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Biomed Res Int. Xiao Z, Xu H. Gender-specific body composition relationships between adipose tissue distribution and peak bone mineral density in young Chinese adults.

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Oxidative stress and reproductive function: oxidative stress and in vitro ageing of the post-ovulatory oocyte: an update on recent advances in the field. Manolopoulos KN, Karpe F, Frayn KN. Gluteofemoral body fat as a determinant of metabolic health.

Int J Obes Lond. Abdo NM, Ahmad H, Loney T, et al. Characterization of fertility clinic attendees in the Abu Dhabi Emirate, United Arab Emirates: a cross-sectional study. Int J Environ Res Public Health.

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A review of disparities in access to infertility care and treatment outcomes among Hispanic women. Reprod Biol Endocrinol. Eller A, Ejzenberg D, Monteleone P, Soares JJ, Baracat EC.

Vitamin D and in vitro fertilization: a systematic review. J Assist Reprod Genet. Hajhashemy Z, Foshati S, Saneei P. Relationship between abdominal obesity based on waist circumference and serum vitamin D levels: a systematic review and meta-analysis of epidemiologic studies.

Nutr Rev. Guerrero R, Vega GL, Grundy SM, Browning JD. Ethnic differences in hepatic steatosis: an insulin resistance paradox? Thong EP, Codner E, Laven J, Teede H. Diabetes: a metabolic and reproductive disorder in women. Article Fertility Health Trying To Conceive Weight. Gynoid Fat Hip Fat and Thigh Fat : Possible Role in Fertility.

Gynoid fat is distributed at the top of the thighs and on the hips. Android fat is distributed on the belly. The female sex hormone oestrogen stimulates hip fat and thigh fat gynoid and the male sex hormone testosterone stimulates belly fat android, around the abdomen.

There is no conclusive data to suggest that having more or less gynoid fat contributes to fertility. Changing body shapes The distribution of body fat varies by age, gender and inheritance. Waist to Hip Ratio WHR The WHR is calculated by dividing waist measurement by hip measurement.

Typically, during the reproductive years, the ratio is lower in females than in males: Healthy, premenopausal women: 0. The benefits of having a low WHR…. and why gynoid fat puts you at an evolutionary advantage Women with more gynoid fat and a lower WHR are considered more attractive.

Sources: Bovet, Jeanne. A Systematic Review. Forte, R, et al. Jasieńska, G, et al. Jenkins, Julian M. Kirchengast, S, and M Gartner. Lassek, William D. Morán, Carlos, et al. Singh, D, and D Singh. Download the Nabta app.

Recommended Products Add to Wishlist. Add to Wishlist. Related Articles. Article Fertility Health. Kate Dudek January 30, Article Body Fertility Infertility Periods Trying To Conceive Weight. Nabta Editorial Team December 11, Am I Pregnant Article Fertility Health Infertility Male Infertility Trying To Conceive.

Kate Dudek December 11, Subscribe Now! Register to get weekly updates. COMPANY About Team Partners Press Careers Podcast Research. CUSTOMER CARE Terms of Use Privacy Policy FAQs Contact. SHOP Payment Information Delivery Information Returns and Refunds Consumer Rights.

DOWNLOAD OUR APP. JOIN OUR COMMUNITY Become part of the Nabta family. We use cookies on our website to give you the most relevant experience by remembering your preferences and repeat visits. In conclusion, in anovulatory women with obesity and infertility, the total amount of abdominal and trunk fat is significantly increased, with an significant increase in the volume of SAF and no difference in the volume of IAF compared with ovulatory women with obesity and infertility.

Abdominal and trunk fat accumulation and SAF accumulation but not the IAF are associated with anovulation. This association is, however, only based on the volume of these fat compartments and does not necessarily reflect the consequences of their metabolic activity.

The authors thank and appreciate Mr. Wim Tukker, radiological technician of the Department of Radiology, for performing the IAF and SAF measurements of the ssCT so meticulously. A grant was received from the University Medical Center Groningen, The Netherlands, for the CT and DEXA scans. A grant was also received from ZonMW Dutch government funding for a subsequent randomized controlled trial on lifestyle intervention in women with obesity and infertility.

Part of these data were presented at the annual meeting of the European Society of Human Reproduction and Embryology Abstract O in Barcelona, Spain, in July Disclosure Summary: W. declares that the disclosure statements of the co-authors have been obtained properly and that no conflicts of interests are known to him.

Haslam DW , James WP Obesity. Lancet : — Google Scholar. Green BB , Weiss NS , Daling JR Risk of ovulatory infertility in relation to body weight. Fertil Steril 50 : — Grodstein F , Goldman MB , Cramer DW Body mass index and ovulatory infertility. Epidemiology 5 : — Wass P , Waldenström U , Rössner S , Hellberg D An android body fat distribution in females impairs the pregnancy rate of in-vitro fertilization-embryo transfer.

Hum Reprod 12 : — Zaadstra BM , Seidell JC , Van Noord PA , te Velde ER , Habbema JD , Vrieswijk B , Karbaat J Fat and female fecundity: prospective study of effect of body fat distribution on conception rates.

BMJ : — Dunaif A Insulin resistance and the polycystic ovary syndrome: mechanism and implications for pathogenesis. Endocr Rev 18 : — Poretsky L On the paradox of insulin-induced hyperandrogenism in insulin-resistant states.

Endocr Rev 12 : 3 — Pasquali R , Casimirri F , Venturoli S , Antonio M , Morselli L , Reho S , Pezzoli A , Paradisi R Body fat distribution has weight-independent effects on clinical, hormonal, and metabolic features of women with polycystic ovary syndrome.

Metabolism 43 : — Pasquali R , Pelusi C , Genghini S , Cacciari M , Gambineri A Obesity and reproductive disorders in women.

Hum Reprod Update 9 : — Franks S , Robinson S , Willis DS Nutrition, insulin and polycystic ovary syndrome. Rev Reprod 1 : 47 — Willis D , Mason H , Gilling-Smith C , Franks S Modulation by insulin of follicle-stimulating hormone and luteinizing hormone actions in human granulosa cells of normal and polycystic ovaries.

J Clin Endocrinol Metab 81 : — Escobar-Morreale HF , San Millán JL Abdominal adiposity and the polycystic ovary syndrome. Trends Endocrinol Metab 18 : — Garg A Regional adiposity and insulin resistance.

J Clin Endocrinol Metab 89 : — Lebovitz HE , Banerji MA Point: visceral adiposity is causally related to insulin resistance. Diabetes Care 28 : — Miles JM , Jensen MD Counterpoint: visceral adiposity is not causally related to insulin resistance.

Guo Z , Hensrud DD , Johnson CM , Jensen MD Regional postprandial fatty acid metabolism in different obesity phenotypes.

Diabetes 48 : — Weiss R Fat distribution and storage: how much, where, and how? Eur J Endocrinol Suppl 1 : S39 — S Carmina E , Bucchieri S , Esposito A , Del Puente A , Mansueto P , Orio F , Di Fede G , Rini G Abdominal fat quantity and distribution in women with polycystic ovary syndrome and extent of its relation to insulin resistance.

J Clin Endocrinol Metab 92 : — Fertil Steril 82 : — Yildirim B , Sabir N , Kaleli B Relation of intra-abdominal fat distribution to metabolic disorders in nonobese patients with polycystic ovary syndrome.

Fertil Steril 79 : — Lord J , Thomas R , Fox B , Acharya U , Wilkin T The central issue? Visceral fat mass is a good marker of insulin resistance and metabolic disturbance in women with polycystic ovary syndrome. BJOG : — Barber TM , Golding SJ , Alvey C , Wass JA , Karpe F , Franks S , McCarthy MI Global adiposity rather than abnormal regional fat distribution characterizes women with polycystic ovary syndrome.

J Clin Endocrinol Metab 93 : — Hum Reprod 19 : 41 — Pratt JJ , Boonman R , Woldring MG , Donker AJ Special problems in the radioimmunoassay of plasma aldosterone without prior extraction and purification. Clin Chim Acta 84 : — Vermeulen A , Verdonck L , Kaufman JM A critical evaluation of simple methods for the estimation of free testosterone in serum.

J Clin Endocrinol Metab 84 : — Muniyappa R , Lee S , Chen H , Quon MJ Current approaches for assessing insulin sensitivity and resistance in vivo: advantages, limitations, and appropriate usage. Am J Physiol Endocrinol Metab : E15 — E Manley SE , Luzio SD , Stratton IM , Wallace TM , Clark PM Preanalytical, analytical, and computational factors affect homeostasis model assessment estimates.

Diabetes Care 31 : — Puder JJ , Varga S , Kraenzlin M , De Geyter C , Keller U , Müller B Central fat excess in polycystic ovary syndrome: relation to low-grade inflammation and insulin resistance.

J Clin Endocrinol Metab 90 : — Freedland ES Role of a critical visceral adipose tissue threshold CVATT in metabolic syndrome: implications for controlling dietary carbohydrates: a review. Nutr Metab Lond 1 : Danforth Jr E Failure of adipocyte differentiation causes type II diabetes mellitus?

Nat Genet 26 : Jensen MD Role of body fat distribution and the metabolic complications of obesity. J Clin Endocrinol Metab 93 11 Suppl 1 : S57 — S Koska J , Stefan N , Permana PA , Weyer C , Sonoda M , Bogardus C , Smith SR , Joanisse DR , Funahashi T , Krakoff J , Bunt JC Increased fat accumulation in liver may link insulin resistance with subcutaneous abdominal adipocyte enlargement, visceral adiposity, and hypoadiponectinemia in obese individuals.

Am J Clin Nutr 87 : — Boden G Obesity and free fatty acids. Endocrinol Metab Clin North Am —, viii — ix. Duggal PS , Van Der Hoek KH , Milner CR , Ryan NK , Armstrong DT , Magoffin DA , Norman RJ The in vivo and in vitro effects of exogenous leptin on ovulation in the rat.

Endocrinology : — Antuna-Puente B , Feve B , Fellahi S , Bastard JP Adipokines: the missing link between insulin resistance and obesity. Diabetes Metab 34 : 2 — Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.

Sign In or Create an Account. Endocrine Society Journals. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Abstract. Subjects and Methods. Journal Article.

The Subcutaneous Abdominal Fat and Not the Intraabdominal Fat Compartment Is Associated with Anovulation in Women with Obesity and Infertility. Kuchenbecker , Walter K. Kuchenbecker, Isala Clinics, Dr.

van Heesweg 2, GK Zwolle, The Netherlands. Oxford Academic. Henk Groen. Tineke M. Johanna H. Riemer H. Erik J. van der Jagt. Anneke C.

The female sex hormone oestrogen stimulates hip fat and thigh fat gynoid and the male sex hormone testosterone stimulates belly fat android, around the abdomen.

There is no conclusive data to suggest that having more or less gynoid fat contributes to fertility. Changing body shapes The distribution of body fat varies by age, gender and inheritance. Waist to Hip Ratio WHR The WHR is calculated by dividing waist measurement by hip measurement. Typically, during the reproductive years, the ratio is lower in females than in males: Healthy, premenopausal women: 0.

The benefits of having a low WHR…. and why gynoid fat puts you at an evolutionary advantage Women with more gynoid fat and a lower WHR are considered more attractive.

Sources: Bovet, Jeanne. A Systematic Review. Forte, R, et al. Jasieńska, G, et al. Jenkins, Julian M. Kirchengast, S, and M Gartner. Lassek, William D. Morán, Carlos, et al. Singh, D, and D Singh. Download the Nabta app. Recommended Products Add to Wishlist. Add to Wishlist. Related Articles.

Article Fertility Health. Kate Dudek January 30, Article Body Fertility Infertility Periods Trying To Conceive Weight. Nabta Editorial Team December 11, Am I Pregnant Article Fertility Health Infertility Male Infertility Trying To Conceive.

Kate Dudek December 11, Subscribe Now! Register to get weekly updates. COMPANY About Team Partners Press Careers Podcast Research. CUSTOMER CARE Terms of Use Privacy Policy FAQs Contact. SHOP Payment Information Delivery Information Returns and Refunds Consumer Rights.

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Visceral fat , for example, is in the abdominal cavity and wraps around organs like the liver, pancreas, and intestines. High amounts of visceral fat can lead to health problems, such as Type 2 diabetes. Conception depends on many factors, including the health and function of your reproductive system, as well as your hormone levels.

An egg and sperm need to meet at just the right time — otherwise known as your fertile window — for fertilization to occur. Your hormones need to be at normal levels for all of this to take place. follicular phase, luteal phase, etc. Estrogens, specifically how much of the hormones you have, play a major role when it comes to weight and fertility.

Estrogens are produced by the ovaries, as well as in fat cells and the adrenal gland. If you have a high BMI, you may have more fat cells. The more fat cells you have, the more estrogens are being produced in your body.

Estrogens are also responsible for the growth of the uterine lining, so more fat cells lead to a thicker uterine lining, and heavier periods.

Enough estrogens can interrupt your cycle, lead to infrequent periods, and prevent you from ovulating. High levels of estrogens can also affect how your body processes insulin, therefore causing problems like diabetes and insulin resistance , as is the case with polycystic ovarian syndrome, or PCOS more on this below.

According to the American Society for Reproductive Medicine ASRM , a higher body-fat percentage can also affect the success of fertility treatments , such as IVF. When this happens, non-essential systems, like reproductive function, slow and shut down.

Your hypothalamus, where hormones such as estrogens are regulated, gets sluggish, and this leads to irregular, or entirely absent, menstrual cycles. For example, research has been looking into how genetics plays a role in your body weight.

There are also treatable medical conditions, like hormonal conditions or eating disorders, that play a role in BMI. Polycystic ovary syndrome PCOS is a hormonal condition that can cause irregular menstrual cycles, extra hair growth, fatigue, and weight gain.

You may also have higher levels of androgens called hyperandrogenism — but not all women with PCOS experience this. This may result in chronically elevated blood sugar and insulin levels. Eating disorders, such as anorexia , can also lead to nutrient deficiencies that decrease levels of estrogens, negatively affecting ovulation and leading to the absence of periods altogether.

When a woman is in recovery, and gaining weight, she might also experience changes in her cycle as her hormones recalibrate. Note: There are also meta-analyses — studies that combine estimates from a whole bunch of studies — that also suggest that weight loss has a positive effect on fertility.

Montenegro recommends talking to a health professional who specializes in metabolic fertility issues.

Slart, Erik J. van der Jagt, Anneke C. Muller Kobold, Bruce H. Wolffenbuttel, Jolande A. Objective: We compared body fat distribution measurements and their contribution to anovulation in obese ovulatory and anovulatory infertile women.

Design: Seventeen ovulatory and 40 anovulatory women age, 30 ± 4 yr; body mass index, Body fat distribution was measured by anthropometrics, dual-energy x-ray absorptiometry, and single-sliced abdominal computed tomography scan.

Multiple logistic regression analysis was applied to determine which fat compartments significantly contributed to anovulation. Results: Anovulatory women had a higher waist circumference ± 11 vs. The volume of intraabdominal fat on single-sliced abdominal computed tomography scan was not significantly different between the two groups ± 56 vs.

After multiple logistic regression analysis, only trunk fat, abdominal fat, and SAF were associated with anovulation. Conclusions: Abdominal fat is increased in anovulatory women due to a significant increase in SAF and not in intraabdominal fat. SAF and especially abdominal and trunk fat accumulation are associated with anovulation.

Overweight [body mass index BMI , 25— Independent of body weight, body fat distribution, expressed by waist-hip ratio WHR , has also been shown to influence the reproductive potential. The differential role and contribution of intraabdominal fat IAF and sc abdominal fat SAF compartments to anovulation are not clear.

Increased IAF is associated with insulin resistance, and the resulting hyperinsulinemia contributes to anovulation by increased ovarian androgen secretion 6 , 7 leading to lower SHBG concentrations 8 , 9 and consequently higher free androgen levels.

Insulin directly influences intraovarian steroidogenesis, which may lead to arrest of follicle growth, as has been shown in women with polycystic ovary syndrome PCOS 10 , Increased androgens in turn contribute to upper body obesity 12 ; thus, a vicious circle evolves where androgens favor abdominal fat accumulation and upper body obesity, which in turn facilitates insulin resistance and androgen production 12 , However, many women with upper body obesity have ovulatory cycles and little or no insulin resistance.

The differential role and contribution of the IAF and SAF compartments to insulin resistance and anovulation have not previously been investigated. There is an ongoing controversy on the relative contribution of the SAF and IAF to insulin resistance and the metabolic syndrome 14 , Some studies 13 , 15 , 16 indicate that SAF contributes to insulin resistance, whereas others 14 , 17 report to the contrary that IAF is associated with insulin resistance and the metabolic complications of obesity.

Some studies have shown more trunk and abdominal fat on dual-energy x-ray absorptiometry DEXA scan in women with PCOS 18 , A study using abdominal ultrasonography to measure the IAF and SAF showed that nonobese women with PCOS have more IAF compared with a group of lean ovulatory women Another study, using single-slice abdominal computed tomography ssCT scan in obese women with PCOS, showed that IAF correlates more strongly with insulin resistance than SAF A cross-sectional study comparing 50 women with PCOS with 28 controls showed that women with PCOS had significantly more SAF and gluteal sc fat.

However, after adjusting for the differences in BMI and total fat mass, there were no significant differences in IAF and SAF between women with PCOS and controls Considering the above-mentioned controversy, questions arise as to whether the IAF and SAF compartments are different in ovulatory and anovulatory infertile women with obesity, and which compartment, IAF or SAF, is associated with anovulation.

The aim of this study was to assess the contribution of different body fat distribution measurements, and especially IAF and SAF, to anovulation in women with obesity and infertility. The study was carried out between and at the Fertility Clinic of the University Medical Center Groningen UMCG.

Of the 60 eligible women that agreed to participate, two did not undergo the baseline assessment due to early dropout and pregnancy.

Except for one anovulatory woman with type 1 diabetes mellitus, no other study subjects were known to have impaired glucose tolerance or type 2 diabetes mellitus.

Except for the one subject with type 1 diabetes mellitus receiving insulin therapy, no other study subject received hormonal preparations or metformin in the 3 months preceding inclusion. All women were Caucasian, except for one woman of Asian origin. Women with cycles of 42 d or less where ovulation could not be identified during ultrasound monitoring as well as women with menstrual cycles between 42 d and 6 months kept a basal body temperature chart.

Hyperprolactinemia, abnormal thyroid function, nonclassical hydroxylase deficiency, and androgen-secreting tumors were excluded in all anovulatory patients. In all study subjects, the Rotterdam consensus diagnostic criteria for PCOS were considered, and subjects were diagnosed as PCOS if two of the following criteria were present: anovulation, hyperandrogenemia clinically or biochemically , or polycystic ovary morphology on ultrasound after the exclusion of other endocrine causes of anovulation Hirsutism was used as a clinical marker of hyperandrogenemia, and a serum testosterone level above 3.

Informed written consent was obtained from all women, and the study was approved by the Medical Ethical Committee of the UMCG. The following anthropometric measurements were determined at intake: body weight kilograms , height centimeters , BMI weight in kilograms divided by height in meters squared , waist circumference Wc; waist measured at the narrowest part of the torso located between the lower rib and the iliac crest and WHR.

The WHR was calculated by dividing Wc by hip circumference measured at the level of the greatest gluteal protuberance in a horizontal plane parallel to the floor.

All measurements were carried out by the same observer. A whole body scan was performed by DEXA using a Hologic A Discovery Bone Densitometer Hologic Inc.

Total fat mass and total fat percentage were determined for the whole body, and two regions trunk and abdominal slice were specified by computer programming and measured as mentioned in previous studies All participants, positioned supine, underwent a ssCT at the level of the umbilicus corresponding well with lumbar vertebrae 4—5 at kv exposure.

Initially, the Siemens Somatom Sensation 16 was used with a total slice thickness of 18 mm four subslices ×0. During the study, a more advanced CT scan, the Siemens Somatom Sensation 64 was used with a slice thickness of 18 mm three subslices ×0. Syngo Volume Siemens, Berlin, Germany was the software used for both apparatus.

The area for measuring IAF was delineated by drawing a line within the muscle wall surrounding the abdominal cavity and letting the computer program calculate the adipose tissue within this area. SAF area was calculated by subtracting IAF from TAF. These measurements were performed by a single observer.

By multiplying the IAF and SAF area square centimeters with each subslice centimeters of the ssCT, the IAF and SAF volume cubic centimeters was calculated, and the mean of the subslices was recorded for analysis. The edited data were archived in Rogan.

All blood samples were taken at intake after an overnight fast of 10 h. Serum total testosterone was measured by RIA, using 1,2,6,7 3 H -testosterone as tracer Amersham Biosciences, Buckinghamshire, UK and antiserum developed by Pratt SHBG was measured with a binding assay using 3 H-dihydrotestosterone Amersham Biosciences and 1 H-dihydrotestosterone Sigma-Aldrich, St.

Louis, MO. The coefficients of intraassay variation were 4. Reference values for women were 0—3. Free testosterone was calculated with the formula according to Vermeulen For insulin measurement, a DSL Insulin RIA Diagnostic Systems Laboratories, Inc.

Radioactivity was measured by a gamma counter. Fasting glucose was determined with a clinical chemistry analyzer. For comparison between groups, subjects were stratified by ovulatory status into anovulatory and ovulatory groups. Normal distribution was tested using the Kolmogorov-Smirnov test.

Multiple logistic regression analyses were used to determine the contribution of various variables to anovulation after correction for BMI, testosterone, and fasting insulin. The goodness of fit of the multiple logistic regression analyses was presented as the Nagelkerke R 2 and P value of the model χ 2 test.

The women ranged in age from 20—38 yr. The BMI ranged from In 14 of the 17 ovulatory patients, PCOS could be excluded. Clinical characteristics comparing anovulatory to ovulatory obese women with infertility. Data are expressed as mean ± sd or median range.

In 33 of the 40 anovulatory women, PCOS could be diagnosed and in three women PCOS could be excluded. In four anovulatory women without clinical or biochemical hyperandrogenemia, PCOS could not be excluded because the ovaries could not be visualized by transvaginal ultrasonography due to morbid obesity.

Despite a nonsignificant difference in BMI, age, and total fat mass on DEXA scan, anovulatory obese women had a significantly higher Wc, WHR, abdominal and trunk fat on DEXA scan and SAF on ssCT compared with the ovulatory obese women. The IAF on ssCT was not significantly different between anovulatory and ovulatory obese women.

Fasting insulin was significantly increased in anovulatory women, but the HOMA-IR was not significantly different. Free testosterone was significantly higher in the anovulatory group compared with the ovulatory group, mainly due to significantly lower levels of SHBG.

To find contributors to the anovulatory status, we performed multivariate logistic regression analysis correcting for BMI, testosterone, and fasting insulin Table 2. Abdominal slice fat and trunk fat on DEXA scan were significant contributors to anovulation, whereas the contribution of SAF on ssCT to anovulation was of borderline significance odds ratio, 0.

The Nagelkerke R 2 on these analyses ranged from 0. The IAF on ssCT showed no contribution to anovulatory status. Wc as a clinical tool did not significantly predict anovulatory status.

Results of multivariate logistic regression analyses of contribution to anovulatory status by different fat measurements in obese women with infertility. This study indicates that the SAF and not the IAF compartment is significantly increased in anovulatory women with obesity and infertility compared with ovulatory counterparts with similar BMI.

Fat accumulation around the trunk and abdomen and the SAF are associated with anovulation, whereas the IAF compartment is not associated with anovulation. Previous studies comparing fat distribution in women with PCOS with ovulatory controls also showed more trunk and abdominal fat on DEXA scan in PCOS women, even in cases with normal BMI One study differentiating SAF from the IAF using abdominal ultrasound indicated that women of normal weight with PCOS have more IAF than normal-weight women with regular menstrual cycles After adjusting for the differences in BMI and total fat mass in a study comparing 50 women with PCOS with 28 controls, no significant differences in IAF and SAF were found between the two groups Using ssCT in obese women with infertility, our study showed that the IAF is not different between anovulatory and ovulatory women of similar BMI.

Considering the difference in mean BMI According to this hypothesis, with increase in body weight, the intraabdominal fat compartment reaches a point of saturation after which fat is shunted to the sc fat compartments This hypothesis could therefore account for increased SAF with increasing BMI.

The ratio of the volume of IAF and SAF on ssCT in the present study population was, however, unchanged across different BMI ranges. On the other hand, the discrepancy of the findings of the present study and previous studies can also be attributed to the hypothesis of dysregulated upper body sc fat 30 , Dysregulated adipocytes of upper body sc fat are resistant to the antilipolytical effects of insulin resulting in the shunting of postprandial free fatty acids FFAs to the liver and skeletal muscles.

This might be mediated by inflammatory changes, increase in adipocyte size, and decreased adiponectin synthesis by the sc fat Fat storage in the liver and skeletal muscles furthermore contributes to insulin resistance Insulin resistance and hyperandrogenemia are pivotal mechanisms through which obesity and fat distribution lead to anovulation 6 , 9.

The finding of significantly higher free testosterone and insulin levels in anovulatory women in the present study supports the findings of previous studies. In the present study, despite significantly higher fasting insulin levels, increased insulin resistance in anovulatory women expressed by the HOMA-IR did not reach statistical significance, possibly due a small sample size.

The present study supports an association of accumulation of sc fat around the abdomen and trunk with anovulation and insulin resistance. Increased FFA delivery to skeletal muscles seems to be the main mediator of insulin resistance The finding of the present study does, however, not necessarily exclude functional mechanisms of IAF contributing to anovulation.

Despite a much smaller volume of IAF compared with SAF and much lower contribution of IAF to the systemic FFA concentration, using multivariate analysis, various studies showed a significant correlation of the IAF with insulin resistance and the metabolic complications of obesity IAF has higher lipolytical activity per unit fat mass, and direct drainage into the portal vein results in increased delivery of FFAs to the liver The differential secretion of adipokines and cytokines by the IAF and SAF compartments might also play a contributory role in obesity-related infertility and anovulation.

In view of a significantly greater amount of SAF, a different obesity-related mechanism contributing to anovulation could also be considered. Leptin, an adipokine mainly produced by SAF, induces anovulation by direct ovarian effects in animal models IAF and SAF compartments are interlinked, and changes in one compartment lead to adaptations in the other The IAF may contribute more to the proinflammatory component of the metabolic syndrome by the secretion of adipokines and cytokines with a different profile compared with sc fat The contributory role of the proinflammatory IAF and the voluminous SAF on infertility and anovulation needs further elucidation.

The finding of this study only shows an association of the volumes of IAF and SAF with anovulation, and no conclusions can be drawn on a cause-and-effect relationship. A limitation of this study was the small sample size.

Larger studies are needed to confirm our data in obese infertile ovulatory and anovulatory women with respect to body fat distribution and the role of these different fat compartments in insulin resistance and anovulation. This study was limited to obese women and cannot be extrapolated to women of normal weight.

In seven of the 57 study subjects, PCOS could not be diagnosed or excluded because the ovaries could not be visualized by transvaginal ultrasonography, therefore limiting the comparison of the findings with previous studies on women with PCOS. Excluding the one anovulatory woman with type I diabetes mellitus would not have changed the outcome of the analysis.

Because 56 of the 57 study subjects were of Caucasian origin, the presented data cannot be extrapolated to non-Caucasian populations.

In conclusion, in anovulatory women with obesity and infertility, the total amount of abdominal and trunk fat is significantly increased, with an significant increase in the volume of SAF and no difference in the volume of IAF compared with ovulatory women with obesity and infertility.

Abdominal and trunk fat accumulation and SAF accumulation but not the IAF are associated with anovulation. This association is, however, only based on the volume of these fat compartments and does not necessarily reflect the consequences of their metabolic activity.

The authors thank and appreciate Mr. Wim Tukker, radiological technician of the Department of Radiology, for performing the IAF and SAF measurements of the ssCT so meticulously.

A grant was received from the University Medical Center Groningen, The Netherlands, for the CT and DEXA scans. A grant was also received from ZonMW Dutch government funding for a subsequent randomized controlled trial on lifestyle intervention in women with obesity and infertility.

Part of these data were presented at the annual meeting of the European Society of Human Reproduction and Embryology Abstract O in Barcelona, Spain, in July Disclosure Summary: W. declares that the disclosure statements of the co-authors have been obtained properly and that no conflicts of interests are known to him.

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J Clin Endocrinol Metab 81 : — Escobar-Morreale HF , San Millán JL Abdominal adiposity and the polycystic ovary syndrome. Trends Endocrinol Metab 18 : — High levels of estrogens can also affect how your body processes insulin, therefore causing problems like diabetes and insulin resistance , as is the case with polycystic ovarian syndrome, or PCOS more on this below.

According to the American Society for Reproductive Medicine ASRM , a higher body-fat percentage can also affect the success of fertility treatments , such as IVF.

When this happens, non-essential systems, like reproductive function, slow and shut down. Your hypothalamus, where hormones such as estrogens are regulated, gets sluggish, and this leads to irregular, or entirely absent, menstrual cycles.

For example, research has been looking into how genetics plays a role in your body weight. There are also treatable medical conditions, like hormonal conditions or eating disorders, that play a role in BMI. Polycystic ovary syndrome PCOS is a hormonal condition that can cause irregular menstrual cycles, extra hair growth, fatigue, and weight gain.

You may also have higher levels of androgens called hyperandrogenism — but not all women with PCOS experience this. This may result in chronically elevated blood sugar and insulin levels. Eating disorders, such as anorexia , can also lead to nutrient deficiencies that decrease levels of estrogens, negatively affecting ovulation and leading to the absence of periods altogether.

When a woman is in recovery, and gaining weight, she might also experience changes in her cycle as her hormones recalibrate. Note: There are also meta-analyses — studies that combine estimates from a whole bunch of studies — that also suggest that weight loss has a positive effect on fertility.

Montenegro recommends talking to a health professional who specializes in metabolic fertility issues. The good news is that there are steps you can take to improve your overall health, especially when it comes to conceiving. One of the things you can be proactive about is getting your hormone levels tested with Modern Fertility.

Knowing your levels can help start a conversation with your doctor about your ability to conceive, and they can work with you to decide whether your BMI could potentially be a factor in getting pregnant. This article was medically reviewed by Dr.

Nataki Douglas, the Chair of the Modern Fertility Medical Advisory Board. Click here to view original article. IVFMD holds a bi-annual raffle for a free IVF cycle.

Enter your email below to access our entry form for your chance to win! Since , IVFMD has helped over 10, individuals and couples achieve their dreams of having a child.

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Research indicates that weight can affect your fertility, but all bodies are different — there are many factors that impact your ability to conceive. Hormones play a major role when it comes to fertility.