Obesity-Related Lipid Profile and Altered Insulin Incretion in Adolescents With Polycystic Ovary Syndrome

Fulghesu, Anna Maria; Magnini, Roberta; Portoghese, Elaine; Angioni, Stefano; Minerba, Luigi; Melis, Gian Benedetto

doi:10.1016/j.jadohealth.2009.10.008

Cited by 46 publications

(31 citation statements)

References 37 publications

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“…Increased body weight is accepted as a major risk factor for MS. Increased body mass and androgen levels were also known to be related to inflammatory response, and proinflammatory cytokine production like TNF-α also contributes to development of insulin resistance and metabolic syndrome in PCOS [18][19][20][21][22][23][24][25]. In accordance to literature, more than half of the Turkish PCOS adolescents were overweight in the present study.…”

Section: Discussionsupporting

confidence: 87%

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The incidence of metabolic syndrome in adolescents with different phenotypes of PCOS

et al. 2017

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Objectives: To evaluate the incidence of metabolic syndrome in Turkish adolescents with different phenotypes of polycystic ovary syndrome (PCOS). Material and methods:This cross-sectional study was performed on the Youth Center clinic of a tertiary referral hospital in Turkey. Adolescents with PCOS (n = 144) were classified into four phenotype groups according to the presence of oligo/anovulation (O), hyperandrogenism (H), and polycystic ovarian morphology (P) as follows: Phenotype A (O + H + P), Phenotype B (H + O), Phenotype C (H + P), Phenotype D (O + P). The adolescents gave early follicular phase blood samples for endocrine and metabolic tests. The incidence and the presence of parameters of metabolic syndrome were assessed among the four groups. Results:In total, 54.9% of the adolescents with PCOS were overweight and 25.7% had metabolic syndrome. The incidence of metabolic syndrome in Phenotypes A-D were as follows: 39.5%, 20.5%, 26.5%, and 15.2%, respectively. Although body mass index was higher in the Phenotype A group, insulin resistance was similar in all of the phenotype groups. The most common dyslipidemia was low HDL-C levels and this was present in more than half of the adolescents with PCOS. Both body mass index and total testosterone levels were significantly higher in adolescents with metabolic syndrome in comparison to those without metabolic syndrome. Conclusions:Although low HDL-C levels and insulin resistance are common PCOS findings in adolescents, the metabolic profile seems to be worse in Phenotype A than the other phenotypes. Therefore, screening programs should evaluate patients based on the known risk factors and phenotypes for adolescents with PCOS.

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Section: Discussionsupporting

confidence: 87%

“…Although the most probable link between PCOS and MS is insulin resistance and hyperinsulinism, the abdominal obesity also supposed to deteriorate the metabolic dysfunction in women with PCOS [21]. The insulin is a known mediator for the development of obesity.…”

Section: Discussionmentioning

confidence: 99%

The incidence of metabolic syndrome in adolescents with different phenotypes of PCOS

et al. 2017

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“…Overall, obese women with HAS are 2.5 times more likely, and nonobese women with HAS are 3.3 times more likely to have IR as assessed with hyperinsulinemic clamps or oral glucose tolerance tests (OGTT) compared with weightmatched controls (14 -16, 38). The reported prevalence of IR and dysglycemia in young girls is much more varied, likely an artifact of the different methods of assessing IR (2,22,23,44,45). For example, Nur et al (44) found that only 6 of 101 obese Hispanic girls with PCOS had IR as assessed by fasting insulin and glucose, and Fruzzetti et al (22) found fasting glucose Ͼ110 mg/dl in only 2% of girls with HAS and varied BMI.…”

Section: E729mentioning

confidence: 99%

Peripheral insulin resistance in obese girls with hyperandrogenism is related to oxidative phosphorylation and elevated serum free fatty acids

Cree-Green

Newcomer

Coe

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

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Cree-Green M, Newcomer BR, Coe G, Newnes L, Baumgartner A, Brown MS, Pyle L, Reusch JE, Nadeau KJ. Peripheral insulin resistance in obese girls with hyperandrogenism is related to oxidative phosphorylation and elevated serum free fatty acids. 31 phosphorus MR spectroscopy before, during, and after near-maximal isometric calf exercise, and peripheral IR was assessed with an 80 mU·m Ϫ2 ·min Ϫ1 hyperinsulinemic euglycemic clamp. Girls with HAS had higher androgens [free androgen index 7.9(6.6,15.5) vs. 3.5(3.0,4.0), P Ͻ 0.01] and more IR [glucose infusion rate 9.4(7.0, 12,2) vs. 14.5(13.2,15.8) mg·kg lean Ϫ1 ·min Ϫ1 , P Ͻ 0.01]. HAS girls also had increased markers of inflammation including CRP, platelets, and white blood cell count and higher serum free fatty acids during hyperinsulinemia. Mitochondrial oxidative phosphorylation was lower in HAS [0.11(0.06,0.19) vs. 0.18(0.12,0.23) mmol/s, P Ͻ 0.05], although other spectroscopy markers of mitochondrial function were similar between groups. In multivariate analysis of the entire cohort, IR related to androgens, oxidative phosphorylation, and free fatty acid concentrations during hyperinsulinemia. These relationships were present in just the HAS cohort as well. Obese girls with HAS have significant peripheral IR, which is related to elevated androgens and free fatty acids and decreased mitochondrial oxidative phosphorylation. These may provide future options as targets for therapeutic intervention.hyperandrogenism; insulin resistance; mitochondria; obesity; hyperandrogenic syndrome HYPERANDROGENIC SYNDROME (HAS), also known as polycystic ovarian syndrome (PCOS), affects at least 10 -15% of the female population in the United States, with a recent increase in prevalence associated with rising obesity rates (32). Women with HAS have a three-to fourfold increased risk of developing type 2 diabetes (T2D) compared with BMI-matched controls (37, 58). This increased risk is thought to be secondary to long-standing insulin resistance (IR) (37). There is also evidence of IR in youth with HAS (2). Similar to findings in T2D, peripheral IR as assessed with a hyperinsulinemic euglycemic clamp has been well documented in adults with HAS (7, 15), with similar but fewer data in youth (2). However, the mechanism of IR in HAS remains uncertain, and as a result the best treatments for HAS are also unclear.A leading theory explaining IR in T2D includes defects in mitochondrial function in combination with excess serum free fatty acids (FFA), which can cause alterations in intracellular insulin signaling (52). Other potential mechanisms involve altered fat metabolism and inflammation, which have been documented in T2D and HAS but have not been examined in adolescents with HAS (14,25,29,33,54). However, data examining the role of mitochondria in IR in HAS are limited and conflicting. Muscle mitochondrial oxidation gene expression for oxidative enzymes such as citrate synthase, or ␤-hydroxyacyl-CoA dehydrogenase were similar between women with and without HAS despite worse IR in the wom...

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“…The manifestation of PCOS in overweight-obese adolescents is likely to originate in prepuberty (Diamanti-Kandarakis et al 2007), predisposing individuals to increased cardiometabolic risk, including dyslipidemia and impaired glucose tolerance, leading to early development of type II diabetes and cardiovascular disease (Alexander et al 2009, Fulghesu et al 2010, Sathyapalan & Atkin 2012, Dantas et al 2013. Insulin resistance (IR) is strongly implicated in the etiology of PCOS (Baillargeon & Nestler 2006, Diamanti-Kandarakis & Dunaif 2012 and hyperinsulinemia has been shown to stimulate androgen production in ovarian thecal cells and to reduce hepatic sex-hormone binding globulin (SHBG) synthesis (Barbieri et al 1984, Nestler et al 1991.…”

Section: Introductionmentioning

confidence: 99%

Cardiometabolic and reproductive benefits of early dietary energy restriction and voluntary exercise in an obese PCOS-prone rodent model

Diané

Kupreeva

Borthwick

et al. 2015

Journal of Endocrinology

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Polycystic ovary syndrome (PCOS) is one of the most common endocrine-metabolic disorders in women of reproductive age characterized by ovulatory dysfunction, hyperandrogenism and cardiometabolic risk. The overweight-obese PCOS phenotype appears to have exacerbated reproductive dysfunction and cardiometabolic risk. In overweight-obese adult women with PCOS, exercise and energy restricted diets have shown limited and inconsistent effects on both cardiometabolic indices and reproductive outcomes. We hypothesized that an early lifestyle intervention involving exercise and dietary energy restriction to prevent or reduce the propensity for adiposity would modulate reproductive indices and cardiometabolic risk in an obese PCOS-prone rodent model. Weanling obese PCOS-prone and Lean-Control JCR:LA-cp rodents were given a chow diet ad libitum or an energyrestricted diet combined with or without voluntary exercise (4 h/day) for 8 weeks. Dietary energy restriction and exercise lowered total body weight gain and body fat mass by 30% compared to free-fed sedentary or exercising obese PCOS-prone animals (P!0.01). Energy restriction induced an increase in exercise intensity compared to free-feeding plus exercise conditions. Energy restriction and exercise decreased fasting plasma triglycerides and apoB48 concentrations in obese PCOS-prone animals compared to free-fed and exercise or sedentary groups. The energy restriction and exercise combination in obese PCOS-prone animals significantly increased plasma sex-hormone binding globulin, hypothalamic cocaine-and amphetamine-regulated transcript (CART) and Kisspeptin mRNA expression to levels of the Lean-Control group, and this was further associated with improvements in estrous cyclicity. The combination of exercise and dietary energy restriction when initiated in early life exerts beneficial effects on cardiometabolic and reproductive indices in an obese PCOS-prone rodent model, and this may be associated with normalization of the hypothalamic neuropeptides, Kisspeptin and CART.

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Obesity-Related Lipid Profile and Altered Insulin Incretion in Adolescents With Polycystic Ovary Syndrome

Cited by 46 publications

References 37 publications

The incidence of metabolic syndrome in adolescents with different phenotypes of PCOS

The incidence of metabolic syndrome in adolescents with different phenotypes of PCOS

Peripheral insulin resistance in obese girls with hyperandrogenism is related to oxidative phosphorylation and elevated serum free fatty acids

Cardiometabolic and reproductive benefits of early dietary energy restriction and voluntary exercise in an obese PCOS-prone rodent model

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