Being born before 37 weeks’ gestation, or preterm birth, is a leading cause of early childhood death and life-long disability. Antenatal steroids (ANS) are recommended for women judged at risk of imminent preterm delivery. The primary intent of ANS treatment is to rapidly mature the fetal lungs to reduce the risk of mortality and lasting morbidity. Despite being used clinically for some 50 years, a large number of uncertainties remain surrounding the use of ANS. In particular, the choice of agent, dose / regimen, and appropriate gestational age range for ANS therapy all remain unclear. Unresolved concerns regarding potential risk of harms from ANS treatment, especially in light of the modest benefits seen with expanding late-preterm administration, make it increasingly important to optimize the dosing and application of this important and widely used treatment. This review will serve to summarize past data, provide an update on recent developments, and chart a way forward to maximize the overall benefit of this important therapy.
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Erin Lesley Fee, Sarah Stock, and Matthew Kemp
Anna G Holmes, Jose L Mesa, Bronwyn A Neill, Jason Chung, Andrew L Carey, Gregory R Steinberg, Bruce E Kemp, Robert J Southgate, Graeme I Lancaster, Clinton R Bruce, Matthew J Watt, and Mark A Febbraio
Chronic elevations in interleukin (IL)-6 have been associated with insulin resistance, but acute IL-6 administration can enhance insulin sensitivity. Our aim was to exogenously administer IL-6 to rats to elicit either chronic or repeated acute elevations in systemic IL-6. We hypothesized that a continuous elevation of IL-6 would inhibit glucose tolerance and insulin sensitivity while acute intermittent elevations would improve it. Male Wistar rats were treated for 14d with recombinant human IL-6 (2.4 μg/day) or saline administered either by miniosmotic pump (continuous IL-6) or via twice-daily injection (intermittent IL-6). Glucose and insulin tolerance tests were performed following 14-d treatment and 24 h later rats were administered a bolus of insulin (150 mU/g) or saline intraperitoneally. Approximately, 10 min after insulin injection soleus, gastrocnemius and liver were excised and rapidly frozen in liquid nitrogen for subsequent metabolic measures. Irrespective of the mode of delivery, IL-6 treatment increased basal insulin sensitivity, as measured by the homeostatic model assessment of insulin resistance, and enhanced glucose clearance during an i.p. glucose tolerance test. IL-6 increased circulating fatty acids, but did not increase triglyceride accumulation in either skeletal muscle or liver, while it increased the protein expression of both PPARα and UCP2 in skeletal muscle, suggesting that IL-6 can enhance fat oxidation via mitochondrial uncoupling. These data demonstrate that, irrespective of the mode of delivery, IL-6 administration over 2 weeks enhances glucose tolerance. Our results do not support the notion that prolonged chronically elevated IL-6 impairs insulin action in vivo.
