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Introduction: A previous study has suggested that with increasing oGTT thresholds there was a statistically increasing risk of maternal and foetal morbidity in the form of hypertensive disorders complicating pregnancy and macrosomia. The present study aims to identify whether this gradient risk is extant with lower blood glucose levels. Methodology: A total of 1289 75-gm oGTTs were performed during pregnancy. These were divided according to their fasting and 2-hour values into categories: A. Fasting values =5.6 mmol/l (n=292); and 2-hour values =9.6 mmol/l (n=208). The incidence of hypertensive disease during pregnancy, the macrosomia rate, and the mean birth weight were assessed in each group. Results: The data confirm that a significant rise in the incidence of hypertensive disease occurs at a fasting vlood glucose value of >=5.6 mmol/l, while the macrosomia rate rises after >=4.6 mmol/l. The mean birth weight increased progressively with increasing fasting blood glucose thresholds. There is furthermore a progressive rise in the incidence of hypertension noted with significance being reached at a 2-hour blood glucose value greater than 9.6 mmol/l. However no such relationship appears to be present for the incidence of macrosomia; and there was no significant differences in mean birth weights with increasing 2-hour post-load glucose values. Conclusions: The study suggests that fasting blood glucose values may be a better indicator of maternal and foetal adverse risk outcomes with increased adverse foetal outcomes being indicated at levels >=4.6 mmol/l. The 2-hour post-75g oGTT values appear to be useful as adverse risk indicators only at levels >-9.6 mmol/l., peer-reviewed

The type 2 iodothyronine deiodinase (D2) is essential for feedback regulation of TSH by T4. We genetically inactivated in vivo D2 in thyrotrophs using a mouse model of Cga-driven cre recombinase. Pituitary D2 activity was reduced 90% in the Cga-cre D2 knockout (KO) mice compared with control Dio2fl/fl mice. There was no growth or reproductive phenotype. Basal TSH levels were increased 1.5- to 1.8-fold, but serum T4 and T3 were not different from the controls in adult mice. In hypothyroid adult mice, suppression of TSH by T4, but not T3, was impaired. Despite mild basal TSH elevation, the TSH increase in response to hypothyroidism was 4-fold reduced in the Cga-cre D2KO compared with control mice despite an identical level of pituitary TSH α- and β-subunit mRNAs. In neonatal Cga-cre D2KO mice, TSH was also 2-fold higher than in the controls, but serum T4 was elevated. Despite a constant TSH, serum T4 increased 2–3-fold between postnatal day (P) 5 and P15 in both genotypes. The pituitary, but not cerebrocortical, D2 activity was markedly elevated in P5 mice decreasing towards adult levels by P17. In conclusion, a congenital severe reduction of thyrotroph D2 causes a major impairment of the TSH response to hypothyroidism. This would be deleterious to the compensatory adaptation of the thyroid gland to iodine deficiency.