Association of Glutathione Peroxidase Activity with Insulin Resistance and Dietary Fat Intake during Normal Pregnancy

Wayne Chris Hawkes

U. S. Department of Agriculture/Agricultural Research Service Western Human Nutrition Research Center, University of California at Davis (UCD) Department of Nutrition, National Center on Minority Health and Health Disparities Center of Excellence for Nutritional Genomics, UCD Medical Center Cancer Center, University of California at Davis, Davis, California 95616-8685

Address correspondence to: Wayne Chris Hawkes, Ph.D., University of California at Davis, 1 Shields Avenue, Davis, California 95616-8685. E-mail: chawkes{at}whnrd.usda.gov.

To the editor:

In a recent article, Chen et al. (1) reported a significant increase in erythrocyte glutathione peroxidase activity during pregnancy. The same article also reported higher glutathione peroxidase activity in Blacks and significant positive correlations with fasting insulin, C-peptide, and insulin resistance. Increased glutathione peroxidase activity during pregnancy is a very surprising finding in light of the many previous reports that selenium status declines significantly during normal pregnancy. This paper by Chen et al. (1) seems to be the first report of increased glutathione peroxidase (or any other parameter of selenium status) during pregnancy.

Lower blood selenium concentrations and glutathione peroxidase activities have been reported in pregnant women relative to prepregnancy levels (2, 3, 4, 5) and relative to nonpregnant control women (6, 7, 8, 9). Glutathione peroxidase activity in erythrocytes (5) and selenium concentration in hair (10) are lower in pregnant women, and amniotic fluid selenium concentrations decline throughout pregnancy (11), suggesting that a real decrease in selenium status occurs during pregnancy. The retention of stable isotopes of selenium is greater in pregnant women than in nonpregnant controls (12), suggesting that the decreased selenium status is driven by an increased requirement for selenium, presumably to support fetal growth.

It seems far more likely that the apparent increase in glutathione peroxidase activity was a result of their choice to express the activity relative to the hemoglobin concentration. It is well known that hemoglobin concentration declines during normal pregnancy (13); however, these authors did not report the hemoglobin data. The paper also does not mention what prenatal nutritional supplements were administered to, or used by, these pregnant women. If supplements were not given, then hemoglobin concentrations very likely declined (14, 15, 16) and would account for the apparent increase in glutathione peroxidase activity. If supplements were given and they contained selenium and/or vitamin E (which may improve selenium utilization) (17), then the supplements may have been the source of a real increase in glutathione peroxidase activity, as has been observed before (18). The apparent racial differences can also be explained by noting that hemoglobin is lower in African-American women than in Caucasian women (19) and anemia is more prevalent in Black women (20, 21, 22), which would cause the ratio of glutathione peroxidase to hemoglobin to appear higher in African-Americans relative to Caucasians.

The authors could have reported the glutathione peroxidase activity as a simple concentration to show that the effect was independent of a change in hemoglobin, or they could have reported the hemoglobin data to show that it did not change. Alternatively, they could have included hemoglobin concentration as a covariate in the statistical analysis of the glutathione peroxidase/hemoglobin ratios. Because these data were not reported and none of these issues were raised in the article, it would seem appropriate to address them now by publishing this letter and the authors’ response.

Received February 18, 2004.

References

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