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Little evidence suggests that PCOS causes CVD, diabetes
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Women with polycystic ovary syndrome often have overweight, which may predispose them to metabolic syndrome; however, the redistribution of subcutaneous fat to the upper body may not explain an increased risk, study data show.
“Obesity is common in women with PCOS, and it can explain most of the metabolic alterations in the syndrome,” Gloria Lena Vega, PhD, professor in the Center for Human Nutrition at the University of Texas Southwestern Medical Center, told Endocrine Today. “Obese PCOS women have a greater upper truncal fat mass relative to lower extremity fat mass. Unexpectedly, most obese women with PCOS do not have more intra-abdominal visceral fat mass than equally obese women without PCOS, but rather, they tend to have more subcutaneous fat. Importantly, the metabolic concomitants of truncal obesity in PCOS women are increased insulin resistance and triglyceride accumulation in the liver. Dyslipidemia does not appear to be a concomitant feature of PCOS, but hypertension is common.”
Scott M. Grundy, MD, PhD, also a professor in the Center for Human Nutrition at the University of Texas Southwestern Medical Center and co-author on the study noted that, “non-obese PCOS women do not have metabolic alterations seen in obese PCOS and non-PCOS women.
Vega, Grundy and colleagues evaluated data from the Reynolds Women Study on 145 women with PCOS and 344 women without PCOS to determine whether women with PCOS have abnormalities of body fat distribution, increased metabolic risk factors and elevated liver triglyceride content independent of percentage of body fat content.
Researchers measured body composition by DXA, abdominal fat masses by MRI and hepatic triglycerides by magnetic resonance spectroscopy. “Obesity” was defined as at least 35% body fat; less than 35% body fat was defined as “no obesity.”
No differences were observed for percent total body fat or distribution between upper and lower body fat in participants without obesity regardless of the presence of PCOS. Percent total body fat was similar in participants with obesity regardless of PCOS status. Participants with obesity and PCOS had significantly higher truncal body fat mass, percent truncal fat and lean-body mass, and lower percentage of total body fat in the trunk and percentage of lower body fat, compared with participants with obesity without PCOS. The natural log of testosterone levels was weakly correlated with percent body fat in participants without PCOS (P < .01); there was no significant correlation in participants with PCOS.
Participants with PCOS and obesity had significantly more subcutaneous and retroperitoneal fat compared with the other groups.
No differences were observed for levels of fasting glucose, fasting insulin, homeostasis model of assessment for insulin resistance (HOMA-IR), fasting lipids, C-reactive protein, leptin, adiponectin or average liver fat content in participants without obesity. Participants with PCOS and obesity had higher fasting insulin and HOMA-IR compared with controls. Participants with PCOS had higher C-reactive protein levels and average liver triglyceride content compared with participants without PCOS.
“This study also showed that in contrast to obese women with PCOS, non-obese PCOS women do not have insulin resistance or fat accumulation in the liver,” Vega said. “The implication of these observations is that reducing or preventing increases in truncal body fat prevent the deleterious metabolic concomitants of obesity. A greater research effort is needed in identifying the molecular factors that trigger susceptibility to insulin resistance and fatty liver in women with PCOS features; epidemiological studies that help to establish thresholds of truncal fat mass that trigger metabolic concomitants in PCOS women; and clinical trials that determine efficacy of lifestyle modification and pharmacotherapy to control truncal body obesity in women with PCOS features.” – by Amber Cox
For more information:
Gloria Lena Vega, PhD, can be reached at gloria.vega@utsouthwestern.edu. Scott M. Grundy, MD, PhD, can be reached at scott.grundy@utsouthwestern.edu.
Disclosures: The authors report no relevant financial disclosures.
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