Maternal high fructose and low protein consumption during pregnancy and lactation share some but not all effects on early-life growth and metabolic programming of rat offspring

Emily J. Arentson-Lantz, Mi Zou, Dorothy Teegarden, Kimberly K. Buhman, Shawn S. Donkin

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Maternal nutritional stress during pregnancy acts to program offspring metabolism. We hypothesized that the nutritional stress caused by maternal fructose or low protein intake during pregnancy would program the offspring to develop metabolic aberrations that would be exacerbated by a diet rich in fructose or fat during adult life. The objective of this study was to characterize and compare the fetal programming effects of maternal fructose with the established programming model of a low-protein diet on offspring. Male offspring from Sprague-Dawley dams fed a 60% starch control diet, a 60% fructose diet, or a low-protein diet throughout pregnancy and lactation were weaned onto either a 60% starch control diet, 60% fructose diet, or a 30% fat diet for 15 weeks. Offspring from low-protein and fructose-fed dam showed retarded growth (P <.05) at weaning (50.3, 29.6 vs 59.1 ± 0.8 g) and at 18 weeks of age (420, 369 vs 464 ± 10.9 g). At 18 weeks of age, offspring from fructose dams expressed greater quantities (P <.05) of intestinal Pgc1a messenger RNA compared with offspring from control or low-protein dams (1.31 vs 0.89, 0.85; confidence interval, 0.78-1.04). Similarly, maternal fructose (P = .09) and low-protein (P <.05) consumption increased expression of Pgc1a in offspring liver (7.24, 2.22 vs 1.22; confidence interval, 2.11-3.45). These data indicate that maternal fructose feeding is a programming model that shares some features of maternal protein restriction such as retarded growth, but is unique in programming of selected hepatic and intestinal transcripts.

Original languageEnglish (US)
Pages (from-to)937-946
Number of pages10
JournalNutrition Research
Volume36
Issue number9
DOIs
StatePublished - Sep 1 2016
Externally publishedYes

Fingerprint

Fructose
Lactation
Mothers
Pregnancy
Growth
Diet
Proteins
Protein-Restricted Diet
Starch
Fats
Confidence Intervals
Liver
Fetal Development
Weaning
Messenger RNA

Keywords

  • Fetal programming
  • Fructose
  • Liver
  • Low protein
  • Rat

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Medicine(all)
  • Endocrinology
  • Nutrition and Dietetics

Cite this

Maternal high fructose and low protein consumption during pregnancy and lactation share some but not all effects on early-life growth and metabolic programming of rat offspring. / Arentson-Lantz, Emily J.; Zou, Mi; Teegarden, Dorothy; Buhman, Kimberly K.; Donkin, Shawn S.

In: Nutrition Research, Vol. 36, No. 9, 01.09.2016, p. 937-946.

Research output: Contribution to journalArticle

Arentson-Lantz, Emily J. ; Zou, Mi ; Teegarden, Dorothy ; Buhman, Kimberly K. ; Donkin, Shawn S. / Maternal high fructose and low protein consumption during pregnancy and lactation share some but not all effects on early-life growth and metabolic programming of rat offspring. In: Nutrition Research. 2016 ; Vol. 36, No. 9. pp. 937-946.
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abstract = "Maternal nutritional stress during pregnancy acts to program offspring metabolism. We hypothesized that the nutritional stress caused by maternal fructose or low protein intake during pregnancy would program the offspring to develop metabolic aberrations that would be exacerbated by a diet rich in fructose or fat during adult life. The objective of this study was to characterize and compare the fetal programming effects of maternal fructose with the established programming model of a low-protein diet on offspring. Male offspring from Sprague-Dawley dams fed a 60{\%} starch control diet, a 60{\%} fructose diet, or a low-protein diet throughout pregnancy and lactation were weaned onto either a 60{\%} starch control diet, 60{\%} fructose diet, or a 30{\%} fat diet for 15 weeks. Offspring from low-protein and fructose-fed dam showed retarded growth (P <.05) at weaning (50.3, 29.6 vs 59.1 ± 0.8 g) and at 18 weeks of age (420, 369 vs 464 ± 10.9 g). At 18 weeks of age, offspring from fructose dams expressed greater quantities (P <.05) of intestinal Pgc1a messenger RNA compared with offspring from control or low-protein dams (1.31 vs 0.89, 0.85; confidence interval, 0.78-1.04). Similarly, maternal fructose (P = .09) and low-protein (P <.05) consumption increased expression of Pgc1a in offspring liver (7.24, 2.22 vs 1.22; confidence interval, 2.11-3.45). These data indicate that maternal fructose feeding is a programming model that shares some features of maternal protein restriction such as retarded growth, but is unique in programming of selected hepatic and intestinal transcripts.",
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