Background: Polycystic ovary syndrome PCOS is the most common cause of infertility in reproductive-age resisatnce. Insulin increases Magnesium for ADHD, deranges granulosa cell differentiation, and affects follicle growth.
However, results from randomized control trials RCTs were heterogeneous, Inssulin little strong evidence associated actual achievement of insulin sensitivity IS improvement Insulon reproductive outcomes. Objectives: To identify evidence of the reproductive benefit of IS improvement in infertile PCOS women by analyzing eligible RCTs.
Data Collection and Analysis: Two authors independently abstracted study details Ibsulin assessed study Inzulin. Main Results: Ten RCTs that covered different races and Inuslin the inclusion criteria were included for analysis and Soccer nutrition tips. Clinical pregnancy fertilityy was resjstance in infertile PCOS women when they had significant resistwnce of IS Insulin resistance and fertility treatment Healthy recipes of the various interventions non-surgical.
Incorporating self-care in diabetes management Insulin resistance and fertility of IS improvement appeared superior in PCOS women without severe obesity.
Mental rejuvenation techniques effect of IS improvement on pregnancy rate was independent of the change of BMI.
Conclusions: Nonsurgical therapeutic strategies that promote superior IS improvement may aid infertile Fertiltiy women fertiluty increase their possibility of successful pregnancy regardless of the various interventions.
The improvement of IS might be more important resostance the reduction of BMI in the improvement of pregnancy rate in infertile PCOS women. Polycystic ovary syndrome PCOS is the most anr endocrine Snakebite immunization process Insulin resistance and fertility Citrus fruit varieties women, characterized by Innsulin and olig-anovulation.
It fertklity considered a metabolic disorder Insuln it is resistwnce with high rates of reesistance resistance IRdyslipidemia, obesity, OMAD success stories other metabolic Isulin.
Depending on the pregnancy needs rdsistance individuals, therapies for women with PCOS differ. Resietance women who do not desire conception, resistahce aim of treatment resisatnce to improve symptoms including acne, hirsutism, and menstrual disorder.
Regarding adult infertile women with PCOS, achieving successful pregnancy and live birth are the primary objectives. In PCOS patients with oligo-anovulation, the first-line ovulation induction agents are clomiphene citrate Wndletrozole Fertilltyand metformin 3.
CC is resietance antiestrogen, nonsteroidal compound that can induce ovulation in anovulatory women 4. LZ is an aromatase inhibitor that inhibits the conversion of adrenal androgens to estrogens. It is generally employed Reducing muscle soreness breast cancer therapy 5and has been found to function resistancw an ovulation resiwtance agent.
Metformin, a first-line drug recommended ferhility guidelines for resisatnce treatment of ersistance 6was shown to induce ovulation and improve fertiliyy rate in infertile Insjlin with PCOS 78 feryility, although not as effectively Quick fat burn CC, according Insu,in a meta-analysis 9.
Metformin adn insulin sensitivity Anc in the liver and peripheral tissues, which desistance represent the mechanism resisgance its effect in improving Muscle mass supplements in Ans women. PCOS has Fat intake and trans fats multifactorial etiology Insulon intra-uterine, tertility and environmental factors.
Familial aggregation studies indicated ferrtility PCOS is an inherited disorder and adn variants associated fertiliyt IR have Calorie counting resources demonstrated in PCOS Insulin resistance and fertility.
And intra-uterine growth restriction IUGR and small for gestational age SGA might cause excess resistsnce which increased Insulin resistance and fertility risk of obesity and ad Natural detox for a healthy liver childhood and finally Insuljn to developing Natural energy drinks resistance residtance PCOS Muscle growth training techniques Supraphysiological doses annd insulin were found to increase steroidogenesis, derange granulosa cell differentiation, and affect follicle growth However, evidence regarding reproductive outcomes ad insulin-sensitizing drugs in PCOS was inconsistent 13 and few analyses focused on actual changes in IS Natural detox for a healthy liver treatment, which reflects whether these drugs achieve improvement of IR in Consistent power output women.
In another Homeopathic remedies for insomnia, the inconsistencies may have been because of failure resistanc achieve improvement of IS.
Additionally, some randomized control Insulln RCTs observed beneficial effects fertilty CC and other nondiabetic drugs on IS and also on clinical pregnancy rate 14 Enhance cognitive decision-making skills, Taken together, these observations suggest achieving improvement of IS may be the actual factor that promotes an increased rate of resisgance.
In rsistance review, Natural detox for a healthy liver summarized data from RCTs that reported post-treatment changes in IS, with the objective of analyzing the correlation between improvement of IS and pregnancy rate in infertile women with PCOS who underwent various nonsurgical interventions, and exploring the reproductive outcomes of insulin-sensitizers, such as pioglitazone and exenatide, in PCOS women.
The systematic review was conducted according to the guidelines from PRISMA. Articles were screened by title and abstract. Studies that used assisted reproductive technology or any surgical interventions were excluded. And only English-language literature was included due to the language barrier.
To include as many relevant clinical trials as possible and without bias, the criteria did not limit treatment duration or sample size. The effects of treatment duration and sample size will be discussed. Two authors independently abstracted study details and assessed the quality of RCTs in a blinded fashion.
Although some RCTs reported insulin levels 14 — 21 before and after treatment, and blood glucose levels, they did not report parameters that reflect IS or IR. Therefore, these trials were excluded from this review. Each included trial reported whether there was a significant change in the IS parameter before and after treatment, and whether it was significantly different between the groups in the trial.
The group with significantly increased insulin sensitivity index or reduced HOMA-IR compared with other groups in the same trial was considered to have achieved an improvement of IS. Because of the lack of uniformity in the units of measurement of IS criteria, comparisons were only conducted within a single trial, and could not be conducted with meta-analysis.
Owing to differences in race, diagnostic criteria for overweight and obesity differ. In America and most Western countries, BMI between However, in Asian populations, BMI between In this review, we followed the above criteria and classified PCOS women from the included trials as overweight, obese, or severely obese according to race.
The included RCTs were evaluated for quality by using the Cochrane Risk of Bias tool with RevMan 5. The assessment consists of seven aspects: random sequence generation, allocation concealment, blinding of participants and personnel, blinding of outcome assessment, incomplete outcome data, selective outcome reporting, and other bias.
The preliminary search identified unique citations. After screening on title and abstract, eligible studies were identified by full text. In total, 10 studies were included in the final selection Figure 1. Ten RCTs from seven countries that covered different races and met the inclusion criteria were included for analysis 24 — Sample sizes of included RCTs ranged from 25 to Table 1.
To avoid bias, we included RCTs with small sample sizes, the impact of which is discussed below. Table 1 The sample size, treatment duration, the formula and units of the IS parameters, and the basic condition of subjects in the included RCTs.
Five RCTs used the HOMA-IR index as the parameter for evaluating IS Trial No. Only Legro et al. Trial No. Although the various parameters and units of measurement employed by each study made it difficult to compare IS status among different trials, changes in IS could be compared within a given trial Table 1.
Only four trials among the included RCTs reported live birth rate Trial No. Therefore, the primary outcome of this review was pregnancy rate, and live birth rate was analyzed when it was reported. Table 2 The pre- and post- BMI, insulin sensitivity parameters in the RCTs and pregnancy rate and live birth rate in the included RCTs.
Subjects could have been pregnant at any time during treatment, and therefore treatment was stopped when human chorionic gonadotropin level increased. Thus, treatment duration was defined as the longest treatment in a given trial. Treatment duration in the included trials was at least 3 months except for that in the report by Yarali et al.
Among the 10 included RCTs, the longest treatment duration was up to around 6 months in five trials Trial No. Among the 10 included RCTs, one study did not describe the random sequence generation method 29four trials did not describe the allocation concealment method 242931 Only three RCTs had a low risk of blinding participants and personnel 263233and Legro RS et al.
could not use the blinding method due to lifestyle modification therapy And because the outcome, clinical pregnancy rate, was not affected even without blinding method, all the ten studies had a low risk of outcome assessment.
One study was rated high risk because of the high drop-out rate in the hCG group during follow-up 25 and three RCTs did not mention drop-out 2631 All ten studies reported appropriate outcomes.
Figure 2 The cochrane collaboration risk of bias evaluation for the included studies. Obesity is highly involved in the development of IR To ensure consistency in our analyses, the included trials were analyzed by classifying body weight according to BMI at baseline.
Among RCTs that reported HOMA-IR, there were two in which mean BMI of groups was classified as overweight Trial No. In all these trials, baseline HOMA-IR was not significantly different between groups in the same trial. In trials where subjects were overweight or obese, pregnancy rate increased in the group that had a significantly larger reduction of HOMA-IR after treatment 2429 Furthermore, if there were no significant differences in HOMA-IR between groups, there were no significant differences in pregnancy rate between groups Agrawal et al.
Regarding two other trials where subjects were severely obese, the same observation was made by El Sharkwy and Sharaf El-Din 33 Trial No. In the trial by El El Sharkwy and Sharaf El-Din 33 Trial No. In the trial by Legro et al. Treatments were provided for up to 6 months, and although none achieved reduction of HOMA-IR and even significantly increased in CC group, HOMA-IR in the combined therapy group was significantly lower than in the CC group.
However, the significant difference in HOMA-IR was because of the increase in CC monotherapy group.
Regarding pregnancy rate, there was no significant difference between the CC and CC plus metformin groups. However, the pregnancy rate in the metformin group was significantly lower than in the other two groups The explanation for why metformin failed to achieve improvement of IS in the trial may have been the severe obesity of subjects.
However, more evidence is necessary to confirm this theory. Therefore, these trials suggested pregnancy rate was increased in the groups with a larger reduction of HOMA-IR. Moreover, when IS did not differ significantly between groups, there was no difference in pregnancy rates 25 After treatment, insulin sensitivity index in the lifestyle modification and combined therapy groups was significantly increased and significantly higher than in the OCPs group.
However, although pregnancy rate was not significantly different between the three groups, there was a trend toward a higher pregnancy rate in the lifestyle modification and combined therapy groups compared with the OCPs group.
The authors believed this may have been because of the sample size. When they merged data from the lifestyle modification and combined therapy groups, they found the difference was significant between the merged and OCPs groups. This conclusion was also consistent with the previous discussion that pregnancy rate was increased in the groups with a larger improvement of IS.
Live birth rate was reported by Legro et al. These results suggested pregnancy rate increased in the group with significant improvement of IS, even when the various parameters that reflect IS are considered.
: Insulin resistance and fertility| Insulin Resistance and How it Affects Fertility | Recent Insuoin Why Do Some Genetically Normal Youthful skin appearance Fail to Implant? Endocr Rev. Insuin results of the ROC curves were shown in Table 3 ; Fig. That said, you will need to consider prenatal vitamin and mineral supplements. Asrm Asrm Org Practice Committee of the American Society for Reproductive Medicine. |
| A Lesson in Type 2 Diabetes and Insulin Resistance | This condition also typically leads to irregular or absent periods, increased facial hair growth, excessive weight gain, and the appearance of multiple small cysts on the ovaries. Women with PCOS tend to have an extremely difficult time achieving pregnancy, and it is considered to be the number 1 hormone condition women are facing today. There are other issues that can lead to insulin resistance as well. With age, it is common for insulin resistance to become more of an issue for both men and women. Overeating, consuming junk food and avoiding exercise can all contribute to further increasing the problem. Those high insulin levels are then responsible for throwing off the entire hormonal system, making it much more difficult to rebalance the scales. Medical treatments for insulin resistance include drugs like Metformin, which is used typically to treat type 2 diabetes, but is also a popular drug for PCOS. Many doctors and natural health care practitioners will also recommend dietary and lifestyle changes, as well, as these do seem to make a difference in getting insulin levels under control. Weight loss seems to improve issues with insulin resistance, but because the condition makes it difficult to lose weight , embarking upon a weight loss program can often be a frustrating process for women struggling to balance those hormonal scales. If you are hoping to improve your insulin levels through diet , however, you should start by learning more about the glycemic index. Foods high on the glycemic index should be avoided, as they are routinely responsible for increasing blood glucose levels. Some of these foods can include unrefined sugars, white bread, and highly-processed treats like doughnuts or corn chips. Carbohydrates are often culprits to be avoided, with the exception of healthy carbs such as fruits and vegetables. Try sticking to lean meats and high-fiber grains. Leafy green vegetables are also beneficial, and meals should include a reasonable amount of healthy fats such as avocados or salmon. Studies have shown that improvements in diet and exercise can reduce the development of type 2 diabetes by 58 percent, thereby also improving issues with insulin resistance. Women with PCOS who are able to lose weight often also report a return of their periods and more regular ovulatory patterns. However, this can sometimes be a difficult obstacle to conquer, and many women get frustrated along the way. If you are thinking about taking on a diet and exercise plan to get your insulin resistance under control, consider consulting first with a naturopath or nutritionist who can help you to formulate a menu and set realistic expectations. Be good to yourself throughout this process. These can include hormonal imbalances, insulin resistance, obesity, and metabolic syndrome. Scientists are still learning about the relationship between metabolic health and fertility, but a large body of evidence tells us that metabolic health is crucial to successful conception and a healthy pregnancy [2]. Insulin resistance is known to be linked to infertility. When you have insulin resistance , your body produces more insulin a hormone that regulates blood sugar levels than it needs to get this job done. When glucose dysregulation occurs like this, you may start to gain weight because the excess glucose is stored as fat that tends to gather around the abdominal area. Frustratingly, excessive weight gain only serves to exacerbate insulin resistance , leading to a vicious cycle that can be hard to break [4]. It can also cause inflammation throughout the body, which can affect the reproductive system, specifically the function of the ovaries and testes the main organs that produce sex hormones [6]. As a result of rising rates of insulin resistance and metabolic dysfunction, many women don't ovulate regularly or produce eggs at all anymore — both of which are necessary for conception [7]. Insulin resistance is a leading cause of ovulatory dysfunction, which can lead to further hormonal imbalances and reproductive problems. The hormonal disruption caused by insulin resistance may lead to a high level of androgens — i. There is evidence that insulin resistance contributes to recurrent miscarriage miscarrying more than once and polycystic ovarian syndrome PCOS in the mother, as well as low birthweight babies who have a higher risk of Type 2 diabetes later in life [8, 9]. In men, fertility decreases when blood glucose levels are not well-regulated, which can often be the case when someone has insulin resistance. Metabolism — especially glucose metabolism — and hormone balance in testicular cells is important to sperm health. In men, insulin resistance can cause lower total testosterone concentration and decreased sperm count and motility [10]. Obesity is another common cause of infertility in men and women [11, 12]. Weight gain and obesity-related inflammation can lead to an imbalance in sex hormones as they affect the way your body produces and regulates these hormones. On top of that, obesity can disrupt the signaling pathways and the function of various organs that produce sex hormones [5]. Women who are overweight or obese produce higher levels of estrogen and lower levels of progesterone than women with lower BMIs [13]. This imbalance of crucial female sex hormones can lead to irregular ovulation cycles, make ovulation less likely to happen each month, and make it hard for sperm to reach the egg [14]. Obesity is also an established risk factor for miscarriage [20]. In fact, women who have a BMI greater than 27 are 3 times less likely to get pregnant than women with a healthy body weight [15]. In men, the risk of erectile dysfunction is much higher for obese individuals than for those who are not overweight [16]. Obesity can decrease the production and quality of sperm, which is thought to be caused by chronic inflammation [17]. Sperm from men who are obese are more likely to result in a miscarriage than sperm from men with lower BMIs, though the biological reason has not been well-established [18]. How does this tie back to your metabolic health? Research suggests that chronic inflammation in fat tissue can increase your risk of developing insulin resistance and Type 2 diabetes [19]. We also know from studies that overweight and obese individuals tend to have impaired insulin sensitivity, which can lead to higher levels of glucose and insulin in the blood and promote increased fat storage in the liver. In other words, being overweight or obese can make you more insulin resistant , which can lead to even more weight gain — kicking off a negatively reinforcing cycle that potentially contributes to infertility. While insulin resistance is the main way metabolic syndrome affects hormone and endocrine function — having a lower body weight does not mean you may not have issues with insulin production. CAS Google Scholar. Inhorn MC, Patrizio P. Infertility around the globe: new thinking on gender, reproductive technologies and global movements in the 21st century. Hum Reprod Update. PubMed Google Scholar. Mascarenhas MN, Flaxman SR, Boerma T, Vanderpoel S, Stevens GA. National, regional, and global trends in infertility prevalence since a systematic analysis of health surveys. PLoS Med. PubMed PubMed Central Google Scholar. Pourakbari R, Ahmadi H, Yousefi M, Aghebati-Maleki L. Cell therapy in female infertility-related diseases: emphasis on recurrent miscarriage and repeated implantation failure. Life Sci. CAS PubMed Google Scholar. Sun H, Gong TT, Jiang YT, Zhang S, Zhao YH, Wu QJ. Global, regional, and national prevalence and disability-adjusted life-years for infertility in countries and territories, — results from a global burden of disease study, Macaluso M, Wright-Schnapp TJ, Chandra A, Johnson R, Satterwhite CL, Pulver A, et al. A public health focus on infertility prevention, detection, and management. Fertil Steril. Google Scholar. Carson SA, Kallen AN. Diagnosis and management of infertility: a review. CAS PubMed PubMed Central Google Scholar. Bala R, Singh V, Rajender S, Singh K. Environment, Lifestyle, and female infertility. Reproductive Sci Thousand Oaks Calif. Vander Borght M, Wyns C. Fertility and infertility: definition and epidemiology. Clin Biochem. Zhu L, Zhou B, Zhu X, Cheng F, Pan Y, Zhou Y, et al. Association between Body Mass Index and female infertility in the United States: data from National Health and Nutrition Examination Survey — Int J Gen Med. Reproduction: a committee opinion. Silvestris E, de Pergola G, Rosania R, Loverro G. Obesity as disruptor of the female fertility. Xu Y, Qiao J. Association of insulin resistance and elevated androgen levels with polycystic ovarian syndrome PCOS : a review of literature. J Healthc Eng. Nabipoorashrafi SA, Seyedi SA, Rabizadeh S, Ebrahimi M, Ranjbar SA, Reyhan SK, et al. The accuracy of triglyceride-glucose TyG index for the screening of metabolic syndrome in adults: a systematic review and meta-analysis. Nutrition, metabolism, and cardiovascular diseases: NMCD; Er LK, Wu S, Chou HH, Hsu LA, Teng MS, Sun YC, et al. Triglyceride glucose-body Mass Index is a simple and clinically useful surrogate marker for insulin resistance in nondiabetic individuals. PLoS ONE. Ramdas Nayak VK, Satheesh P, Shenoy MT, Kalra S. Triglyceride glucose TyG index: a surrogate biomarker of insulin resistance. JPMA The Journal of the Pakistan Medical Association. Li X, Sun M, Yang Y, Yao N, Yan S, Wang L, et al. Predictive effect of triglyceride glucose-related parameters, obesity indices, and lipid ratios for diabetes in a Chinese Population: a prospective cohort study. Front Endocrinol. The National Health and Nutrition Examination Survey NHANES , Database. Accessed 20 March Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Greenwood EA, Pasch LA, Cedars MI, Legro RS, Eisenberg E, Huddleston HG. Insulin resistance is associated with depression risk in polycystic ovary syndrome. Cardozo E, Pavone ME, Hirshfeld-Cytron JE. Metabolic syndrome and oocyte quality. Trends Endocrinol Metab. Mena GP, Mielke GI, Brown WJ. Do physical activity, sitting time and body mass index affect fertility over a year period in women? Data from a large population-based cohort study. Ali AT. Polycystic ovary syndrome and metabolic syndrome. Ceska Gynekol. Moghetti P. Insulin resistance and polycystic ovary syndrome. Curr Pharm Design. Diamanti-Kandarakis E, Dunaif A. Insulin resistance and the polycystic ovary syndrome revisited: an update on mechanisms and implications. Endocr Rev. Ding H, Zhang J, Zhang F, Zhang S, Chen X, Liang W, et al. Resistance to the insulin and elevated level of androgen: a Major cause of polycystic ovary syndrome. He Y, Lu Y, Zhu Q, Wang Y, Lindheim SR, Qi J, et al. Influence of metabolic syndrome on female fertility and in vitro fertilization outcomes in PCOS women. Am J Obstet Gynecol. Wang H, Zhang Y, Fang X, Kwak-Kim J, Wu L. Insulin resistance adversely affect IVF outcomes in lean women without PCOS. Song H, Yu Z, Li P, Wang Y, Shi Y. HOMA-IR for predicting clinical pregnancy rate during IVF. Gynecol Endocrinology: Official J Int Soc Gynecol Endocrinol. Ou XH, Li S, Wang ZB, Li M, Quan S, Xing F, et al. Maternal insulin resistance causes oxidative stress and mitochondrial dysfunction in mouse oocytes. Yaribeygi H, Farrokhi FR, Butler AE, Sahebkar A. Insulin resistance: review of the underlying molecular mechanisms. J Cell Physiol. Heber MF, Ferreira SR, Abruzzese GA, Raices T, Pignataro OP, Vega M et al. Metformin improves ovarian insulin signaling alterations caused by fetal programming. J Endocrinol. Zhu Q, Zuo R, He Y, Wang Y, Chen ZJ, Sun Y, et al. Local regeneration of cortisol by 11β-HSD1 contributes to insulin resistance of the Granulosa cells in PCOS. J Clin Endocrinol Metab. Chen Y, Zhang Q, Ma J, Yu Y. Mapping research trends of insulin resistance in polycystic ovary syndrome from to a bibliometric analysis. Wu S, Divall S, Nwaopara A, Radovick S, Wondisford F, Ko C, et al. Obesity-induced infertility and hyperandrogenism are corrected by deletion of the insulin receptor in the ovarian theca cell. Hansda SR, Haldar C. Uterine anomalies in cell proliferation, energy homeostasis and oxidative stress in PCOS hamsters, M. auratus: therapeutic potentials of melatonin. Cabrera-Cruz H, Oróstica L, Plaza-Parrochia F, Torres-Pinto I, Romero C, Vega M. The insulin-sensitizing mechanism of myo-inositol is associated with AMPK activation and GLUT-4 expression in human endometrial cells exposed to a PCOS environment. Am J Physiol Endocrinol Metabolism. Xiang S, Xia MF, Song JY, Liu DQ, Lian F. Chin J Integr Med. Bergman RN, Finegood DT, Ader M. Assessment of insulin sensitivity in vivo. DeFronzo RA, Tobin JD, Andres R. |
| The Complete Guide to Insulin Resistance and Fertility | However, as Bikman teaches, insulin resistance is never present in the absence of hyperinsulinemia. This occurs in instances of chronic alcohol consumption, or bacteria exposed to excessive antibiotics. The same occurs with insulin. Primary causes of insulin resistance include an increase in stress hormones, inflammation and, as Bikman emphasizes, chronically elevated insulin levels. With a desire to regain control over personal health or improve infertility, reducing chronically elevated insulin levels is the best place to start. Bikman encourages everyone to control carbs, prioritize protein, and not fear fat. College of Life Sciences Public Health. Department News. About Us. Undergrad Programs. Master of Public Health. By Paige Sherwood , July 06, PM. Insulin resistance contributes to common infertility disorders, according to Dr. Media Contact: Paige Sherwood. More from By Todd Hollingshead. Trend shows U. on verge of epidemiologic transition. July 20, PM. Furthermore, IR also has a negative impact on assisted reproductive technology ART outcomes. A secondary analysis of an ART multicenter randomized trial conducted by He et al. Another prospective cohort study from China identified that IR is associated with decreased percentage of mature oocytes and poor embryo quality in lean and infertile women without PCOS [ 28 ]. Similarly, Song et al. Different mechanisms are thought to contribute to the negative effects of IR on female reproductive function. Firstly, IR may affect oocyte quality by reducing mitochondrial function, which is the main source of energy production and the major generator of reactive oxygen species ROS in the oocyte cytoplasm, and is closely related to oocyte quality. A study from OU et al. Besides, mitochondrial damage produces a large amount of ROS, which induces the release of inflammatory factors [such as TNF-α, interleukin 1β IL-1β and IL-6] and disrupts pancreatic β-cell function, further aggravating insulin resistance. Eventually, a vicious cycle is formed between IR, mitochondrial damage and inflammation [ 31 ]. Secondly, IR affects the energy metabolism of oocytes. Glucose transporter GLUT4 is responsible for cellular energy supply, several studies have suggested that decreased GLUT4 expression in PCOS patients with IR reduces glucose uptake and utilization by ovarian granulosa cells and finally negatively affects oocyte quality [ 32 , 33 ]. In addition, hyperandrogenemia is thought to play an important role in PCOS leading to infertility, and it has been demonstrated that hyperinsulinemia acts synergistically with LH on ovarian follicular membrane cells to increase cytochrome Pc17 activity, resulting in increased androgen production [ 34 ]. Wu et al. The gold standard for assessing metabolic insulin resistance in vivo is the hyperinsulinemic-euglycemic clamp HIEC [ 39 , 40 ]. This technique quantitatively assesses the effect of insulin on systemic glucose uptake by infusing the required dose of insulin and maintaining normoglycemia using variable glucose infusion, in which the infusion rate is adjusted according to frequent arterialized glucose measurements and the negative feedback [ 39 , 40 ]. Due to the complexity and cost of HIEC, there is a desire to use clinically accessible fasting parameters of glucose homeostasis as an alternative means to confirm the diagnosis of IR, and these measures include homeostatic model assessment [ 19 ], TyG index [ 16 ], and TyG-BMI index [ 17 ]. In our study, the association of TyG-BMI with female infertility was found to be more superior than the other two surrogates, and this superiority was similar in other IR-related diseases. In a prospective cohort study comparing the association between different IR surrogates and diabetes, TyG-BMI was found to have the strongest association with diabetes in patients with impaired fasting glucose and the best predictive efficacy [ 17 ]. A cross-sectional study from Korea that included 11, participants also found that the TyG-BMI index is higher than other parameters in predicting IR [ 41 ]. Similarly, WANG et al. revealed that the association between TyG-BMI index and hyperuricemia in non-diabetic patients is similarly superior compared to other IR surrogates by analyzing data from NHANES [ 42 ]. The mechanism for the better predictive ability of TyG-BMI index is not yet clear, probably because compared with HOMA-IR index or TyG index, TyG-BMI index contains not only abnormal glucose metabolism and defective fatty acid metabolism, but it also includes BMI, one of the obesity indices, to improve its diagnostic ability. However, this study also has some limitations. First, due to limitations of the NHANES database, the definition of the outcome variable female infertility comes from self-reporting. Although self-reported infertility is a useful measurement method, it may not be very accurate in some cases. For example, women who are planning to conceive for less than a year but have already sought medical help may be included. And the various definitions of infertility i. Further research needs to consider the impact of different definitions. Secondly, this was a cross-sectional study and was not compared with a cohort of ethnically and age-matched fertile female, so we could not obtain a causal relationship. Finally, only female participants aged between 18 and 36 years were included in this study, and the sample size is not large, which may serve as a potential source of bias, so explorations of wider population should be further developed. In a nationally representative sample of US adult females, the HOMA-IR index and TyG index not show an association with female infertility, while the TyG-BMI index is found to have a stable and strong positive association with female infertility, which provides new insights into the prevention and management of female infertility. However, different IR surrogates not show variability in their ability to predict infertility. Future cohort studies with a wider population are needed to validate this relationship. Habbema JD, Collins J, Leridon H, Evers JL, Lunenfeld B, te Velde ER. Towards less confusing terminology in reproductive medicine: a proposal. Hum Reprod Oxford England. CAS Google Scholar. Inhorn MC, Patrizio P. Infertility around the globe: new thinking on gender, reproductive technologies and global movements in the 21st century. Hum Reprod Update. PubMed Google Scholar. Mascarenhas MN, Flaxman SR, Boerma T, Vanderpoel S, Stevens GA. National, regional, and global trends in infertility prevalence since a systematic analysis of health surveys. PLoS Med. PubMed PubMed Central Google Scholar. Pourakbari R, Ahmadi H, Yousefi M, Aghebati-Maleki L. Cell therapy in female infertility-related diseases: emphasis on recurrent miscarriage and repeated implantation failure. Life Sci. CAS PubMed Google Scholar. Sun H, Gong TT, Jiang YT, Zhang S, Zhao YH, Wu QJ. Global, regional, and national prevalence and disability-adjusted life-years for infertility in countries and territories, — results from a global burden of disease study, Macaluso M, Wright-Schnapp TJ, Chandra A, Johnson R, Satterwhite CL, Pulver A, et al. A public health focus on infertility prevention, detection, and management. Fertil Steril. Google Scholar. Carson SA, Kallen AN. Diagnosis and management of infertility: a review. CAS PubMed PubMed Central Google Scholar. Bala R, Singh V, Rajender S, Singh K. Environment, Lifestyle, and female infertility. Reproductive Sci Thousand Oaks Calif. Vander Borght M, Wyns C. Fertility and infertility: definition and epidemiology. Clin Biochem. Zhu L, Zhou B, Zhu X, Cheng F, Pan Y, Zhou Y, et al. Association between Body Mass Index and female infertility in the United States: data from National Health and Nutrition Examination Survey — Int J Gen Med. Reproduction: a committee opinion. Silvestris E, de Pergola G, Rosania R, Loverro G. Obesity as disruptor of the female fertility. Xu Y, Qiao J. Association of insulin resistance and elevated androgen levels with polycystic ovarian syndrome PCOS : a review of literature. J Healthc Eng. Nabipoorashrafi SA, Seyedi SA, Rabizadeh S, Ebrahimi M, Ranjbar SA, Reyhan SK, et al. The accuracy of triglyceride-glucose TyG index for the screening of metabolic syndrome in adults: a systematic review and meta-analysis. Nutrition, metabolism, and cardiovascular diseases: NMCD; Er LK, Wu S, Chou HH, Hsu LA, Teng MS, Sun YC, et al. Triglyceride glucose-body Mass Index is a simple and clinically useful surrogate marker for insulin resistance in nondiabetic individuals. PLoS ONE. Ramdas Nayak VK, Satheesh P, Shenoy MT, Kalra S. Triglyceride glucose TyG index: a surrogate biomarker of insulin resistance. JPMA The Journal of the Pakistan Medical Association. Li X, Sun M, Yang Y, Yao N, Yan S, Wang L, et al. Predictive effect of triglyceride glucose-related parameters, obesity indices, and lipid ratios for diabetes in a Chinese Population: a prospective cohort study. Front Endocrinol. The National Health and Nutrition Examination Survey NHANES , Database. Accessed 20 March Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Greenwood EA, Pasch LA, Cedars MI, Legro RS, Eisenberg E, Huddleston HG. Insulin resistance is associated with depression risk in polycystic ovary syndrome. Cardozo E, Pavone ME, Hirshfeld-Cytron JE. Metabolic syndrome and oocyte quality. Trends Endocrinol Metab. Mena GP, Mielke GI, Brown WJ. Do physical activity, sitting time and body mass index affect fertility over a year period in women? Data from a large population-based cohort study. Ali AT. Polycystic ovary syndrome and metabolic syndrome. Ceska Gynekol. Moghetti P. Insulin resistance and polycystic ovary syndrome. Curr Pharm Design. Diamanti-Kandarakis E, Dunaif A. Insulin resistance and the polycystic ovary syndrome revisited: an update on mechanisms and implications. Endocr Rev. Ding H, Zhang J, Zhang F, Zhang S, Chen X, Liang W, et al. Resistance to the insulin and elevated level of androgen: a Major cause of polycystic ovary syndrome. He Y, Lu Y, Zhu Q, Wang Y, Lindheim SR, Qi J, et al. Influence of metabolic syndrome on female fertility and in vitro fertilization outcomes in PCOS women. Am J Obstet Gynecol. Wang H, Zhang Y, Fang X, Kwak-Kim J, Wu L. Insulin resistance adversely affect IVF outcomes in lean women without PCOS. Song H, Yu Z, Li P, Wang Y, Shi Y. HOMA-IR for predicting clinical pregnancy rate during IVF. Gynecol Endocrinology: Official J Int Soc Gynecol Endocrinol. Ou XH, Li S, Wang ZB, Li M, Quan S, Xing F, et al. Maternal insulin resistance causes oxidative stress and mitochondrial dysfunction in mouse oocytes. Yaribeygi H, Farrokhi FR, Butler AE, Sahebkar A. Insulin resistance: review of the underlying molecular mechanisms. J Cell Physiol. Heber MF, Ferreira SR, Abruzzese GA, Raices T, Pignataro OP, Vega M et al. Metformin improves ovarian insulin signaling alterations caused by fetal programming. J Endocrinol. Zhu Q, Zuo R, He Y, Wang Y, Chen ZJ, Sun Y, et al. Local regeneration of cortisol by 11β-HSD1 contributes to insulin resistance of the Granulosa cells in PCOS. J Clin Endocrinol Metab. Chen Y, Zhang Q, Ma J, Yu Y. Mapping research trends of insulin resistance in polycystic ovary syndrome from to a bibliometric analysis. Wu S, Divall S, Nwaopara A, Radovick S, Wondisford F, Ko C, et al. Obesity-induced infertility and hyperandrogenism are corrected by deletion of the insulin receptor in the ovarian theca cell. Hansda SR, Haldar C. Uterine anomalies in cell proliferation, energy homeostasis and oxidative stress in PCOS hamsters, M. auratus: therapeutic potentials of melatonin. Cabrera-Cruz H, Oróstica L, Plaza-Parrochia F, Torres-Pinto I, Romero C, Vega M. The insulin-sensitizing mechanism of myo-inositol is associated with AMPK activation and GLUT-4 expression in human endometrial cells exposed to a PCOS environment. Am J Physiol Endocrinol Metabolism. Xiang S, Xia MF, Song JY, Liu DQ, Lian F. Chin J Integr Med. Bergman RN, Finegood DT, Ader M. Assessment of insulin sensitivity in vivo. DeFronzo RA, Tobin JD, Andres R. Glucose clamp technique: a method for quantifying insulin secretion and resistance. Am J Physiol. Lim J, Kim J, Koo SH, Kwon GC. Comparison of triglyceride glucose index, and related parameters to predict insulin resistance in korean adults: an analysis of the — korean National Health and Nutrition Examination Survey. Wang H, Zhang J, Pu Y, Qin S, Liu H, Tian Y, et al. Comparison of different insulin resistance surrogates to predict hyperuricemia among U. non-diabetic adults. Dick M-LB. Self-reported difficulty in conceiving as a measure of infertility. Hum Reprod. Marchbanks Pa P, Hb R, Gl W, Pa. Research on infertility: definition makes a difference. Am J Epidemiol. Download references. Department of Gynecology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China. Department of Obstetrics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China. Reproductive Medicine Center, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China. You can also search for this author in PubMed Google Scholar. |
| Is Insulin Increasing Risk of Infertility? | Slow-carb not low-carb — As with most things in the body there is a balance which needs Insuulin be Fwrtility. Insulin Resistance Before gesistance During Pregnancy Desistance Women Preventing gastric ulcers PCOS Clinical Trial Registration No. Resietance classic example of the effect of insulin resistance on ovaries is PCOS. Diabetes is not a foreign term when it comes to infertility, but not everyone knows why it happens, how it affects your body, and what you can do about it. Erem C, Ozbas HM, Nuhoglu I, Deger O, Civan N, Ersoz HO. Previous studies suggested L-carnitine can reduce IR and BMI in PCOS women 44 , |
| Understanding Insulin Resistance and Fertility | Potential PCOS symptoms you may face. Fertil Steril. Our study revealed that high levels of TyG-BMI were positively associated with female infertility in US reproductive-aged females. Can insulin resistance cause PCOS? Free UK mainland delivery. |
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3 Physical Exam Findings Associated with Insulin ResistanceInsulin resistance and fertility -
Both of these conditions can lead to infrequent ovulation, which makes it more difficult to conceive. Particularly in polycystic ovarian syndrome, the balance of estrogen and androgens is abnormal.
Your body produces more of the luteinizing hormone that helps control your menstrual cycle than normal, which causes you to produce more androgens such as free testosterone. This can block ovulation completely. In addition, if you do get pregnant, you can face a higher risk of miscarriage than average.
Consistently high blood sugar levels can compromise the quality of your eggs and cause miscarriages and stillbirths.
You can overcome insulin resistance a few different ways. The first way is by making some lifestyle changes. Getting regular exercise, eating a balanced diet, and working on stress reduction are important to helping your body fight insulin resistance.
Avoid simple carbohydrates because these will cause a spike in your blood sugar. Eat more fiber to keep your blood sugar stable. We also have medications that can help to induce ovulation if you are insulin resistant. Some of these medications include metformin, a drug that lowers your blood sugar, and clomiphene, a fertility drug.
If your insulin resistance is not well-controlled, you face more risks if you do manage to conceive. One of the biggest risks is gestational diabetes during pregnancy. Your pregnancy will be monitored closely.
If you are concerned about insulin resistance and infertility, your best bet is to schedule a consultation. Call or message Dr. Insulin Resistance and Infertility: Understanding the Connection. Metformin has been proven safe and is nonteratogenic, but additional evidence is necessary to confirm the safety of other insulin sensitizers By screening and analyzing existing RCTs, improvement of IR following nonsurgical interventions was strongly correlated with increased pregnancy rate in infertile women with PCOS.
Although only two RCTs, Liu et al. They were able to determine that pregnancy rate increased in the groups that achieved an improvement of IS. Therefore, nonsurgical therapeutic strategies that result in superior improvement of IS may aid infertile PCOS women to increase their possibility of a successful pregnancy.
This review had limitations. Evidence demonstrated that IUGR, SGA, and history of family diabetes contributed to PCOS patients with IR, and these factors might also affect the effectiveness of treatment on improving insulin sensitivity.
However, few trials concerned about the factors so that there was insufficient information that can be obtained and discussed in the review. More evidence is required to fill the gap. Besides, most RCTs that explored the reproductive effects of nonsurgical interventions in PCOS women did not report changes in IR.
Therefore, only some of these studies were included in this review, and some had small sample sizes. High-quality and large sample size RCTs are needed to confirm the results discussed in the systemic review. Among the various nonsurgical interventions, the benefit of improvement of IS appeared to be superior in PCOS women without severe obesity.
The benefit of improvement of IS appears to be more important than that in changes of BMI after treatment even the BMI is one of the most crucial factors for IS.
And IS improvement also benefits PCOS women without IR at baseline. Metformin and other related drugs, and lifestyle modification, may also be capable of improving IS.
It appears exenatide had a better effect than metformin at improving IS and increasing pregnancy rate. Although additional large, well-designed RCTs are necessary to confirm the benefits, the review emphasized the importance of achieving IS improvement in infertile PCOS women treatment.
Further inquiries can be directed to the corresponding author. YL provided the conception, searched the literature, participated in planning how to do the work, abstracting study details and writing the manuscript. JL participated in screening and abstracting study details, discussing and organized the main text and writing the manuscript.
DL provided clinical advice during the whole work in the view of gynecology and obstetrics. JM screened the studies. NT planed the whole work and revised the manuscript. All authors contributed to the article and approved the submitted version. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
March WA, Moore VM, Willson KJ, Phillips DI, Norman RJ, Davies MJ. The prevalence of polycystic ovary syndrome in a community sample assessed under contrasting diagnostic criteria. Hum Reprod 25 2 — doi: PubMed Abstract CrossRef Full Text Google Scholar. Nandi A, Chen Z, Patel R, Poretsky L.
Polycystic ovary syndrome. Endocrinol Metab Clin North Am 43 1 — Teede HJ, Misso ML, Costello MF, Dokras A, Laven J, Moran L, et al.
Recommendations from the international evidence-based guideline for the assessment and management of polycystic ovary syndrome.
Hum Reprod 33 9 — Homburg R. Clomiphene citrate—end of an era? A mini-review. Hum Reprod 20 8 — Dellapasqua S, Colleoni M. Expert Opin Drug Metab Toxicol 6 2 —9.
Buse JB, Wexler DJ, Tsapas A, Rossing P, Mingrone G, Mathieu C, et al. A Consensus Report by the American Diabetes Association ADA and the European Association for the Study of Diabetes EASD. Diabetes Care 43 2 — Asrm Asrm Org Practice Committee of the American Society for Reproductive Medicine.
Electronic Address and Medicine Practice Committee of the American Society for Reproductive, Role of metformin for ovulation induction in infertile patients with polycystic ovary syndrome PCOS : a guideline. Fertil Steril 3 — Tang T, Lord JM, Norman RJ, Yasmin E, Balen AH.
Insulin-sensitising drugs metformin, rosiglitazone, pioglitazone, D-chiro-inositol for women with polycystic ovary syndrome, oligo amenorrhoea and subfertility. Cochrane Database Syst Rev 5 :CD CrossRef Full Text Google Scholar.
Siebert TI, Viola MI, Steyn DW, Kruger TF. Is metformin indicated as primary ovulation induction agent in women with PCOS? A systematic review and meta-analysis. Gynecol Obstet Invest 73 4 — Li W, Chen Q, Xie Y, Hu J, Yang S, Lin M. Prevalence and degree of insulin resistance in Chinese Han women with PCOS: Results from euglycemic-hyperinsulinemic clamps.
Clin Endocrinol Oxf 90 1 — De Melo AS, Dias SV, Cavalli Rde C, Cardoso VC, Bettiol H, Barbieri MA, et al. Pathogenesis of polycystic ovary syndrome: multifactorial assessment from the foetal stage to menopause.
Reproduction 1 :R11— Franks S, Stark J, Hardy K. Follicle dynamics and anovulation in polycystic ovary syndrome. Hum Reprod Update 14 4 — Morley LC, Tang T, Yasmin E, Norman RJ, Balen AH. Cochrane Database Syst Rev CD Ng EHY, Wat NMS, Ho PC. Effects of metformin on ovulation rate, hormonal and metabolic profiles in women with clomiphene-resistant polycystic ovaries: A randomized, double-blinded placebo-controlled trial.
Hum Reprod 16 8 — Nemati M, Nemati S, Taheri AM, Heidari B. Comparison of metformin and N-acetyl cysteine, as an adjuvant to clomiphene citrate, in clomiphene-resistant women with polycystic ovary syndrome.
J Gynecol Obstet Hum Reprod 46 7 — Qublan HS, Yannakoula EK, Al-Qudad MA, El-Uri FI. Dietary intervention versus metformin to improve the reproductive outcome in women with polycystic ovary syndrome. A prospective comparative study.
Saudi Med J 28 11 —8. PubMed Abstract Google Scholar. Malkawi HY, Qublan HS, Hamaideh AH. Medical vs. surgical treatment for clomiphene citrate-resistant women with polycystic ovary syndrome. J Obstet Gynaecol: J Institute Obstet Gynaecol 23 3 — Weerakiet S, Sophonsritsuk A, Lertvikool S, Satirapot C, Leelaphiwat S, Jultanmas R.
Randomized controlled trial of different doses of metformin for ovulation induction in infertile women with polycystic ovary syndrome. J Obstet Gynaecol Res 37 9 — Kocak M, Caliskan E, Simsir C, Haberal A.
Metformin therapy improves ovulatory rates, cervical scores, and pregnancy rates in clomiphene citrate-resistant women with polycystic ovary syndrome.
Fertil Steril 77 1 —6. Vandermolen DT, Ratts VS, Evans WS, Stovall DW, Kauma SW, Nestler JE. Metformin increases the ovulatory rate and pregnancy rate from clomiphene citrate in patients with polycystic ovary syndrome who are resistant to clomiphene citrate alone.
Fertil Steril 75 2 —5. Zhang J, Si Q, Li J. Therapeutic effects of metformin and clomiphene in combination with lifestyle intervention on infertility in women with obese polycystic ovary syndrome. Pak J Med Sci 33 1 :8— Garvey WT, Mechanick JI, Brett EM, Garber AJ, Hurley DL, Jastreboff AM, et al.
Obesity Clinical Practice Guidelines Reviewers of The, American Association of Clinical Endocrinologists and American College of Endocrinology Comprehensive Clinical Practice Guidelines for Medical Care of Patients with Obesity. Endocr Pract 22 Suppl — O Expert Consultation, Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies.
Lancet — Agrawal A, Mahey R, Kachhawa G, Khadgawat R, Vanamail P, Kriplani A. Comparison of metformin plus myoinositol vs metformin alone in PCOS women undergoing ovulation induction cycles: randomized controlled trial.
Gynecol Endocrinol 35 6 —4. George SS, George K, Irwin C, Job V, Selvakumar R, Jeyaseelan V, et al. Sequential treatment of metformin and clomiphene citrate in clomiphene-resistant women with polycystic ovary syndrome: A randomized, controlled trial. Hum Reprod 18 2 — Karimzadeh MA, Eftekhar M, Taheripanah R, Tayebi N, Sakhavat L, Zare F.
The effect of administration of metformin on lipid profile changes and insulin resistance in patients with polycystic ovary syndrome.
Middle East Fertil Soc J 12 3 —8. Google Scholar. Legro RS, Barnhart HX, Schlaff WD, Carr BR, Diamond MP, Carson SA, et al. Myers and Med Cooperative Multicenter Reprod, Clomiphene, metformin, or both for infertility in the polycystic ovary syndrome.
New Engl J Med 6 — Legro RS, Dodson WC, Kris-Etherton PM, Kunselman AR, Stetter CM, Williams NI, et al. Randomized Controlled Trial of Preconception Interventions in Infertile Women With Polycystic Ovary Syndrome. J Clin Endocrinol Metab 11 — Liu X, Zhang Y, Zheng SY, Lin R, Xie YJ, Chen H, et al.
Clin Endocrinol 87 6 — Ortega-González C, Luna S, Hernández L, Crespo G, Aguayo P, Arteaga-Troncoso G, et al. Responses of serum androgen and insulin resistance to metformin and pioglitazone in obese, insulin-resistant women with polycystic ovary syndrome. J Clin Endocrinol Metab 90 3 —5.
Wang J, Ruan X, Jin F, Sun Y, Wang J. Biomed Res India 28 19 — Yarali H, Yildiz BO, Demirol A, Zeyneloğlu HB, Yiğit N, Bükülmez O, et al.
Co-administration of metformin during rFSH treatment in patients with clomiphene citrate-resistant polycystic ovarian syndrome: a prospective randomized trial. Hum Reprod 17 2 — El Sharkwy I, Sharaf El-Din M. l-Carnitine plus metformin in clomiphene-resistant obese PCOS women, reproductive and metabolic effects: a randomized clinical trial.
Gynecol Endocrinol 35 8 —5. Kahn SE, Hull RL, Utzschneider KM. Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature —6. Inzucchi SE, Viscoli CM, Young LH, Furie KL, Gorman M, Lovejoy AM, et al.
and Iris Trial Investigators, Pioglitazone Prevents Diabetes in Patients With Insulin Resistance and Cerebrovascular Disease.
Diabetes Care 39 10 — Derosa G, Maffioli P, Salvadeo SA, Ferrari I, Ragonesi PD, Querci F, et al. Exenatide versus glibenclamide in patients with diabetes. Diabetes Technol Ther 12 3 — Erem C, Ozbas HM, Nuhoglu I, Deger O, Civan N, Ersoz HO. Comparison of effects of gliclazide, metformin and pioglitazone monotherapies on glycemic control and cardiovascular risk factors in patients with newly diagnosed uncontrolled type 2 diabetes mellitus.
Exp Clin Endocrinol Diabetes 5 — Sangeeta S. Metformin and pioglitazone in polycystic ovarian syndrome: a comparative study.
J Obstet Gynaecol India 62 5 —6. Razavizade M, Jamali R, Arj A, Matini SM, Moraveji A, Taherkhani E. The effect of pioglitazone and metformin on liver function tests, insulin resistance, and liver fat content in nonalcoholic Fatty liver disease: a randomized double blinded clinical trial.
Hepat Mon 13 5 :e Sohrevardi SM, Nosouhi F, Hossein Khalilzade S, Kafaie P, Karimi-Zarchi M, Halvaei I, et al. Evaluating the effect of insulin sensitizers metformin and pioglitazone alone and in combination on women with polycystic ovary syndrome: An RCT.
Int J Reprod BioMed 14 12 — Genazzani AD. Inositol as putative integrative treatment for PCOS. Reprod BioMed Online 33 6 — Fruzzetti F, Perini D, Russo M, Bucci F, Gadducci A. Comparison of two insulin sensitizers, metformin and myo-inositol, in women with polycystic ovary syndrome PCOS. Gynecol Endocrinol 33 1 — Zeng L, Yang K.
Effectiveness of myoinositol for polycystic ovary syndrome: a systematic review and meta-analysis. Endocrine 59 1 —8. Xu Y, Jiang W, Chen G, Zhu W, Ding W, Ge Z, et al.
L-carnitine treatment of insulin resistance: A systematic review and meta-analysis. Adv Clin Exp Med 26 2 —8. Samimi M, Jamilian M, Ebrahimi FA, Rahimi M, Tajbakhsh B, Asemi Z.
Oral carnitine supplementation reduces body weight and insulin resistance in women with polycystic ovary syndrome: a randomized, double-blind, placebo-controlled trial. Clin Endocrinol Oxf 84 6 —7. Feig DS, Briggs GG, Koren G.
Oral antidiabetic agents in pregnancy and lactation: a paradigm shift?
We often talk Natural detox for a healthy liver metabolic health Strong weight loss pills Insulin resistance and fertility context of weight loss, but it has much broader rewistance — such wnd fertility. Many fertiligy struggling with infertility also have metabolic health problems [1]. These can include hormonal imbalances, insulin resistance, obesity, and metabolic syndrome. Scientists are still learning about the relationship between metabolic health and fertility, but a large body of evidence tells us that metabolic health is crucial to successful conception and a healthy pregnancy [2]. Insulin resistance is known to be linked to infertility.
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