During the past 2 decades, the consumption of fructose (a monosaccharide) has doubled due to the availability of high fructose corn syrup. Fructose is absorbed more slowly than glucose. It is less insulinogenic and does not require the presence of insulin for its uptake by cells. Therefore, fructose has been recommended to diabetic and obese patients to replace sucrose as a sweetener. However, more research evidence has now revealed that fructose consumption can cause hyperinsulinemia, hypertriglyceridemia and insulin resistance (IR) in humans and animals. With increased fructose consumption, certain populations with mild IR would be more susceptible to the effect of fructose. Pregnancy is another IR state. When IR produced by pregnancy is superimposed on the IR produced by fructose ingestion, an additive effect may be seen. In this proposed research, the hypothesis that fructose ingestion will potentiate gestation induced IR will be tested. It is expected that the aggravated IR will predispose the pups to obesity and diabetes in adult life. The roles of prenatal fructose expose and postnatal factors (i.e. changes in milk composition or lipid profile) play in fructose and gestation induced IR will be examined. The second hypothesis to be tested is that IR exposure during pre-weaning period will have a trans-generation effect. The parameters for studying these hypotheses are; glucose tolerance, blood substrate and hormone levels, hepatic gluconeogenic and lipogenic enzyme activities, insulin binding and receptor function, liver fat and glycogen content, pancreatic insulin content, milk substrate levels and profile, as well as body composition. This proposed research will provide valuable information regarding the factor and mechanisms of fructose or gestation will afford effective dietary recommendations and treatments in order to warrant the well-being of mothers and their offspring.
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