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By David Douglas
Reuters Health Information
In women with polycystic ovary syndrome (PCOS), obstructive sleep apnea is associated with insulin resistance, glucose intolerance and type 2 diabetes, according to a study from the University of Chicago.
“Our findings,” investigator Dr. David A. Ehrmann told Reuters Health, “suggest that the metabolic disturbances seen commonly among women with PCOS are due, at least in part, to the effects of sleep disordered breathing.”
“In the absence of obstructive sleep apnea,” he added, “metabolic disturbances in PCOS are modest and are not significantly different from those seen among obese women without PCOS.”
In the October issue of the Journal of Clinical and Endocrinological Metabolism, Dr. Ehrmann and colleagues describe their prospective study of 52 women with PCOS and 21 comparable women without the disorder.
With polysomnography, the team diagnosed obstructive sleep apnea in 29 women with PCOS (56%) and 4 controls (19%). After adjustment for risk factors, the PCOS patients with sleep apnea were more insulin resistant than those without apnea. Further, impaired glucose tolerance was observed in 16 of the 29 women (55%) with PCOS and sleep apnea versus only 6 of the 23 (26%) PCOS patients without sleep apnea.
“Insulin resistance and glucose tolerance were highly correlated with the presence and severity of obstructive sleep apnea,” the authors report.
They also found that in PCOS patients with normal glucose tolerance, sleep apnea was associated with an almost twofold higher fasting insulin level and homeostatic model assessment (HOMA) index.
Moreover, the severity of sleep apnea was a highly significant predictor of the fasting concentrations of glucose and insulin as well as 2-hour glucose concentration and HOMA index.
Dr. Ehrmann’s team is now “actively engaged in clinical studies designed to determine the direction of causality between obstructive sleep apnea and the metabolic disturbances characteristic of PCOS.”
J Clin Endocrinol Metab 2008;93:3878-3884.
Science Daily
Nov. 6, 2008
A two-year study conducted by researchers at George Mason University, INOVA Fairfax Hospital and the National Cancer Institute may open the door to new therapies for combating chronic diseases associated with obesity, a condition that affected more than 33 percent of American adults in 2005-06 according to the Centers for Disease Control and Prevention.
While analyzing samples taken from morbidly obese patients undergoing weight loss surgery, the researchers discovered that substantial quantities of melanin—a pigment that gives the skin, the hair and the iris of the eye their natural color—were being produced in the study participants’ fat tissue.
Ancha Baranova, assistant professor in George Mason University’s Department of Molecular and Microbiology and the paper’s lead author, explains that melanin production has never before been identified in fat tissue. She believes that the antioxidant, which has been shown to have anti-inflammatory properties, could be the body’s natural defense against obesity-related conditions such as type 2 diabetes, coronary heart disease, fatty liver disease, polycystic ovary syndrome and some cancers.
“Stockpiling extra calories is difficult even for specialized fat cells; having too much lipid molecules takes its toll on the fat cells, producing oxidative stress,” says Baranova. “It’s not unthinkable that these cells would adapt and produce melanin as a form of self-protection. As a side benefit, melanin may suppress inflammatory properties of the extra pounds of the fat.”
Baranova notes that a larger study is needed in order to confirm the role that the body’s production of this compound plays in fat tissue. However, the discovery suggests that melanin-based therapies may one day be used to reduce the incidence of chronic diseases among the morbidly obese.
“This opens an entirely new avenue for medical interventions because the process of biosynthesis of melanin is relatively easy to meddle with,” says Baranova. “We hope that this study will spur the development of preventive medications aimed at curtailing devastating metabolic complications in obese and overweight populations.”
The paper was co-authored by Manpreet Randhawa, Tom Huff and Vikas Chandhoke of George Mason University; Julio C. Valencia and Vincent J. Hearing of the National Cancer Institute; and Zobair Younossi of INOVA Fairfax Hospital. The study was funded by the Thomas F. Jeffress and Kate Miller Jeffress Memorial Trust and by the Intramural Research Program of the National Cancer Institute at the U.S. National Institutes of Health.
The findings appear in the current Web edition of the FASEB (Federation of American Societies for Experimental Biology) Journal and will be published in the March 2009 print edition.
Journal reference:
1. Randhawa et al. Evidence for the ectopic synthesis of melanin in human adipose tissue. The FASEB Journal, 2008; DOI: 10.1096/fj.08-116327
Adapted from materials provided by George Mason University.
http://www.sciencedaily.com/releases/2008/11/081106164818.htm
Sathyapalan T, Kilpatrick ES, Coady AM, Atkin SL
Department of Diabetes and Endocrinology, University of Hull, Hull, UK; Department of Clinical Biochemistry, Hull Royal Infirmary, Hull, UK; Department of Obstetric Ultrasound, Hull & East Yorkshire Women’s & Children’s Hospital, Hull, UK.
Source J Clin Endocrinol Metab 2008 Oct 21.
Abstract Context: Polycystic ovary syndrome (PCOS) is associated with increased risk of cardiovascular morbidity whereas statins are proven to reduce cardiovascular mortality and morbidity through lipid lowering and perhaps through their pleotrophic effects. Statins can also reduce testosterone in vitro by inhibiting ovarian theca-interstitial cell proliferation, steroidogenesis and reducing inflammation in vivo.
Objective: To assess the effect of atorvastatin on inflammatory markers, insulin resistance and biochemical hyperandrogenemia in patients with PCOS.
Design: Randomised, double blind placebo controlled study.
Setting: Tertiary care setting in United Kingdom.
Patients: Forty medication naïve patients with PCOS and biochemical hyperandrogenaemia.
Methods: Patients were randomised to either atorvastatin 20mg daily or placebo.
Main outcome measures: The primary end point of the study was a change in the inflammatory marker hsCRP. The secondary end points were a change in insulin resistance and total testosterone.
Results: After 12 weeks of atorvastatin there was a significant reduction (mean+/-SEM) in total cholesterol (4.6+/-0.2 vs. 3.4+/-0.2 mmol/L,p<0.01), LDL cholesterol (2.9+/-0.2vs.1.8+/-0.2 mmol/L,p<0.01), triglycerides (1.34+/-0.08vs.1.08+/-0.13mmol/L,p<0.01), hsCRP (4.9+/-1.4vs.3.4+/-1.1mg/Lp=0.04), free androgen index (13.4+/-0.6vs.8.7+/-0.4 p<0.01), testosterone[4.1+/-0.2vs.2.9+/-0.1 nmol/Lp<0.01) and insulin resistance as measured by HOMA-IR(3.3+/-0.4vs.2.7+/-0.4). There was a significant increase in SHBG (31.1+/-1.0vs.35.3+/-1.2 nmol/L,p<0.01). There was a positive correlation between the reduction in HOMA-IR in the atorvastatin group with the reduction in triglycerides and the reduction of FAI. There was a significant deterioration of HOMA-IR in the placebo group (3.0+/-0.4vs.3.8+/-0.5).
Conclusions: This study suggests that atorvastatin is effective in reducing inflammation, biochemical hyperandrogenemia and metabolic parameters in patients with polycystic ovary syndrome after a 12 week period.
PubMed ID 18940877