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Journal ArticleDOI

Impact of obesity on infertility in women.

01 Jun 2015-Journal of The Turkish German Gynecological Association (J Turk Ger Gynecol Assoc)-Vol. 16, Iss: 2, pp 111-117
TL;DR: Overweight women have a higher incidence of menstrual dysfunction and anovulation, and are at a high risk for reproductive health, and weight loss has beneficial effects on the reproductive outcomes in patients.
Abstract: The prevalence of obesity and overweight are increasing and have become an epidemic worldwide. Obesity has detrimental influences on all systems, including reproductive health. The prevalence of obesity in infertile women is high, and it is well known that there is an association between obesity and infertility. The relationship between obesity and reproductive functions is still being explored. Overweight women have a higher incidence of menstrual dysfunction and anovulation. Overweight and obese women are at a high risk for reproductive health. The risk of subfecundity and infertility, conception rates, miscarriage rates, and pregnancy complications are increased in these women. They have poor reproductive outcomes in natural as well as assisted conception. These poor reproductive outcomes include assisted reproduction such as ovulation induction, in vitro fertilization/intracytoplasmic sperm injection (IVF/ICSI), and ovum donation cycles. Weight loss has beneficial effects on the reproductive outcomes in these patients.
Citations
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Journal ArticleDOI
TL;DR: Findings provide evidence for the significant influence of body composition on oocyte transcript abundance in women undergoing hormonal induction to retrieve oocytes and identify the potential for maternal diet to influence oocyte gene expression.
Abstract: Context It is hypothesized that obesity adversely affects the ovarian environment, which can disrupt oocyte maturation and embryonic development. Objective This study aimed to compare oocyte gene expression profiles and follicular fluid (FF) content from overweight/obese (OW) women and normal-weight (NW) women who were undergoing fertility treatments. Design Using single-cell transcriptomic analyses, we investigated oocyte gene expression using RNA sequencing. Patients or Other Participants Eleven OW women and 13 NW women undergoing fertility treatments were enrolled. Main Outcome Measures Oocyte messenger RNA profiles as well as serum and FF hormone and lipid levels were assessed. Results OW women had significantly higher body mass index, body fat percentage, and serum homeostatic model assessment-insulin resistance index compared with NW women (P < 0.01). Serum leptin and C-reactive protein (CRP) levels as well as FF leptin, CRP, and triglyceride levels were increased (P < 0.05) in OW compared with NW women. Oocytes from OW women had increased expression of proinflammatory (CXCL2; P = 0.071) and oxidative stress-related (DUSP1; P = 0.051) genes but had decreased expression of GAS7 (fat metabolism; P = 0.065), TXNIP (oxidative stress; P = 0.055), and transcription factors ID3 (P = 0.075) and TWIST1 (P = 0.099) compared with NW women. Conclusions These findings provide evidence for the significant influence of body composition on oocyte transcript abundance in women undergoing hormonal induction to retrieve oocytes. They further identify the potential for maternal diet to influence oocyte gene expression. The preconception period is, therefore, an important window of opportunity to consider for lifestyle interventions.

57 citations


Cites background from "Impact of obesity on infertility in..."

  • ...During in vitro fertilization (IVF) procedures, OW women have significantly lower numbers of oocytes retrieved, decreased numbers of cleaved embryos, reduced high-grade embryos, and increased number of miscarriages compared with normal-weight (NW) women (2, 3)....

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  • ...of obesity on pregnancy and/or fertility outcomes (2, 3)....

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  • ...25 kg/m(2)] and are predisposed to higher risk of infertility and pregnancy complications, leading to higher rates of fertility treatments (1, 2)....

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Journal ArticleDOI
15 Jun 2010
TL;DR: In this article, the authors examined the association between anthropometric factors and TTP among I65I Danish women participating in an inter-net-based prospective cohort study of pregnancy planners (2007―2008).
Abstract: BACKGROUND: Recent studies have shown that both female and male obesity may delay time-to-pregnancy (TTP). Little is known about central adiposity or weight gain and fecundability in women. METHODS: We examined the association between anthropometric factors and TTP among I65I Danish women participating in an inter-net-based prospective cohort study of pregnancy planners (2007―2008). We categorized body mass index (BMI = kg/m 2 ) as underweight (<20), normal weight (20-24), overweight (25-29), obese (30-34) and very obese (≥35). We used discrete-time Cox regression to estimate fecundability ratios (FRs) and 95% confidence intervals (CI), controlling for potential confounders. RESULTS: We found longer TTPs for overweight (FR = 0.83, 95% CI = 0.70―I.00), obese (FR = 0.75, 95% CI = 0.58-0.97), and very obese (FR = 0.61, 95% CI = 0.42―0.88) women, compared with normal weight women. After further control for waist circumference, FRs for overweight, obese, and very obese women were 0.72 (95% CI = 0.58―0.90), 0.60 (95% CI = 0.42-0.85) and 0.48 (95% CI = 0.3I-0.74), respectively. Underweight was associated with reduced fecundability among nulliparous women (FR = 0.82, 95% CI = 0.63- I.06) and increased fecundability among parous women (FR = 1.61, 95% CI = 1.08-2.39). Male BMI was not materially associated with TTP after control for female BMI. Compared with women who maintained a stable weight since age I7 (―5 to 4 kg), women who gained ≥ 15 kg had longer TTPs (FR = 0.72, 95% CI = 0.59-0.88) after adjustment for BMI at age I7. Associations of waist circumference and waist-to-hip ratio with TTP depended on adjustment for female BMI: null associations were observed before adjustment for BMI and weakly positive associations were observed after adjustment for BMI. CONCLUSIONS: Our results confirm previous studies showing reduced fertility in overweight and obese women. The association between underweight and fecundability varied by parity.

49 citations

Journal ArticleDOI
TL;DR: The data suggest that male obesity negatively impacts on male reproductive potential, not only through altering hormone levels, but also by directly altering sperm function.
Abstract: Male infertility is a complex, multifactorial and polygenic disease that contributes to ~50% cases of infertility. Previous studies have demonstrated that excess weight and obesity factors serve an important role in the development of male infertility. An increasing number of studies have reported that resveratrol may regulate the response of cells to specific stimuli that induce cell injury, as well as decrease germ cell apoptosis in mice or rats. In the present study, the semen quality and serum sex hormone levels were evaluated in 324 men, which included 73 underweight, 82 normal weight, 95 overweight and 74 obese men. All patients were referred to The Reproductive Medicine Center of Shanxi Women and Infants Hospital (Taiyuan, China) between January 2013 and January 2015. The aim of the present study was to investigate the effects of resveratrol treatment on the motility, plasma zinc concentration and acrosin activity of sperm from obese males. The sperm concentration, normal sperm morphology, semen volumes, DNA fragmentation rates and testosterone levels in men from the overweight and obese groups were markedly decreased when compared with men in the normal weight group. In addition, the progressive motility, seminal plasma zinc concentration and spermatozoa acrosin activity were notably decreased in the obese group compared with the normal weight group. However, estradiol levels were significantly increased in the overweight, obese and underweight groups compared with the normal weight group. Notably, semen samples from obese males with astenospermia treated with 0‑100 µmol/l resveratrol for 30 min demonstrated varying degrees of improvement in sperm motility. When these semen samples were treated with 30 µmol/l resveratrol, sperm motility improved when compared to other doses of resveratrol. Therefore, 30 µmol/l resveratrol was selected for further experiments. Upon treatment of semen samples with resveratrol (30 µmol/l) for 30 min, the seminal plasma zinc concentration and spermatozoa acrosin activity increased significantly in the experimental group compared with the control group. These data suggest that male obesity negatively impacts on male reproductive potential, not only through altering hormone levels, but also by directly altering sperm function. In addition, resveratrol may have a therapeutic and protective effect against obesity-induced abnormalities in semen.

46 citations


Cites background or result from "Impact of obesity on infertility in..."

  • ...These results are consistent with those reported in previous studies (6-8)....

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  • ...In parallel, obesity rates are increasing rapidly worldwide (6,7), which is not only associated with an increased risk of developing chronic diseases, but has also been demonstrated to increase the risk of developing...

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Journal ArticleDOI
TL;DR: This review aims to dissect the plausible interconnection of lifestyle and environmental factors with various neuroendocrine pathways and to discuss how it can affect the female physiology in the long-term, resulting in reproductive incompetence.
Abstract: Lifestyle factors, which include the practices we adopt in our daily life, have a significant role in shaping our overall health. These lifestyle choices are mainly centered on personal preferences and our surrounding social environment. In addition to lifestyle factors, we continuously interact with our environment, which impacts physiology. Several factors have been claimed to affect women's fertility; lifestyle-related factors, in particular, have received great attention in the last decade. Due to societal and professional pressure, childbearing age in women has gradually shifted to the 30s. Delayed age of childbearing along with modern lifestyle offers a wider window of opportunity for various lifestyle and genetic perturbations to penetrate to affect fertility. While clinical studies have strengthened a direct correlation between lifestyle, environment, and female reproductive health; experimental studies on animal models have investigated their mechanism of action. In most instances, these factors target the neuroendocrine pathways, resulting in metabolic derangements. This review aims to dissect the plausible interconnection of lifestyle and environmental factors with various neuroendocrine pathways and to discuss how it can affect the female physiology in the long-term, resulting in reproductive incompetence.

41 citations

Journal ArticleDOI
TL;DR: It is advisable to delay pregnancy for at least 12 months following bariatric surgery and a multidisciplinary approach to care is desirable with close monitoring for deficiencies at each trimester.
Abstract: The widespread use of bariatric surgery for the treatment of morbid obesity has led to a dramatic increase in the numbers of women who become pregnant post-surgery. This can present new challenges, including a higher risk of protein and calorie malnutrition and micronutrient deficiencies in pregnancy due to increased maternal and fetal demand. We undertook a focused, narrative review of the literature and present pragmatic recommendations. It is advisable to delay pregnancy for at least 12 months following bariatric surgery. Comprehensive pre-conception and antenatal care is essential to achieving the best outcomes. Nutrition in pregnancy following bariatric surgery requires specialist monitoring and management. A multidisciplinary approach to care is desirable with close monitoring for deficiencies at each trimester.

37 citations

References
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Journal ArticleDOI
18 Jan 2001-Nature
TL;DR: It is shown that adipocytes secrete a unique signalling molecule, which is named resistin (for resistance to insulin), which circulating resistin levels are decreased by the anti-diabetic drug rosiglitazone, and increased in diet-induced and genetic forms of obesity.
Abstract: Diabetes mellitus is a chronic disease that leads to complications including heart disease, stroke, kidney failure, blindness and nerve damage. Type 2 diabetes, characterized by target-tissue resistance to insulin, is epidemic in industrialized societies and is strongly associated with obesity; however, the mechanism by which increased adiposity causes insulin resistance is unclear. Here we show that adipocytes secrete a unique signalling molecule, which we have named resistin (for resistance to insulin). Circulating resistin levels are decreased by the anti-diabetic drug rosiglitazone, and increased in diet-induced and genetic forms of obesity. Administration of anti-resistin antibody improves blood sugar and insulin action in mice with diet-induced obesity. Moreover, treatment of normal mice with recombinant resistin impairs glucose tolerance and insulin action. Insulin-stimulated glucose uptake by adipocytes is enhanced by neutralization of resistin and is reduced by resistin treatment. Resistin is thus a hormone that potentially links obesity to diabetes.

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TL;DR: The pathophysiology of adiponectin and adiponECTin receptors in insulin resistance, diabetes, and the metabolic syndrome is described and potential versatile therapeutic targets to combat obesity-linked diseases characterized by insulin resistance are described.
Abstract: Adiponectin is an adipokine that is specifically and abundantly expressed in adipose tissue and directly sensitizes the body to insulin. Hypoadiponectinemia, caused by interactions of genetic factors such as SNPs in the Adiponectin gene and environmental factors causing obesity, appears to play an important causal role in insulin resistance, type 2 diabetes, and the metabolic syndrome, which are linked to obesity. The adiponectin receptors, AdipoR1 and AdipoR2, which mediate the antidiabetic metabolic actions of adiponectin, have been cloned and are downregulated in obesity-linked insulin resistance. Upregulation of adiponectin is a partial cause of the insulin-sensitizing and antidiabetic actions of thiazolidinediones. Therefore, adiponectin and adiponectin receptors represent potential versatile therapeutic targets to combat obesity-linked diseases characterized by insulin resistance. This Review describes the pathophysiology of adiponectin and adiponectin receptors in insulin resistance, diabetes, and the metabolic syndrome.

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TL;DR: It is shown that AdipoR1 and AdIPoR2 serve as receptors for globular and full-length adiponectin and mediate increased AMP-activated protein kinase, peroxisome proliferator-activated receptor-alpha ligand activities, and glucose uptake and fatty-acid oxidation by adiponECTin.
Abstract: Metabolic syndrome is thought to result from obesity and obesity-linked insulin resistance. Obesity in adulthood is characterized by adipocyte hypertrophy. Adipose tissue participates in the regulation of energy homeostasis as an important endocrine organ that secretes a number of biologically active “adipokines.” Heterozygous peroxisome proliferator-activated receptor- knockout mice were protected from high-fat diet induced obesity, adipocyte hypertrophy, and insulin resistance. Systematic gene profiling analysis of these mice revealed that adiponectin/Acrp30 was overexpressed. Functional analyses including generation of adiponectin transgenic or knockout mice have revealed that adiponectin serves as an insulinsensitizing adipokine. In fact, obesity-linked down-regulation of adiponectin was a mechanism whereby obesity could cause insulin resistance and diabetes. Recently, we have cloned adiponectin receptors in the skeletal muscle (AdipoR1) and liver (AdipoR2), which appear to comprise a novel cell-surface receptor family. We showed that AdipoR1 and AdipoR2 serve as receptors for globular and full-length adiponectin and mediate increased AMP-activated protein kinase, peroxisome proliferator-activated receptorligand activities, and glucose uptake and fatty-acid oxidation by adiponectin. Obesity decreased expression levels of AdipoR1/R2, thereby reducing adiponectin sensitivity, which finally leads to insulin resistance, the so-called “vicious cycle.” Most recently, we showed that osmotin, which is a ligand for the yeast homolog of AdipoR (PHO36), activated AMPK via AdipoR in C2C12 myocytes. This may facilitate efficient development of adiponectin receptor agonists. Adiponectin receptor agonists and adiponectin sensitizers should serve as versatile treatment strategies for obesitylinkeddiseasessuchasdiabetesandmetabolicsyndrome.(Endocrine Reviews 26: 439–451, 2005)

2,525 citations

Journal ArticleDOI
TL;DR: A newly identified adipocytokine, visfatin, that is highly enriched in the visceral fat of both humans and mice and whose expression level in plasma increases during the development of obesity is isolated.
Abstract: Recent studies of obesity show that fat tissue fulfills an endocrine function by producing a variety of secreted proteins, called adipocytokines, that may play key metabolic roles. The present investigators have isolateda newly identified adipocytokine, visfatin, from visceral fat of both mice and humans. Expression of visfatin in the plasma increases as obesity develops. This substance corresponds to a protein identified as preB cell colony-enhancing factor (PBEF), a cytokine expressed in lymphocytes. In a study of 101 human males and females, plasma levels of PBEF correlated closely with the amount of visceral fat as estimated by computed tomography. Correlation with the amount of subcutaneous fat was weak. Significant elevations of PBEF mRNA were also found in KKAy mice, which serve as a model for obesity-related type 2 diabetes. These mice become obese at age 6 to 12 weeks and, at the same time, plasma PBEF levels increase significantly, as do levels of PBEF mRNA in visceral fat. Levels in subcutaneous fat change very little. Mice fed a high-fat diet had higher plasma PBEF concentrations than those fed normal chow. When recombinant visfatin was administered intravenously to c57BL/6J mice, plasma glucose decreased within 30 minutes in a dose-dependent manner. The same effect was noted in insulin-resistant obese KKAy mice, mimicking the effect of insulin injection. Visfatin also had insulin-like effects on cultured cells. In both strains of mice, chronic exposure to visfatin, using adenovirus, significantly lowered plasma levels of both glucose and insulin. Visfatin was found to bind to-and activate-the insulin receptor but in a way different from insulin. These studies indicate that visfatin shares properties of insulin both in vitro and in vivo. In addition to helping to understand glucose and lipid homeostasis and adipocyte proliferation, visfatin may prove to be a useful target when developing drug treatments for diabetes.

1,131 citations

Journal ArticleDOI
TL;DR: Weight loss should be considered as a first option for women who are infertile and overweight, and the cost savings of the programme were considerable.
Abstract: Obesity affects ovulation, response to fertility treatment, pregnancy rates and outcome. In this prospective study, a weight loss programme was assessed to determine whether it could help obese infertile women, irrespective of their infertility diagnosis, to achieve a viable pregnancy, ideally without further medical intervention. The subjects underwent a weekly programme aimed at lifestyle changes in relation to exercise and diet for 6 months; those that did not complete the 6 months were treated as a comparison group. Women in the study lost an average of 10.2 kg/m2, with 60 of the 67 anovulatory subjects resuming spontaneous ovulation, 52 achieving a pregnancy (18 spontaneously) and 45 a live birth. The miscarriage rate was 18%, compared to 75% for the same women prior to the programme. Psychometric measurements also improved. None of these changes occurred in the comparison group. The cost savings of the programme were considerable. Prior to the programme, the 67 women had had treatment costing a total of A$550,000 for two live births, a cost of A$275,000 per baby. After the programme, the same women had treatment costing a total of A$210,000 for 45 babies, a cost of A$4600 per baby. Thus weight loss should be considered as a first option for women who are infertile and overweight.

729 citations

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