The state of the intrauterine environment plays a significant role in the development of disease in adult life, with recent interest in the effects of perturbations around conception [periconceptional (PC) period]. This corresponds to the time period when women are unaware of their pregnancy and thus may partake in risky behaviours including alcohol consumption. We have a model of periconceptional ethanol (PCEtOH) exposure in rats which results in offspring with glucose intolerance and insulin insensitivity (1). Recent research suggests that metabolic dysfunction may arise from disturbances to circadian rhythms. As such this study aimed to determine if PCEtOH resulted in changes to peripheral circadian rhythms.
Sprague-Dawley rats consumed either a control liquid diet or an ethanol diet (12.5% v/v ethanol) from four days before mating until four days post mating. Blood was collected every 4 hours over a 24-hour period, to determine glucose and corticosterone concentrations in both male and female rat offspring at 6 months of age. Whole-blood glucose was measured using an Accucheck Performa glucometer with plasma corticosterone measured via radioimmunoassay.
PCEtOH resulted in alterations in the circadian pattern of glucose and plasma corticosterone concentrations in a sex specific manner. Female offspring exhibited a phase shift with peak glucose and corticosterone occurring ~4 hours later in animals exposed to PCEtOH. This resulted in a significantly higher blood glucose and plasma corticosterone at Zeitgeber Time (ZT) 18.5 (P<0.05). No differences were observed between control and PCEtOH exposed male offspring in whole blood glucose or plasma corticosterone at any time point.
These results suggest a sex specific alteration to the circadian regulation of blood glucose and plasma corticosterone in response to PCEtOH exposure. Disturbances to circadian rhythms as a result of periconceptional ethanol exposure may contribute to metabolic deficits in later life.