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ABSTRACT: To get further insights on the estrogen regulation of the uteroglobin (UG) gene, the 5'-flanking region of the UG gene from the brown hare (Lepus capensis) (Lc) was cloned and compared with those from two phylogenetically related species: the rabbit (Orictolagus cuniculus) (Oc) and the volcano rabbit (Romerolagus diazi) (Rd). The Lc-UG gene is very similar to those from rabbits (94%) and volcano rabbits (95%), and shares a number of genetic elements, including an estrogen response element (ERE). The estrogen-regulated transcription of a series of progressive 5́-deletion mutants of the Lc-UG gene, identified a functional ERE in the promoter region exhibiting the same orientation and relative position than that previously described in rabbits. The Lc-ERE is identical to the Oc-ERE, but different from both the Rd-ERE and the consensus ERE (c-ERE) by one nucleotide. We also detected important species-specific differences in the estrogen-regulated transcription of the UG gene. A luciferase reporter driven by 333 base pairs (bp) of the Lc-UG promoter elicited a higher response to estradiol than its related counterparts when expressed in estrogen-sensitive MCF-7 cells. Several ERE-like motifs which failed to act as functional EREs were also identified; one of them exhibited two mismatches in its palindromic sequence, a characteristic exhibited in many other natural occurring EREs, including the Rd-ERE.
General and Comparative Endocrinology 01/2014;
Accountability in Research Policies and Quality Assurance 01/2014; 21(2):138-141.
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Because the role of 2-h postload glucose and insulin levels as confounders in the relationship between hypertriglyceridemia and development of metabolic glucose disorders (MGD) has not been elucidated, the aim of this study was to determine whether triglyceride levels ≥ 1.7 mmol/L are a risk factor of developing MGD in otherwise healthy men and women.
A total of 341 healthy men and non-pregnant women, 30 to 50 years of age, were enrolled in a 15-year follow-up study and allocated into the exposed (triglycerides ≥ 1.7 mmol/L) and non-exposed (triglycerides < 1.7 mmol/L) groups. Follow-up visits were scheduled every 3 years to complete 5 visits (mean 3.8 visits). At final follow-up, about 15 years later (mean 13.6 years), contact was re-established in 236 individuals to complete 3540 person-years of follow-up. At baseline, all subjects in both groups were required to be free of impaired fasting glucose (IFG), impaired glucose tolerance (IGT), IFG + IGT, and type 2 diabetes.
The Poisson regression models, adjusted by age, sex, family history of diabetes, waist circumference, body mass index, total body fat, blood pressure, fasting and postload glucose, fasting and postload insulin, and HOMA-IR index, showed a significant association between triglycerides ≥ 1.7 mmol/L and IFG (relative risk – RR – 1.40; 95% CI 1.2–2.2), IGT (RR 1.60; 95% CI 1.3–2.2), IFG + IGT (RR 1.80; 95% CI 1.5–2.7), and type 2 diabetes (RR 3.0; 95% CI 2.5–3.8).
Serum triglyceride levels ≥ 1.7 mmol/L are an independent risk factor of developing IFG, IGT, IFG + IGT, and type 2 diabetes in young and middle-aged, men and women.
European Journal of Internal Medicine 01/2014;
Mexico City, Mexico
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