Striking differences in estimates of infant adiposity by new and old DXA software, PEAPOD and skin-folds at 2 weeks and 1 year of life.

BACKGROUND: Infant adiposity better predicts childhood obesity/metabolic risk than weight, but technical challenges fuel controversy over the accuracy of adiposity estimates. OBJECTIVE: We prospectively measured adiposity (%fat) in term newborns (NB) at 2 weeks (n = 41) and 1 year (n = 30). METHODS: %fat was measured by dual X-ray absorptiometry (DXA), PEAPOD and skin-folds (SF). DXAs were analyzed using Hologic Apex software 3.2(DXAv1) and a new version 5.5.2(DXAv2). RESULTS: NB %fat by DXAv2 was 55% higher than DXAv1 (14.2% vs. 9.1%), 45% higher than SF (9.8%), and 36% higher than PEAPOD (10.4%). Among NB, Pearson correlations were 0.73-0.89, but agreement (intra-class correlations) poor between DXAv2 and DXAv1 (0.527), SF (0.354) and PEAPOD (0.618). At 1 year, %fat by DXAv2 was 51% higher than DXAv1 (33.6% vs. 22.4%), and twice as high compared with SF (14.6%). Agreement was poor between DXAv2 and DXAv1 (0.204), and SF (0.038). The absolute increase in %fat from 2 weeks to 1 year was 19.7% (DXAv2), 13.6% (DXAv1) and only 4.8% by SF. CONCLUSION: Analysis of the same DXA scans using new software yielded considerably higher adiposity estimates at birth and 1 year compared with the previous version. Using different modalities to assess body composition longitudinally is problematic. Standardization is gravely needed to determine how early life exposures affect childhood obesity/metabolic risk.

Maternal and perinatal long-chain fatty acids: possible roles in preterm birth.

OBJECTIVE: We conducted a case-control study to evaluate whether maternal and fetal omega-3 and omega-6 essential fatty acid status play possible roles in the pathogenesis of preterm birth. STUDY DESIGN: Essential fatty acid status in blood and trophoblast tissues was measured in (1) women and their newborns with spontaneous preterm birth and (2) control women and newborns at 34 weeks' gestation (maternal blood) and at term delivery. RESULTS: Thirty-seven preterm (mean gestational age 34 weeks) and 34 control mother-baby dyads (gestational age 40 weeks) were evaluated. The maternal percent of total arachidonic acid in red blood cells and plasma was increased in preterm cases versus controls at delivery (3.8- and 1.6-fold, respectively, p < 0.05). Maternal red blood cell eicosapentaenoic acid (1.98 +/- 0.15, p < 0.0001) and omega-3/omega-6 ratios (0.58 +/- 0.22, p < 0.009) were lower in preterm cases than in controls at delivery (4.64 +/- 0.32 and 1.27 +/- 0.12, respectively). Docosapentaenoic acid, a marker of omega-3 essential fatty acid deficiency, was higher in preterm maternal red blood cells (1.26 +/- 0.18, p < 0.0001) and amnion (1.27 +/- 0.19, p < 0.001) compared with term controls (0.12 +/- 0.07 and 0.58 +/- 0.13, respectively). CONCLUSION: Women delivered preterm demonstrated higher arachidonic acid and docosapentaneoic acid levels in maternal blood and trophoblast tissue than did women delivered at term. This suggests (1) altered essential fatty acid intake or metabolism in a portion of women delivered preterm and (2) increased maternal red blood cell arachidonic acid is associated with an increased risk of preterm birth.

Prostaglandins in selected reproductive tissues in preterm and full-term gestations.

We investigated differences in maternal plasma and trophoblast prostaglandin metabolism associated with preterm births. Tissue prostaglandins (PGs) E2 and F2 alpha and the stable plasma PGF2 alpha metabolite, 13,14-dihydro-15-keto-PGF2 alpha, were measured in preterm (< 37 weeks) and term (< or = 37 weeks) births. Amnion PGE2 in preterm (106.1 +/- 15.7 ng/g wet weight tissue; x +/- SEM; n = 37) was lower than in term (176.6 +/- 22.7 ng/g wet weight; x +/- SEM; n = 34, P < 0.02). Placenta PGE2 was lower in preterm (34.7 +/- 19.7 ng/g wet weight; x +/- SEM) than in term (103.3 +/- 28.0 ng/g wet weight; x +/- SEM, P < 0.04). Preterm PGF2 alpha was consistently lower in the amnion (106.8 +/- 17.5 ng/g wet weight) and placenta (102.5 +/- 8.7 ng/g wet weight) than in term amnion (188.2 +/- 24.8 ng/g wet weight; P < 0.01) and placenta (128.9 +/- 7.8 ng/g wet weight; P < 0.03). Chorionic PGE2 and plasma PGF2 alpha metabolite followed this trend but did not reach significance. These findings suggest qualitative and quantitative differences in maternal and trophoblast eicosanoid metabolism between term and preterm parturition.

Persistence of infertility in GnRH immunized male rats treated with subdermal implants of dihydrotestosterone (DHT).

Male hormonal contraception has been limited to date because two fundamental requirements have not been concurrently satisfied, these are, consistent and dependable azoospermia and infertility coupled with maintenance of libido. The objective of this study was to determine the extent to which implants of potent androgen (DHT) will restore androgenization and spermatogenesis in hypogonadotropic infertile male rats. Twenty-five sexually mature male rats of proven fertility were actively immunized against gonadotropin releasing hormone (GnRH) to induce azoospermia. After azoospermia was achieved, GnRH immunized rats received subdermal DHT-filled Silastic implants of 2, 4, 6, or 8 cm, or empty implants (n=5/group). Five untreated control rats received empty capsules. Eight weeks later, fertility was evaluated, sperm number was obtained from the testis, and weights of androgen-dependent organs were measured. The results indicate that immunoneutralization of GnRH induced complete azoospermia, and subsequent treatment with DHT implants of 2 or 4 cm for 8 wk restored accessory organ weights, but did not restore spermatogenesis or fertility. In addition, DHT implants of 6 to 8 cm partially restored spermatogenesis, but not fertility. We conclude that low-dose DHT supplementation of GnRH-immunized rats may be a suitable alternate therapy able to maintain androgenization in the face of persistent azoospermia in the rat. This may be an effective model for development of a male contraceptive.

Maintenance of sexual function with testosterone in the gonadotropin-releasing hormone-immunized hypogonadotropic infertile male rat.

We have previously shown that active immunization against GnRH in the mature male rat can predictably produce hypogonadotropic hypogonadism and azoospermia and, further, that normospermia and normal fertility can be restored by testosterone (T) administration alone. The objective of this study was to explore the hypothesis that GnRH-immunized azoospermic rats could be supplemented with T doses sufficient to restore sexual behavior, but insufficient to support adequate spermatogenesis or to allow restoration of fertility. Adult male rats of proven fertility were immunized against GnRH and supplemented with 2-, 4-, or 8-cm T implants or with empty implants. Eight weeks later, fertility was evaluated; concentrations of serum T, LH, FSH, growth hormone (GH), prolactin (PRL), and thyroid-stimulating hormone (TSH) were determined; sperm number was obtained from the testis; and weights of androgen-dependent organs were measured. GnRH immunization and T supplementation resulted in restoration of organ weights and of fertility in a dose-dependent manner. GnRH immunization with or without T supplementation resulted in the absence of circulating gonadotropins, but had no effect on serum GH, PRL, or TSH levels. Whereas all control animals were fertile, rats that received either empty or 2-cm T implants were completely infertile. Rats that received 4-cm or 8-cm T implants were fertile in 60% and 100% of cases, respectively. Sexual behavior of rats with empty and with 2-cm T implants was compared at 10-18 wk after immunization with GnRH. GnRH-immunized rats given empty implants displayed negligible sexual activity, but those with 2-cm T implants displayed sexual activity equivalent to that of untreated controls despite complete infertility.(ABSTRACT TRUNCATED AT 250 WORDS)