Preconception Alcohol Drinking Alters Glucose Homeostasis and Increases Diabetes Susceptibility in the Offspring

Presentation Number: SUN 585
Date of Presentation: April 2nd, 2017

Ali Mosa Rashid Al-Yasari*, Shaima Jabbar, Miguel Cabrera, Kamil Sochacki, Nickolas Lisanti, Srinivas Gumudavelli and Dipak K Sarkar
Rutgers University, New Brunswick, NJ


In the U.S, it is estimated that about 60% of women have at least one drink a year. Among those who drank, the prevalence of binge drinking was 15.0%. The effect of preconception alcohol exposure (PCAE) on the offspring has not been studied. In this study we evaluated the effect of (PCAE) on glucose homeostasis in the offspring by feeding adult female rats with 6.7% alcohol in their diet for thirty days, went without alcohol for three weeks (AF) and were bred to generate male and female offspring compared with control group receiving rat chow ad libitum (AD), and the pair fed (PF) group receiving an isocaloric liquid control diet to match the daily intake of AF rats. The pups were kept with their mothers until age of weaning on postnatal day (PND)25. At PND60, a group of AD, PF and AF offspring animals were tested for glucose tolerance test (OGTT), glucose-stimulated insulin secretion (GSIS), and glucagon measurement. A separate group of AD, PF and AF offspring animals were tested for diabetes susceptibility by feeding the animals with 40% HFD for two weeks followed by single STZ (40 mg/kg) injection. OGTT results, in both control and HFD/STZ-treated groups, showed that blood glucose levels were increased significantly in AF offspring group in comparison with AD & PF groups. Glucagon levels were decreased in blood and increased in pancreatic tissue of AF animals. Furthermore, blood and pancreatic tissue insulin levels were decreased significantly in AF group. Immunohistochemical measurements in non-HFD/STZ-treated animals revealed that pancreatic tissues of AF offspring had increased COX-2, IFN-γ, and CD3 levels but no changes in Ki67 and caspase-3 levels. Gene expression analysis of liver tissues of the non-HFD/STZ-treated animals identified changes in the levels of FOXO1 and Glucose-6-Phosphatase but not Glucokinase, GLUT2 and PEPCK in AF offspring. These data suggest that PCAE alters the normal glucose homeostasis by increasing pancreatic inflammation and consequently lowers insulin production and secretion which enhances glycogenolysis and increases blood glucose level. Furthermore, PCAE alters glucose homeostasis and increases susceptibility to diabetes in offspring (Supported by NIH grant R37AA08757).


Nothing to Disclose: AMRA, SJ, MC, KS, NL, SG, DKS