Background Although a great deal of scientific evidence on the epidemiological risk factors for diabetes and prediabetes has been accumulated, there is still insufficient evidence to explore sex-related differences. The aim of this study was to examine sex-specific differences in the effect of the atherogenic index of plasma (AIP) on prediabetes and diabetes. Methods This cross-sectional study included data from 10099 American adults. The exposure variable was the AIP, which was defined as log10 (triglycerides/high-density lipoprotein cholesterol). The outcome variables included prediabetes and diabetes defined by the 2013 American Diabetes Association guidelines. Results The median age (mean ± SD) was 48.51 ± 18.42 years, and the average value (SD) of the AIP was − 0.09 (0.34). The prevalence of prediabetes was 40.24%, and that of diabetes was 21.32%. Overall, there was a significant positive association between the AIP and prediabetes and diabetes (per 1-unit increment in the AIP: OR, 2.49; 95% CI 1.75, 3.54). The multivariate logistic regression model demonstrated that for each unit increment in the AIP, the prediabetes and diabetes prevalence increased 4.96-fold among female participants (OR 4.96, 95% CI 2.68, 9.18) but not among male participants. We found that the AIP was not related to the prevalence of prediabetes or diabetes (OR 1.41; 95% CI 0.87, 2.29) among males. There was an interaction between sex and the AIP (P for interaction < 0.0001). Conclusions This study showed that a higher AIP was significantly associated with an increased prevalence of prediabetes and diabetes, and the above relationships occurred only among women and not men.

Background Association between age at menarche (AAM) and hypertension remains a controversial topic, and data in China were sparse. Therefore, we aimed to investigate the association between AAM and hypertension in Chinese female population. Methods In this cross-sectional study, 5,102 females aged ≥15 years were enrolled. Self-reported AAM was assessed by the questionnaire. Multiple linear regression analysis was used to evaluate the association between systolic blood pressure (SBP), diastolic blood pressure (DBP), and AAM. Logistic regression analysis was performed to evaluate the association between hypertension and AAM. Generalized additive model (GAM) and smooth curve fitting (penalized spline method) were conducted to explore the exact shape of curve between them. Results The overall mean of AAM was 15.5 years. Each additional year of AAM was associated with a 15% higher risk of hypertension (odds ratio (OR) = 1.15, 95% confidence interval (CI): 1.11–1.19). Among females with hypertension, there was a significant positive association between AAM and SBP (β = 0.88, 95% CI: 0.29–1.46) and DBP (β = 0.80, 95% CI: 0.47–1.13). A significantly higher risk of hypertension was found in younger subjects (15–44 y: OR = 1.37, 95% CI: 1.21–1.55; P for interaction = 0.009) compared with those aged between 62 and 97 y.Conclusions AAM was positively associated with hypertension and blood pressure, especially among females in early adulthood from southern China.

In TEA3A1 rat thymic epithelial cells, ATP stimulates prostaglandin E2 (PGE2) production through activation of phospholipase A2 (PLA2) enzymic activity. The stimulation of PGE2 production tested with other nucleotides indicated the agonist potency of adenosine 5'-[gamma-thio]triphosphate (ATP[S]) > or = UTP > ATP, with ED50 of about 10 microM for ATP[S]. In TEA3A1 cells, cross-linking studies with ATP[35S] revealed the presence of four cell-surface cross-linked bands of 42 kDa, 53 kDa, 83 kDa and 100 kDa in Triton X-100 extracts of TEA3A1 cells by fluorography. Guanosine 5'-[gamma-thio]triphosphate specifically blocked the cross-linking of ATP[35S] to the 53 kDa, 83 kDa and 100 kDa ATP-binding proteins, and inhibited the ATP[S]-mediated stimulation of PGE2 production with an ED50 of about 25 microM. On the other hand, 2-methylthioadenosine triphosphate (2MeSATP) blocked ATP[35S] cross-linking to the 42 kDa protein, but had no effect on ATP[S]-mediated stimulation of PGE2 production. In a variant cell line, TEAvarl, derived from TEA3A1 cells that lost their response to ATP in the activation of PLA2, the presence of 83 kDa ATP-binding protein was not detected. Results from our study suggest that ATP activates PLA2 enzymic activity in TEA3A1 cells by binding to an atypical ATP receptor that has not been described previously.

The stimulation of both phospholipase A2 (PLA2) enzymic activity and the production of prostaglandin E2 (PGE2) by transforming growth factor-alpha (TGF-alpha) and Ca2+ ionophore A23187 in TEA3A1 rat thymic epithelial cells were studied. TGF-alpha by itself at various concentrations (5-200 ng/ml) had no effect on the stimulation of PGE2 production. A23187 (1 microgram/ml) by itself stimulated PGE2 production on average by 18-fold over the control. When TGF-alpha (50 ng/ml) was added to the cells in the presence of A23187, a synergistic stimulation (on average 45-fold) of PGE2 production was observed. Synergistic stimulation was also observed at the level of arachidonic acid released from phospholipid pools, suggesting the activation of PLA2 enzymic activity. We have found that this synergistic activation of PLA2 enzymic activity and subsequent stimulation of PGE2 production required the activation of epidermal growth factor (EGF) receptor tyrosine kinase and Ca2+ influx. This was shown by the fact that genistein, an inhibitor of tyrosine kinase, blocks the synergistic stimulation by TGF-alpha and A23187 and by the fact that the stimulation of PGE2 production by TGF-alpha and A23187 is dependent on the culture-medium Ca2+ concentrations. The requirement for Ca2+ influx instead of intracellular mobilization of Ca2+ was shown by the fact that PGE2 production was not stimulated when cells were treated with TGF-alpha and thapsigargin. Moreover, the synergistic stimulation of PGE2 production by TGF-alpha and A23187 was not affected in protein kinase C down-modulated cells. In addition, the synergistic stimulation was not observed in cells treated with either phorbol 12-myristate 13-acetate (PMA) and TGF-alpha or PMA and A23187, and in cells treated with TGF-alpha and thapsigargin. The requirement for the activation of receptor tyrosine kinase seems to be specific to the EGF receptor, since a synergistic stimulation of PGE2 production was not observed when cells are treated with either insulin-like growth factor-I or fibroblast growth factor-I in the presence of A23187.

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