Serum and adipocyte resistin in polycystic ovary syndrome with insulin resistance

Seow, Kok-Min; Juan, Chi Chang; Wu, Liang; Hsu, Yung Pei; Wei, Yang; Tsai, Yieh-Loong; Hwang, Jiann Loung; Ho, Low Tone

doi:10.1093/humrep/deh010

Cited by 98 publications

(63 citation statements)

References 36 publications

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“…However, serum resistin levels were found to be higher in obese and non-obese Chinese PCOS groups in comparison with controls, suggesting that resistin may be implicated in the regulation of insulin resistance in this PCOS ethnic group (Wang et al 2010). In terms of gene expression, Seow et al (2004) reported data on resistin mRNA expression in isolated adipocytes from OM adipose tissue of Taiwanese women with PCOS and age-and weightmatched non-PCOS. An overexpression of the resistin gene was found in adipocytes from PCOS, suggesting that resistin may play a role in the local pathogenesis of PCOS.…”

Section: Resistinmentioning

confidence: 99%

Adipose tissue dysfunction, adipokines, and low-grade chronic inflammation in polycystic ovary syndrome

Spritzer¹,

Lecke²,

Satler³

et al. 2015

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258

206

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Polycystic ovary syndrome (PCOS), a complex condition that affects women of reproductive age, is characterized by ovulatory dysfunction and androgen excess. Women with PCOS present higher prevalence of obesity, central adiposity, and dyslipidemia, and face increased risk of type 2 diabetes. PCOS is closely linked to functional derangements in adipose tissue. Adipocytes seem to be prone to hypertrophy when exposed to androgen excess, as experienced by women with PCOS, and both adipose tissue hypertrophy and hyperandrogenism are related to insulin resistance. Hypertrophic adipocytes are more susceptible to inflammation, apoptosis, fibrosis, and release of free fatty acids. Disturbed secretion of adipokines may also impact the pathophysiology of PCOS through their influence on metabolism and on sex steroid secretion. Chronic low-grade inflammation in PCOS is also related to hyperandrogenism and to the hypertrophy of adipocytes, causing compression phenomena in the stromal vessels, leading to adipose tissue hypoperfusion and altered secretion of cytokines. Lifestyle changes are the first-line intervention for reducing metabolic risks in PCOS and the addition of an insulin-sensitizing drug might be required. Nevertheless, there is not sufficient evidence in favor of any specific pharmacologic therapies to directly oppose inflammation. Further studies are warranted to identify an adipokine that could serve as an indirect marker of adipocyte production in PCOS, representing a reliable sign of metabolic alteration in this syndrome.

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Section: Resistinmentioning

confidence: 99%

Adipose tissue dysfunction, adipokines, and low-grade chronic inflammation in polycystic ovary syndrome

Spritzer¹,

Lecke²,

Satler³

et al. 2015

Reproduction

258

206

View full text Add to dashboard Cite

show abstract

“…Indeed, due to its low mRNA expression level in human adipose tissue, it was initially concluded that this molecule was unlikely to be an important factor linking human obesity to insulin resistance. [71][72][73] However, several recent studies reported that resistin serum levels are increased in obesity [74][75][76] or type 2 diabetes, 77,78 with significant correlations often being observed between resistin levels and the BMI, 75 basal glycemia, 77 insulin resistance, 75,79,80 C-reactive peptide, 78 and hepatic lipid content. 80 In keeping with these observations, as well as with the well-known association among central obesity, insulin resistance, and type 2 diabetes, resistin mRNA and protein expression were shown to be higher in human central adipose tissue depots compared with thigh and breast adipose tissue.…”

Section: Resistinmentioning

confidence: 99%

Role of glucocorticoids in the physiopathology of excessive fat deposition and insulin resistance

2004

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Glucocorticoids are important hormones in the regulation of metabolic homeostasis. We infused normal rats with dexamethasone given intracerebroventricularly (i.c.v.) for 3 days. This resulted in hyperphagia, hyperinsulinemia, and marked insulin resistance. Similar metabolic defects were observed following i.c.v. infusion of neuropeptide Y (NPY) in normal rats. As central dexamethasone infusion enhanced NPY content in the arcuate nucleus, it suggested that its metabolic effects are mediated by NPY. Moreover, due to the lack of effects observed in vagotomized animals, activation of the parasympathetic nervous system by central dexamethasone infusion is proposed. Glucocorticoid action is known to involve prereceptor metabolism by enzymes such as 11b-HSD-1 that converts inactive into active glucocorticoids. Mice overexpressing 11b-HSD-1 in adipose tissue were shown to be obese and insulin resistant. We recently observed that adipose tissue 11b-HSD-1 mRNA expression is increased at the onset of high-fat diet-induced obesity and positively correlated with the degree of hyperglycemia. In human obesity, increased adipose tissue 11b-HSD-1 expression and activity were also reported. Resistin is a new adipose tissue-secreted hormone shown to play a role in glucose homeostasis by increasing hepatic glucose production and inhibiting muscle and adipose tissue glucose utilization. We observed increased adipose tissue resistin expression in the early phase of highfat diet-induced obesity as well as decreased resistin expression in response to leptin. A positive correlation between glycemia and adipose tissue resistin expression further suggested a role of this hormone in the development of insulin resistance. The melanocortin system is another important player in the regulation of energy balance. Peripheral administration of a melanocortin agonist decreased food intake and body weight and favored lipid oxidation, effects that were more marked in obese than in lean rats. It is proposed that both resistin and melanocortin agonists may influence adipose tissue 11b-HSD-1, thereby decreasing or enhancing glucose metabolism.

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“…A significant correlation between resistin and BMI had also been demonstrated. Resistin mRNA levels in adipocytes were increased 2-fold in PCOS patients (Seow et al, 2004), suggesting that the resistin gene may be a local determining factor in the pathogenesis of PCOS. Our study aims: (1) to measure serum and follicular resistin, steroids hormone levels in women with PCOS; (2) to assess possible correlations of resistin to the hormonal and metabolic parameters; (3) to analyze the clinical outcomes of in vitro fertilization-embryo transfer (IVF-ET) in women with PCOS and tubal infertility.…”

Section: Introductionmentioning

confidence: 98%

Resistin levels of serum and follicular fluid in non-obese patients with polycystic ovary syndrome during IVF cycles

Lu¹,

Huang²,

Li³

et al. 2005

J. Zhejiang Univ. Sci.

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Abstract:Objectives: To measure serum and follicular resistin, steroids hormone levels in women with PCOS (polycystic ovary syndrome) (BMI (body mass index)<25 kg/m 2 ), to assess possible correlations of resistin to hormonal and metabolic parameters and to analyze the clinical outcomes of in vitro fertilization-embryo transfer (IVF-ET) in women with PCOS and tubal infertility. Study design: We analyzed the clinical outcomes of IVF-ET in women with PCOS (BMI<25 kg/m 2 ) and tubal infertility during the years 2002 to 2004 and compared the serum and follicular fluid resistin levels, estradiol (E 2 ), progesterone (P), testosterone (T) levels in 20 PCOS and 20 healthy, age-matched women without PCOS during IVF-stimulated cycles. The correlations between the resistin levels and the outcomes of IVF-ET were evaluated. Results: No significant differences in resistin levels of either serum or follicular fluid between PCOS and control group were found. However, resistin levels in serum were higher than that in follicular fluid in both groups. Multiple regression analysis showed that resistin levels in serum did not correlate with BMI, estradiol, LH (luteinizing hormone) and insulin level in fasting blood. No significant correlations were found between follicular fluid reisistin levels and fertilization rate, implantation rate, clinical pregnancy rate or early miscarriage rate in both PCOS and control groups. Conclusion: Our results show that resistin does not have correlation with the hormonal and metabolic parameters as well as the outcomes of IVF. These data suggest that resistin is unlikely to be a local determinant factor in steroidogenesis and growth and maturation of oocytes during IVF-ET in lean women with PCOS.

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Serum and adipocyte resistin in polycystic ovary syndrome with insulin resistance

Abstract: These results suggest that overexpression of the resistin gene in adipocytes may be a local determinant factor in the pathogenesis of PCOS.

Cited by 98 publications

References 36 publications

Adipose tissue dysfunction, adipokines, and low-grade chronic inflammation in polycystic ovary syndrome

Adipose tissue dysfunction, adipokines, and low-grade chronic inflammation in polycystic ovary syndrome

Role of glucocorticoids in the physiopathology of excessive fat deposition and insulin resistance

Resistin levels of serum and follicular fluid in non-obese patients with polycystic ovary syndrome during IVF cycles

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