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Hyperinsulinemia And Pcos

Hyperinsulinemia In Polycystic Ovary Syndrome: Relationship To Clinical And Hormonal Factors

Hyperinsulinemia In Polycystic Ovary Syndrome: Relationship To Clinical And Hormonal Factors

, Volume 72, Issue11 , pp 853857 | Cite as Hyperinsulinemia in polycystic ovary syndrome: relationship to clinical and hormonal factors We analyzed the association between hyperandrogenism and hyperinsulinemia, and their relationship to body mass index, in a large series of patients with polycystic ovary syndrome (PCOS). A characteristic hormonal profile was sought in women with marked hyperinsulinemia. The patient group consisted of 73 women with PCOS, ranging in age from 16 to 29 years. The control group consisted of 34 healthy women with no evidence of hyperandrogenism, aged 1930 years. None of the patients or control women had a body mass index above 27 kg/m2. Follicle-stimulating hormone, luteinizing hormone, prolactin, testosterone, estradiol, androstenedione, dehydroepiandrosterone sulfate, sex hormone binding globulin, 17-hydroxyprogesterone, and free cortisol were determined by radioimmunoassay. The free testosterone index was calculated. The oral glucose tolerance test was used to analyze basal insulinemia, maximum insulin peak, and the insulinemia/glycemia index. In the group with PCOS body mass index was greater, free testosterone index was higher, and levels of dehydroepiandrosterone sulfate, testosterone, 17-hydroxyprogesterone (P < 0.001) and androstenedione (P < 0.05) were higher than in the control group. Of the insulin parameters, basal insulinemia, maximum insulin peak, and insulinemia/glycemia index were higher in the patient group (P < 0.001). In patients with marked insulinemia, free testosterone index was more markedly elevated, and gonadotrophin levels were normal. Our data confirm that a characteristic pattern of hyperinsulinemia is associated with PCOS. We found no causal relationship between hyperinsulinemia and androgen levels. A characteris Continue reading >>

Polycystic Ovary Syndrome

Polycystic Ovary Syndrome

Description Polycystic ovary syndrome (PCOS) is the most common cause of anovulatory infertility. Its prevalence among women of reproductive age is estimated to be between 5-10%. PCOS is classified as a syndrome because it is a heterogeneous disorder: not all of the women with PCOS will express all of the symptoms associated with the disorder. A diagnosis of PCOS is made if a woman has chronic problems with ovulation coupled with hyperandrogenism (excess secretion of androgens). Problems with ovulation will manifest themselves as amenorrhea (lack of menstruation) or oligomenorrhea (irregular menstruation). Hyperandrogenism may cause hirsutism, which is a masculine pattern of hair growth on the body, and acne, because androgens have an effect on the sebaceous glands of the skin that promotes acne. Androgens may also cause hair loss on the scalp. PCOS gets its name from the changes seen in the ovary (although not all women with PCOS have polycystic ovaries). Polycystic ovaries are enlarged and contain multiple (greater than 10) immature follicles. The immature follicles show a relative hyperplasia of theca cells, and fewer granulosa cells. Development of these follicles is arrested well before the point of dominant follicle selection, so the LH surge doesn't occur, and therefore, neither does ovulation. There are also metabolic disturbances associated with PCOS. Frequently, women with PCOS are found to be insulin resistant. Because insulin resistance is a decreased sensitivity to insulin, this means that more insulin is necessary to achieve the same effect. For this reason, individuals who are insulin resistant have higher levels of insulin secretion or hyperinsulinemia. Because women with PCOS are insulin resistant, they are at a greater risk for developing type 2 diabet Continue reading >>

Correlation Of Hyperandrogenism With Hyperinsulinism In Polycystic Ovarian Disease*

Correlation Of Hyperandrogenism With Hyperinsulinism In Polycystic Ovarian Disease*

Background: According to NIH criteria for PCOS, the estimated prevalence of this disorder has been reported to range from 4% to 10% of women in their reproductive years, which designates PCOS as the most common endocrinopathy of women. Insulin resistance is common in PCOS and obesity contributes an additional component to insulin resistance in obese PCOS.Methods: The study was a prospective study. One-hundred and twenty PCOS women were divided into two groups: Group O - obese (n = 60) and Group L - lean (body mass index [BMI] cutoff <23 kg/m2). Oral glucose tolerance test, serum fasting insulin and HOMA- IR were compared between these groups.Results: Impaired glucose tolerance was seen in 33.3 % of lean PCOS and 36.7% of obese PCOS women. 5% of lean PCOS and 10% of obese PCOS women had hyperinsulinemia. 38.3% of lean PCOS and 51.7% of obese PCOS women had insulin resistance. But the differences were not statistically significant. However, HOMA-IR and fasting insulin values showed a significant positive correlation with BMI.Conclusions: Both obese and lean women with PCOS are vulnerable to the problems of insulin resistance irrespective of BMI and insulin resistance shows a positive correlation with BMI. Background: The objective of this study was to describe the association between luteinizing hormone (LH)/ follicle-stimulating hormone (FSH) ratio and demographic variables and maturation stage of oocytes in insulinresistant and insulin-sensitive patients with polycystic ovary syndrome (PCOS) in comparison with control group.Materials and methods: In this case-control study, 60 patients with in vitro fertilization (IVF)/intracytoplasmic sperm injection (ICSI) indication were subdivided into 3 groups as follow: 20 subjects were assigned to control (fertile women with mal Continue reading >>

Polycystic Ovarian Syndrome (pcos)

Polycystic Ovarian Syndrome (pcos)

What is polycystic ovary syndrome (PCOS)? Polycystic ovary syndrome (also called PCOS or Stein Leventhal syndrome) is the most common hormonal and reproductive problem affecting women of childbearing age. It's estimated that about5 percent of women in the U.S.have this disorder. PCOShas beendefinedas the presence of any two of the following characteristics: Lack of ovulation for an extended period of time Many small cysts (fluid-filled sacs) on the ovaries The exact cause of PCOS is unclear. It's common for sisters or a mother and daughter to have PCOS, but a definite genetic link hasn't been found. PCOS results from a combination of several related factors. Many women with PCOS have insulin resistance, in which the body can't use insulin efficiently. This leads to high circulating blood levels of insulin, called hyperinsulinemia. It's believed that hyperinsulinemia is related to increased androgen levels, as well as obesity and type 2 diabetes. In turn, obesity can increase insulin levels, causing worsening of PCOS. Ovulation is a process in which a mature egg cell (also called an ovum), ready for fertilization by a sperm cell, is released from one of the ovaries (two female reproductive organs located in the pelvis). If the egg doesn't become fertilized as it travels down the fallopian tube on its way to the uterus, the endometrium (lining of the uterus) is shed and passes through the vagina (the passageway through which fluid passes out of the body during menstrual periods; also called the birth canal), in a process called menstruation. With an ovulatory problem, the woman's reproductive system doesn't produce the proper amounts of hormones necessary to develop, mature, and release a healthy egg. When the ovaries don't produce the hormones needed for ovulation and p Continue reading >>

Pcos And Hyperinsulinemia

Pcos And Hyperinsulinemia

The most iconic feature of PCOS and what the syndrome is named for is the presence of the multiple cysts on the ovary. Many women have a few cysts on their ovary, but the sheer number of cysts distinguishes this syndrome from virtually all others. Almost no other human disease causes polycystic ovaries. These cysts develop from a group of cells known as follicles. Normal ovaries are endowed at birth with a finite pool of primordial follicles, which have the potential to develop into a mature egg. Primordial follicles remain quiescent for many years until recruited for growth into a primary follicle during the menstrual cycle. From birth to menarche, all primordial follicles remain dormant. Follicle numbers gradually decrease with age as used follicles are never replaced. When the follicles are fully depleted, women undergo menopause and can no longer have children. At the start of each menstrual cycle, a few primordial follicles grow into primary and then secondary follicles. Only one of these follicles is selected to become the dominant follicle and the rest simply shrivel away (involute) and are reabsorbed by the body. The dominant follicle alone continues to grow. At ovulation, in response to a surge in luteinizing hormone (LH), the egg is expelled into the respective fallopian tube which carries it to the uterus. The rest of the dominant follicle becomes the corpus luteum, which secretes estrogen and progesterone to support the hoped-for pregnancy. Primary follicles are generally detectable by ultrasound when they reach 2mm in size. The key growth signal for the primary follicle is testosterone . Insulin is important, too, but acts indirectly by increasing testosterone. The dominant follicle typically measures 2224 mm. While the follicle is growing, the lining of t Continue reading >>

Hyperinsulinemia Vs Hyperglycemia - The Story Of Pcos & Obesity

Hyperinsulinemia Vs Hyperglycemia - The Story Of Pcos & Obesity

The ZRT Blog is an extensive resource for patients and health care providers searching for health and hormone testing information. Here, you can read about ZRTs cutting edge research, advances in testing, wellness advice, and health industry highlights. Posted by Dr. Alison McAllister on Wednesday, 20 January 2016 Hyperinsulinemia vs Hyperglycemia - the Story of PCOS & Obesity Many times when I am talking to a practitioner about a patient with PCOS and/or weight issues, I commonly get the response "His/her blood sugar is normal." However, when we are looking at the health of PCOS and weight-challenged patients, their insulin response is of primary importance, and not just their blood sugar. When we are fasting, both blood sugar and insulin levels should be at a steady state. Blood sugar is generally between 70-90 mg/dL and insulin levels between 1-8 IU/mL. When we eat a meal, blood sugar increases. In response, insulin is produced by the pancreatic beta cells to help shepherd glucose into all cells to be used as energy. Within 2 hours, insulin and glucose levels should have essentially returned to normal. Thus, our cells exposure to glucose and insulin is only for short blips of time within a 24 hour cycle. Excess glucose that is not used for energy is stored as glycogen in the liver and muscle cells to be used for energy between meals, where it is rapidly available for sudden energy needs such as "fight or flight" situations; but once these stores are full, the body stores extra glucose as fat in adipose cells and we gain weight. If we allow this hyperinsulinemia to continue the body will lose the ability to manufacture enough insulin to control postprandial glucose levels. When we become insulin resistant, things change. The first tissue to become insulin resistant i Continue reading >>

Polycystic Ovarian Syndrome (pcos)

Polycystic Ovarian Syndrome (pcos)

PCOS is characterized by hyperandrogenism, irregular ovulatory cycles, and a metabolic derangement including glucose intolerance and hyperinsulinemia. Manifestations of PCOS are heterogeneous, and several consensus definitions of the disorder have been produced to describe the disease, with various emphases on clinical or biochemical hyperandrogenism, polycystic ovaries, and oligoanovulation. The Rotterdam Consensus (2003) defines PCOS as at least two of the following characteristics: Clinical hyperandrogenism and/or hyperandrogenemia Oligoanovulation Polycystic ovaries on ultrasound Although other definitions emphasize the presence of clinical or biochemical hyperandrogenism as an important characteristic of the disease, there is some debate as to the centrality of hyperandrogenism in PCOS. The more inclusive Rotterdam criteria may be appropriate in patients where clinical hyperandrogenism is difficult to assess. Genetics: PCOS is believed to be a complex disorder, with genetic as well as environmental factors contributing to development of the disease. 20-40% of female first-degree relatives of women with PCOS also have the syndrome, suggesting that the disease is partially heritable and clusters in families. Prevalence and severity of presentation vary with ethnicity, with South Asians at a higher risk of disease. Some candidate genes have been identified as contributing to risk of the disease, including 7β-hydroxysteroid-dehydrogenase type 6 (HSD17B6). Intrauterine exposures: exposures to testosterone in utero may predispose to the later development of PCOS. Animal studies have demonstrated that in utero exposure is correlated with development of a PCOS-like syndrome including hyperinsulinemia, hyperandrogenism, oligoanovulation, and polycystic ovaries. Exposure to Continue reading >>

Insulin Resistance And Hyperinsulinism In The Polycystic Ovary Syndrome

Insulin Resistance And Hyperinsulinism In The Polycystic Ovary Syndrome

Insulin Resistance and Hyperinsulinism in the Polycystic Ovary Syndrome Part of the Contemporary Endocrinology book series (COE) Insulin resistance with compensatory hyperinsulinemia has been demonstrated to occur in 5070% of women with polycystic ovary syndrome (PCOS), regardless of weight. Hyperinsulinemia stimulates excess ovarian androgen production, thereby contributing to the hyperandrogenism and chronic anovulation characteristic of PCOS. The exact cause of insulin resistance in PCOS is unknown, but it appears to be related to a postbinding defect in insulin receptor-mediated signal transduction. Because of insulin resistance, women with PCOS are at risk for several long-term metabolic complications, including type 2 diabetes and cardiovascular disease. Insulin resistancehyperinsulinisminsulin receptor-mediated signal transduction This is a preview of subscription content, log in to check access. Unable to display preview. Download preview PDF. Burghen GA, Givens JR, Kitabchi AE. Correlation of hyperandrogenism with hyperinsulinism in polycystic ovarian disease. J Clin Endocrinol Metab 1980;50:113116. PubMed Google Scholar Reaven GM. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes 1988;37:15951607. PubMed CrossRef Google Scholar Nestler JE, Clore JN, Strauss JF, III, Blackard WG. Effects of hyperinsulinemia on serum testosterone, progesterone, dehydroepiandrosterone sulfate, and cortisol levels in normal women and in a woman with hyperandrogenism, insulin resistance and acanthosis nigricans. J Clin Endocrinol Metab 1987;64:180184. PubMed Google Scholar Nestler JE, Barlascini CO, Matt DW, et al. Suppression of serum insulin by diazoxide reduces serum testosterone levels in obese women with polycystic ovary syndrome. J Clin Endocrinol M Continue reading >>

Insulin Resistance And The Polycystic Ovary Syndrome: Mechanism And Implications For Pathogenesis

Insulin Resistance And The Polycystic Ovary Syndrome: Mechanism And Implications For Pathogenesis

POLYCYSTIC ovary syndrome (PCOS) is an exceptionally common disorder of premenopausal women characterized by hyperandrogenism and chronic anovulation ( 1 , 2 ). Its etiology remains unknown. Although there have been no specific population-based studies, a 510% prevalence of this disorder in women of reproductive age is probably a reasonable conservative estimate. This is based as an upper limit on studies of the prevalence of polycystic ovaries, which found that 20% of self-selected normal women had polycystic ovary morphology on ovarian ultrasound ( 3 ). Many of these women had subtle endocrine abnormalities ( 3 ). The lower estimate is based on the reported 3% prevalence rate of secondary amenorrhea for 3 or more months ( 4 ) and the fact that up to 75% of women with secondary amenorrhea will fulfill diagnostic criteria for PCOS ( 5 ). PCOS women can also have less profound disturbances in menstrual function ( 1 , 3 , 6 ). Since the report by Burghen et al. ( 7 ) in 1980 that PCOS was associated with hyperinsulinemia, it has become clear that the syndrome has major metabolic as well as reproductive morbidities. The recognition of this association has also instigated extensive investigation of the relationship between insulin and gonadal function ( 1 , 8 11 ). This review will summarize our current understanding of insulin action in PCOS, address areas of controversy, and propose several hypotheses for this association. Abnormalities of steroidogenesis and gonadotropin release will not be discussed in detail; these changes have been reviewed recently by Erhmann and colleagues ( 12 ) and by Crowley ( 13 ), respectively. The association between a disorder of carbohydrate metabolism and hyperandrogenism was first described in 1921 by Achard and Thiers ( 14 ) and was call Continue reading >>

Role Of Hyperinsulinemia In The Pathogenesis Of The Polycystic Ovary Syndrome,and Its Clinical Implications.

Role Of Hyperinsulinemia In The Pathogenesis Of The Polycystic Ovary Syndrome,and Its Clinical Implications.

1. Semin Reprod Endocrinol. 1997 May;15(2):111-22. Role of hyperinsulinemia in the pathogenesis of the polycystic ovary syndrome,and its clinical implications. (1)Department of Internal Medicine, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298-0111, USA. The polycystic ovary syndrome (PCOS) is a prevalent disorder affectingapproximately 6% of women of reproductive age, and is characterized byanovulation and hyperandrogenism. It has also become apparent that a frequentfeature of women with PCOS is insulin resistance accompanied by compensatoryhyperinsulinemia, and increasing evidence suggests that hyperinsulinemia plays animportant role in the pathogenesis of PCOS. This article will review (1) evidenceindicating that insulin contributes to the hyperandrogenism of PCOS bystimulating ovarian androgen production and decreasing serum sex hormone-binding globulin (SHBG) concentrations; (2) possible direct effects of hyperinsulinemiaon folliculogenesis; (3) the relationship between insulin and adrenal androgensin women; and (4) therapeutic and clinical implications of these findings. Continue reading >>

Hyperinsulinemia And Men's Health Is There A Male Equivalent To Pcos?

Hyperinsulinemia And Men's Health Is There A Male Equivalent To Pcos?

Hyperinsulinemia and Men's Health: Is There a Male Equivalent to PCOS? It has long been known that polycystic ovarian syndrome (PCOS) is driven largely by chronically elevated insulin (hyperinsulinemia) . PCOS is the most common endocrine abnormality among reproductive age women, affecting as much as 10% of the population ( 1 ). But if insulin is primarily a blood sugar hormone, why would chronic hyperinsulinemia affect female fertility? Why would it contribute to irregular or absent menstrual periods, facial hair, acne, and other signs and symptoms of PCOS? The answer is that insulin is not just a blood sugar hormone. In fact, insulin has such surprising and far-reaching effects throughout the whole body that lowering blood sugar might actually be one of the least notable things this hormone does. In a past KetoDiet post exploring chronic hyperinsulinemia , I mentioned that high insulin plays a driving role in such diverse issues as hypertension, skin tags, gout, and migraines . A quick flip through a biochemistry or endocrinology textbook shows that hormones dont exist in a vacuum. They interact with and influence each other in complex ways, with multiple control mechanisms and feedback loops, so that changing the levels of one inevitably causes changes in the levels of others, too. If hyperinsulinemia produces multiple hormonal abnormalities in women leading to PCOS, might it also produce hormonal abnormalities in men? Is there a male equivalent to PCOS? Insulin Isnt the Enemy; Chronically High Insulin Is Insulin has gotten a very negative reputation in the keto community. But by itself, insulin isnt a bad thing. Insulin is an essential hormone that performs numerous critical functions. Insulin is only a problem when theres too much of it in the bloodstream too ofte Continue reading >>

Hyperinsulinemia, Not Ovaries, At Core Of Pcos

Hyperinsulinemia, Not Ovaries, At Core Of Pcos

Hyperinsulinemia, Not Ovaries, at Core of PCOS Hyperinsulinemia, Not Ovaries, at Core of PCOS. DALLAS Polycystic ovary syndrome is in sore need of a new name, Dr. Barbara S. Apgar said at the annual meeting of the American Academy of Family Physicians. Put aside the traditional notion that the primary defect in polycystic ovary syndrome (PCOS) involves the ovaries. Focus instead on hyperinsulinemia, which lies at the core of this common endocrinopathy, advised Dr. Apgar, a family physician at the University of Michigan, Ann Arbor. Indeed, the finding of enlarged ovaries on palpation or polycystic ovaries on ultrasound in merely a sign of PCOS. Insulin abnormalities precede the elevated androgen levels that characterize PCOS. And switching off the ovaries via a GnRH agonist doesnt affect the hyperinsulinemia and insulin resistance, she noted. PCOS is probably the most common endocrine disorder in women. Its estimated that up to 10% of premenopausal women are affected. In PCOS, hyperinsulinemia leads to hyperandrogenism, resulting in chronically elevated LH levels. The hair follicles are genetically sensitive to androgen stimulation, so acne and hirsutism are commonly part of the PCOS picture. Glucose intolerance, type 2 diabetes, and lipid abnormalities also are common. And 40%-60% of patients with PCOS are obese. Treatment is not directed at the ovary. Its directed at the hair follicle level and also at the pancreatic level, where we see the insulin resistance, she explained. The disorder requires a multimodal approach. Treatment may include clomiphene citrate (Clomid) to stimulate ovulation, OCs or a progestin to prevent endometrial hyperplasia, and statins or other lipid-lowering agents for cardiovascular protection. Spironolactone is probably the best option for tre Continue reading >>

Hyperandrogenism And Hyperinsulinemia

Hyperandrogenism And Hyperinsulinemia

INTRODUCTION Hyperinsulinemia and hyperandrogenism represent a tangled web that reaches its greatest complexity in women with polycystic ovary syndrome (PCOS). Researchers are beginning to separate the strands of the relationship between the two, but the pattern is still not clear. Initial data seem to suggest that the hyperinsulinemia, rather than the hyperandrogenemia, holds perhaps the gravest implications for long-term complications of the syndrome, such as cardiovascular disease and development of non - insulin-dependent diabetes mellitus (NIDDM). But the data supporting these long-term complications in women with PCOS are still scant. As gynecologists, we have traditionally focused on the hyperandrogenic aspects of this syndrome: hirsutism, dysfunctional uterine bleeding, and infertility. But as we identify the long-term sequelae, our primary concern for these patients may become improving insulin sensitivity. Because they frequently develop symptoms at the time of menarche, they represent an ideal target group for early intervention. This chapter will focus mainly on insulin resistance in PCOS, but other causes of hyperandrogenism and hyperinsulinemia also will be discussed. INSULIN RESISTANCE Insulin is the primary glucoregulatory hormone and is secreted by the beta cells of the pancreas. Its primary target tissues are skeletal muscle, liver, and adipose tissue. Of these, skeletal muscle is the largest target for insulin action. In the liver, insulin promotes glycogen formation and inhibits gluconeogenesis and glycogenolysis. In fat and muscle, insulin promotes glucose utilization and storage. Insulin is a potent growth factor, and its effects on peripheral tissues are pleiotropic and potentially not all favorable. In high doses, it may be directly atherogenic o Continue reading >>

Polycystic Ovary Syndrome

Polycystic Ovary Syndrome

J Midwifery Womens Health.2006;51(6):415-422. A complete understanding of the underlying pathophysiology of PCOS is still lacking. Because of the heterogeneity of this disorder, there are most likely multiple underlying pathophysiologic mechanisms. Several theories have been proposed to explain the pathogenesis of PCOS.[ 8 ] 1) An alteration in gonadotropin-releasing hormone secretion results in increased luteinizing hormone (LH) secretion. 2) An alteration in insulin secretion and insulin action results in hyperinsulinemia and insulin resistance. 3) A defect in androgen synthesis that results in increased ovarian androgen production. We will discuss each of these theories in more detail. LH hypersecretion is a characteristic hallmark of PCOS. LH is secreted in a pulsatile manner. Women with PCOS have an increase in both the LH pulse frequency and amplitude, resulting in increased 24-hour secretion. This increase in LH secretion is thought to occur as a result of increased frequency of hypothalamic gonadotropin-releasing hormone (GnRH) pulses. Increased LH, in turn, leads to an increase in androgen production by the theca cells within the ovary.[ 3 , 8 ] Insulin resistance, defined as reduced glucose response to a given amount of insulin, is a characteristic metabolic disturbance associated with PCOS. Both obese and nonobese women with PCOS have a higher incidence of insulin resistance and hyperinsulinemia than age-matched controls; however, obese women with PCOS have significantly decreased insulin sensitivity compared with nonobese women who have PCOS. Insulin resistance is known to precede the development of type 2 diabetes mellitus. Studies have shown that 30% to 40% of women with PCOS have impaired glucose tolerance, and as many as 10% develop type 2 diabetes mell Continue reading >>

Substituting Poly And Mono-unsaturated Fat For Dietary Carbohydratereduces Hyperinsulinemia In Women With Polycystic Ovary Syndrome

Substituting Poly And Mono-unsaturated Fat For Dietary Carbohydratereduces Hyperinsulinemia In Women With Polycystic Ovary Syndrome

Received date: September 29, 2015 Accepted date: November 12, 2015 Published date: November 19, 2015 Citation: Dalia P, Nicole C, Cindy L, Susan C, Fahim A, et al. (2015) Substituting Poly and Mono-unsaturated Fat for Dietary Carbohydrate Reduces Hyperinsulinemia in Women with Polycystic Ovary Syndrome. J Nutr Food Sci 5:429. doi: 10.4172/2155-9600.1000429 Copyright: 2015 Dalia P, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Objective: Hyperinsulinemia is a prevalent feature of Polycystic Ovary Syndrome (PCOS), contributing to metabolic and reproductive manifestations of the syndrome. Weight loss reduces hyperinsulinemia but weight regain is the norm, thus preventing long-term benefits. In the absence of weight loss, replacement of dietary carbohydrate (CHO) with mono/polyunsaturated fat reduces ambient insulin concentrations in non-PCOS subjects. The current study evaluated whether this dietary intervention could ameliorate hyperinsulinemia in women with PCOS. Design/Setting/Patients: Obese women with PCOS (BMI 39 7 kg/m2) and insulin resistance completed a crossover study (Stanford University Clinical Research Center) comparing two isocaloric diets, prepared by research dietitians, containing 60% CHO/25% fat versus 40% CHO/45% fat (both 15% protein and 7% saturated fat). After 3 weeks on each diet, day-long glucose, insulin, and fasting lipid/lipoproteins were measured. Results: Day-long glucose did not differ according to diet. Day-long insulin concentrations were substantially (30%) and significantly lower on the low-CHO/higher fat diet. Beneficial changes in lipid profi Continue reading >>

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