Posted on 02/24/2011 6:54:26 AM PST by decimon
Study finds maternal fructose consumption may also effect placental development
Chevy Chase, MDA recent study accepted for publication in Endocrinology, a publication of The Endocrine Society, reports for the first time that maternal fructose intake during pregnancy results in sex-specific changes in fetal and neonatal endocrinology.
Fructose is a simple sugar found naturally in honey, fruit and some vegetables. Diets high in dietary fructose, particularly due to calorically sweetened beverages, are now increasingly common and have been shown to be detrimental to the regulation of energy intake and body adiposity. With the increasing prevalence of maternal obesity and its association with gestational diabetes, there has been growing interest in maternal nutrition on the risk of childhood and adult disease in the offspring.
"There has been a marked increase in the consumption of fructose-sweetened beverages and foods, particularly among women of reproductive age," said Mark Vickers PhD, of the University of Auckland in New Zealand and lead author of the study." This is the first time that it has been suggested that female and male fetuses react differently to maternal fructose consumption, and that these sex-specific changes may be associated in changes in placental development."
In this study, researchers examined female Wistar rats that were time-mated and allocated to receive either water or a fructose solution designed to provide 20 percent of caloric intake from fructose. Only female fetuses in the fructose-fed rats had higher leptin, fructose and blood glucose levels than their control counterparts. Male and female offspring of fructose-fed rats both showed higher plasma fructose levels and were hypoinsulinemic. Researchers also found that the placenta of female fetuses in the fructose-fed rats were lighter than the female fetuses in the control group.
"Further studies are now critical to establish the long-term effects of maternal fructose intake on the health and well-being of offspring and whether this study's observed sex differences elicit different risk profiles for metabolic disease into the post-weaning period," said Deborah Sloboda, PhD, also of the University of Auckland and co-author of the study. Dr Vickers is currently conducting a follow-up study in rats.
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Other researchers working on the study include: Z.E. Clayton and C. Yap of the Liggins Institute and the National Research Centre for Growth and Development, University of Auckland in New Zealand.
The article, "Maternal fructose intake during pregnancy and lactation alters placental growth and leads to sex-specific changes in fetal and neonatal endocrine function," appears in the April 2011 issue of Endocrinology.
Founded in 1916, The Endocrine Society is the world's oldest, largest and most active organization devoted to research on hormones and the clinical practice of endocrinology. Today, The Endocrine Society's membership consists of over 14,000 scientists, physicians, educators, nurses and students in more than 100 countries. Society members represent all basic, applied and clinical interests in endocrinology. The Endocrine Society is based in Chevy Chase, Maryland. To learn more about the Society and the field of endocrinology, visit our site at www.endo-society.org.
Honeychild ping.
Doesn’t fructose get converted to glucose before it hits the bloodstream?
Threads involving fructose often generate great arguments over such questions. Check back later and you may have at least two answers to choose from.
Sucrose (table sugar) gets converted to fructose and glucose before it hits the bloodstream.
Only one answer to that one.
Girls are fructose and spice.
“body adiposity” = fat
Not according to this:
Figure 2
Hepatic fructose metabolism: A highly lipogenic pathway. Fructose is readily absorbed from the diet and rapidly metabolized principally in the liver. Fructose can provide carbon atoms for both the glycerol and the acyl portions of triglyceride. Fructose is thus a highly efficient inducer of de novo lipogenesis. High concentrations of fructose can serve as a relatively unregulated source of acetyl CoA. In contrast to glucose, dietary fructose does NOT stimulate insulin or leptin (which are both important regulators of energy intake and body adiposity). Stimulated triglyceride synthesis is likely to lead to hepatic accumulation of triglyceride, which has been shown to reduce hepatic insulin sensitivity, as well as increased formation of VLDL particles due to higher substrate availability, increased apoB stability, and higher MTP, the critical factor in VLDL assembly.
Figure 2 is at the end of the conclusion of:
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