Body and pancreas weight, and pancreatic histomorphology of Control and prenatal ethanol (EtOH)-exposed rats at 30 days of age.

<p>Offspring were prenatally exposed to a control (Control) or 6% EtOH containing diet for the entirety of gestation and pancreatic histomorphology determined at postnatal day 30 (n = 8–9 male and female Control and EtOH-exposed). A Students t-test was used to compare groups within each sex. Data are expressed as mean±SEM. wt – weight; BW – body wt.</p

Daily pattern of ethanol (EtOH) consumption by pregnant dams.

<p>The average amount of EtOH consumed within each (A) 15 minute interval during the first hour (n = 5), (B) one hour interval during the first 5 hours (n = 4) and (C) from 0–5 hours and 5–21 hours (n = 38). Data are expressed as mean of mean±SEM.</p

Plasma glucose and insulin response curves during the glucose tolerance test and insulin challenge.

<p>Response curves during the (A, B, C, D) intraperitoneal glucose tolerance test (IPGTT) and (E, F) insulin challenge. Plasma glucose (A, B) and insulin (C, D) concentrations during the IPGTT and plasma glucose concentrations (E, F) during the insulin challenge are shown for male (A, C, E) and female (B, D, F) Control and EtOH-exposed offspring. Data are expressed as mean±SEM.</p

Relative hepatic, abdominal adipose and gastrocnemius gene expression of eight month old control and prenatal ethanol (EtOH)-exposed rats.

<p>Rats were prenatally exposed to a control or 6% EtOH containing diet for the entirety of gestation. Group sizes were n = 6–12 per group. Data are expressed as mean±SEM (comparison of data from same-sex groups via Students t-test) or median [25%, 75% confidence intervals] (comparison of data from same-sex groups via Mann-Whitney Rank Sum test). GLUT – glucose transporter; PEPCK – phosphoenolpyruvate carboxykinase 1; PGC-1α – peroxisome proliferator-activated receptor gamma, coactivator 1α; G6Pase – glucose-6-pohosphotase; GK – glucokinase; InsR – insulin receptor; FoxO1– forkhead box protein 1.</p

Impact of low dose prenatal ethanol exposure on glucose homeostasis in Sprague-Dawley rats aged up to eight months

Excessive exposure to alcohol prenatally has a myriad of detrimental effects on the health and well-being of the offspring. It is unknown whether chronic low-moderate exposure of alcohol prenatally has similar and lasting effects on the adult offspring's health. Using our recently developed Sprague-Dawley rat model of 6% chronic prenatal ethanol exposure, this study aimed to determine if this modest level of exposure adversely affects glucose homeostasis in male and female offspring aged up to eight months. Plasma glucose concentrations were measured in late fetal and postnatal life. The pancreas of 30 day old offspring was analysed for beta-cell mass. Glucose handling and insulin action was measured at four months using an intraperitoneal glucose tolerance test and insulin challenge, respectively. Body composition and metabolic gene expression were measured at eight months. Despite normoglycaemia in ethanol consuming dams, ethanol-exposed fetuses were hypoglycaemic at embryonic day 20. Ethanol-exposed offspring were normoglycaemic and normoinsulinaemic under basal fasting conditions and had normal pancreatic b-cell mass at postnatal day 30. However, during a glucose tolerance test, male ethanol-exposed offspring were hyperinsulinaemic with increased first phase insulin secretion. Female ethanol-exposed offspring displayed enhanced glucose clearance during an insulin challenge. Body composition and hepatic, muscle and adipose tissue metabolic gene expression levels at eight months were not altered by prenatal ethanol exposure. Low-moderate chronic prenatal ethanol exposure has subtle, sex specific effects on glucose homeostasis in the young adult rat. As aging is associated with glucose dysregulation, further studies will clarify the long lasting effects of prenatal ethanol exposure