April 20, 2016
American Journal of Obstetrics and Gynecology
TAKE-HOME MESSAGE
Pregnant mice were randomized to receive 10% fructose solution or water as the sole drinking fluid throughout pregnancy to assess the effect of fructose-rich diets on cardiovascular disease risk factors in the offspring. Maternal and birth weights were similar in the two groups. At 1 year, offspring in the fructose group had higher peak glucose, higher area under the intraperitoneal glucose tolerance testing curve, and higher mean arterial pressure compared with the control offspring. In addition, female offspring in the fructose group had a higher weight, higher percent visceral adipose tissue, more liver fat infiltrates, higher insulin resistance scores, higher insulin area under the intraperitoneal glucose tolerance testing curve, higher serum concentrations of leptin, and lower concentrations of adiponectin than females from the control group. These differences were not seen in male mice. Triglycerides and total cholesterol levels were similar in the two groups.
High fructose intake in pregnancy predisposes offspring, particularly female offspring, to adult obesity, hypertension, and metabolic dysfunction, which increase cardiovascular risk. Limiting fructose intake in pregnancy could have significant, durable benefits.
Abstract
BACKGROUND
Consumption of fructose-rich diets in the United States is on the rise and thought to be associated with obesity and cardiometabolic diseases.
OBJECTIVE
We sought to determine the effects of antenatal exposure to high-fructose diet on offspring’s development of metabolic syndrome-like phenotype and other cardiovascular disease risk factors later in life.
STUDY DESIGN
Pregnant C57BL/6J dams were randomly allocated to fructose solution (10% wt/vol, n = 10) or water (n = 10) as the only drinking fluid from day 1 of pregnancy until delivery. After weaning, pups were started on regular chow, and evaluated at 1 year of life. We measured percent visceral adipose tissue and liver fat infiltrates using computed tomography, and blood pressure using CODA/noninvasive monitor. Intraperitoneal glucose tolerance testing with corresponding insulin concentrations were obtained. Serum concentrations of glucose, insulin, triglycerides, total cholesterol, leptin, and adiponectin were measured in duplicate using standardized assays. Fasting homeostatic model assessment was also calculated to assess insulin resistance. P values
RESULTS
Maternal weight, pup number, and average weight at birth were similar between the 2 groups. Male and female fructose group offspring had higher peak glucose and area under the intraperitoneal glucose tolerance testing curve compared with control, and higher mean arterial pressure compared to control. Female fructose group offspring were heavier and had higher percent visceral adipose tissue, liver fat infiltrates, homeostatic model assessment of insulin resistance scores, insulin area under the intraperitoneal glucose tolerance testing curve, and serum concentrations of leptin, and lower concentrations of adiponectin compared to female control offspring. No significant differences in these parameters were noted in male offspring. Serum concentrations of triglycerides or total cholesterol were not different between the 2 groups for either gender.
CONCLUSION
Maternal intake of high fructose leads to fetal programming of adult obesity, hypertension, and metabolic dysfunction, all risk factors for cardiovascular disease. This fetal programming is more pronounced in female offspring. Limiting intake of high fructose-enriched diets in pregnancy may have significant impact on long-term health.