Abstract
Early life exposure to certain environmental stimuli is related to the development of alternative phenotypes in mammals. A number of these phenotypes are related to an increased risk of disease later in life, creating a massive healthcare burden. With recent focus on the determination of underlying causes of common metabolic disorders, parental nutrition is of great interest, mainly due to a global shift towards a Western-type diet. Recent studies focusing on the increase of food or macronutrient intake don’t always consider the source of these nutrients as an important factor. In our study, we concentrate on the effects of high-sucrose diet, which provides carbohydrates in form of sucrose as opposed to starch in standard diet, fed in pregnancy and lactation in two subsequent generations of spontaneously hypertensive rats (SHR) and congenic SHR-Zbtb16 rats. Maternal sucrose intake increased fasting glycaemia in SHR female offspring in adulthood and increased their chow consumption in gravidity. High-sucrose diet fed to the maternal grandmother increased brown fat weight and HDL cholesterol levels in adult male offspring of both strains, i.e., the grandsons. Fasting glycaemia was however decreased only in SHR offspring. In conclusion, we show the second-generation effects of maternal exposition to a high-sucrose diet, some modulated to a certain extent by variation in the Zbtb16 gene.
Highlights
The early development of a mammalian organism represents a critical time in the determination of health and disease in its adult life
F2 programmed spontaneously hypertensive rats (SHR) males displayed lower fasting glycaemia compared to their control group significant difference test of the two-way ANOVA for STRAIN and PROGRAM as major factors are (Figure 7a), indicated with no ascorresponding difference in SHR-Zbtb16
predictive adaptive responses (PARs) presumably evolved to enable organisms to cope with transient changes in the environment and “provide a process by which individuals adapt to their future postnatal environment by restricting their range of possible phenotypes to a narrower spectrum, without changing the genotype [28]”
Summary
The early development of a mammalian organism represents a critical time in the determination of health and disease in its adult life. Diet as well as other environmental factors influence the establishment or maintenance of specific epigenetic patterns through the activity of methyltransferases [2] or histone modifications [3,4]. When it comes to DNA methylation, do the activity of methyltransferases matter. Due to the raised interest in environmental factors able to alter the mammalian development towards disease in adult life (DOHAD, developmental origins of health and disease), many studies using animal models have focused on understanding the underlying mechanisms in past years. Since the genetic difference between the two used strains is only subtle, we opted to enhance homogeneity of the experimental groups by using highly inbred strains of animals and limiting our focus only to male F2 offspring of F1 programmed rat dams
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
