity represent the major potential factor by which obesity may negatively impact on the oocyte health thus
obesity 42605 elucidated yet, their altered concentrations due to obesity represent the major potential factor by which obesity may negatively impact on the oocyte health thus affecting the fertility in women.Obesity and miscarriage
obesity 42746 oocyte health thus affecting the fertility in women.Obesity and miscarriage rateThe association between obesity and miscarriage has been assessed in a number of studies in both natural and assisted conceptions in
obesity 45107 via modulating adiposity, AMH and fertility in obese women with or without PCOS [[72]].Influence of obesity on fertility treatmentsOverweight and obese women have lower outcomes following fertility treatments
obesity 49920 primarily alert overweight and obese women on their potentially defective fertility. The impact of obesity on reproductive function, especially associated with ovulatory disorders, is mainly due to neuroendocrine
obesity 50375 gonadotropins, estradiol and inhibin in the follicular phase, suggesting an inhibitory effect of the obesity condition per se on the production of these hormones.Since the obesity is pathogenically associated
obesity 50447 an inhibitory effect of the obesity condition per se on the production of these hormones.Since the obesity is pathogenically associated to inflammation, all mechanisms enrolled in oocyte differentiation and
obesity 51048 through the hypothalamus hypophysis ovaries axis.In conclusion, in terms of human and social impact of obesity in women during the reproductive phase, this disease does not affect only the cardiovascular system
osteoporosis 11227 sports may typically produce the ‘female athlete triad’, a syndrome characterized by amenorrhea, osteoporosis and eating disorder as defined by the American College of Sports Medicine [[17]].Environmental pollutants
osteoporosis 51205 disease does not affect only the cardiovascular system and the skeleton health for higher incidence of osteoporosis and dramatically restrains the physical activity in addition to the unfavourable aesthetic impact in
ovarian dysfunction 42141 adiponectin synthesis is reduced in obesity, this defect may play a substantial role in obesity-related ovarian dysfunction [[64]].Other adipokines such as interluekin-6 (IL6), plasminogen activator inhibitor (PAI) type-1, or
polycystic ovary syndrome 684 anovulation and infertility. Besides the hormone disorders and subfertility that are common in the polycystic ovary syndrome (PCOS), in obesity the adipocytes act as endocrine organ. The adipose tissue indeed, releases a number
polycystic ovary syndrome 4051 these mechanisms may influence its physiology. The most common cause of ovulation failure includes the polycystic ovary syndrome (PCOS) [[6]]. This condition is related to the arrest of the follicle maturation resulting in formation
polycystic ovary syndrome 44534 parameters in PCOS and normo-ovulatory women, conducting a one-year study among obese women with or without polycystic ovary syndrome . All patients were classified into three age-matched groups; group A: controls, group B: PCOS patients
type 2 diabetes mellitus 18004 levels of these factors have been shown to be strongly associated with both insulin resistance (IR) and type 2 diabetes mellitus (T2DM) and in patients with the PCOS, a severe dysfunction of adipose tissue has been observed leading
type 2 diabetes mellitus 24053 omentin-1 and omentin-2 are located as adjacent to each other at 1q22-q23, exactly in the region linked to type 2 diabetes mellitus . Both omentin homologues as circulating forms correlate with expression in visceral fat tissue [[37]].

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