High-fat feeding during pregnancy and lactation affects offspring metabolism in rats

Guo, Feng; Jen, K.‐L. Catherine

doi:10.1016/0031-9384(94)00342-4

Cited by 224 publications

(174 citation statements)

References 30 publications

Supporting

Mentioning

149

Contrasting

Unclassified

Order By: Relevance

“…Relatively little is known about the persistent consequences of maternal obesity for the developing offspring. Some studies in rodents have assessed influences of maternal high-energy diets using only a short time window, generally less than 14 days prior to mating or only during gestation and/or lactation, and have generally failed to achieve obesity in the dam [16,19,20,[24][25][26]. A few, using a prolonged feeding period to induce obesity [17,27,28], have generally switched from a high-energy diet to a control diet postdelivery [28], potentially inducing changes of the milk composition [29].…”

Section: Discussionmentioning

confidence: 99%

“…Studies from our laboratories and others have shown that a maternal diet rich in animal fat during gestation and lactation leads to the development of an offspring phenotype with characteristics of the metabolic syndrome even when offspring are reared on a normal diet [16][17][18][19][20]. However, these dietary manipulations were made only during the short period of gestation and lactation and rodents fed a diet rich in fat alone are generally resistant to the development of obesity [16].…”

mentioning

confidence: 99%

See 1 more Smart Citation

Established diet-induced obesity in female rats leads to offspring hyperphagia, adiposity and insulin resistance

et al. 2009

View full text Add to dashboard Cite

Aims/hypothesis Accumulating evidence suggests that maternal obesity may increase the risk of metabolic disease in the offspring. We investigated the effects of established maternal diet-induced obesity on male and female offspring appetite, glucose homeostasis and body composition in rats. Methods Female Wistar rats were fed either a standard chow (3% fat, 7% sugar [wt/wt]) or a palatable obesogenic diet (11% fat, 43% sugar [wt/wt]) for 8 weeks before mating and throughout pregnancy and lactation. Male and female offspring of control and obese dams were weaned on to standard chow and assessed until 12 months of age. Results At mating, obese dams were heavier than control with associated hyperglycaemia and hyperinsulinaemia. Male and female offspring of obese dams were hyperphagic (p<0.0001) and heavier than control (p<0.0001) until 12 months of age. NEFA were raised at 2 months but not at 12 months. At 3 months, OGTT showed more pronounced alteration of glucose homeostasis in male than in female offspring of obese animals. Euglycaemic-hyperinsulinaemic clamps performed at 8 to 9 months in female and 10 to 11 months in male offspring revealed insulin resistance in male offspring of obese dams (p<0.05 compared with control). Body compositional analysis at 12 months also showed increased fat pad weights in male and female offspring of obese animals. Conclusions/interpretation Diet-induced obesity in female rats leads to a state of insulin resistance in male offspring, associated with development of obesity and increased adiposity. An increase in food intake may play a role.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Established diet-induced obesity in female rats leads to offspring hyperphagia, adiposity and insulin resistance

et al. 2009

View full text Add to dashboard Cite

show abstract

“…Considering that a typical Western diet is rich in dietary fat content (17), especially saturated fatty acids (SFA), some studies have investigated the role of high-fat feeding in the concept of developmental origins of health and disease (3)(4)(5). These studies indicate that maternal high-SFA consumption during pregnancy can induce features of metabolic syndrome including dyslipidemia (26,27,35), insulin resistance (57), and hypertension (36,35) in the adult offspring. However, the underlying mechanisms of these effects are not known.…”

mentioning

confidence: 99%

Developmental programming of lipid metabolism and aortic vascular function in C57BL/6 mice: a novel study suggesting an involvement of LDL-receptor

Chechi

McGuire²,

Cheema³

2009

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Chechi K, McGuire JJ, Cheema SK. Developmental programming of lipid metabolism and aortic vascular function in C57BL/6 mice: a novel study suggesting an involvement of LDL-receptor. Am J Physiol Regul Integr Comp Physiol 296: R1029 -R1040, 2009. First published February 4, 2009 doi:10.1152/ajpregu.90932.2008We have previously shown that a maternal high-fat diet, rich in saturated fatty acids (SFA), alters the lipid metabolism of their adult offspring. The present study was designed to investigate 1) whether alterations in hepatic LDL-receptor (LDL-r) expression may serve as a potential mechanism of developmental programming behind the altered lipid metabolism of the offspring, 2) whether altered lipid metabolism leads to aortic vascular dysfunction in the offspring, 3) whether deleterious effects of SFA exposure preweaning are influenced by postweaning diet, and 4) whether gender-specific programming effects are observed. Female C57Bl/6 mice were fed a high-SFA diet or regular chow during gestation and lactation while their pups, both male and female, received either SFA or a chow diet after weaning. Male offspring obtained from mothers fed an SFA diet and those who continued on chow postweaning had higher plasma triglycerides and total cholesterol, whereas female offspring had higher plasma total and LDL cholesterol levels, lower hepatic LDL-r mRNA expression, and reduced aortic contractile responses compared with the offspring that were fed chow throughout the study. A comparison of the postweaning diet revealed significantly lower hepatic LDL-r expression along with significantly higher plasma LDL-cholesterol concentration in the female offspring that were obtained from mothers fed an SFA diet and who continued on an SFA diet postweaning, compared with the female offspring that were obtained from mothers fed an SFA diet but who continued on chow postweaning. In conclusion, we report a novel observation of hepatic LDL-r-mediated programming of altered lipid metabolism, along with aortic vascular dysfunction, in the female offspring of mothers fed a high-SFA diet. Male offspring only exhibited dyslipidemia, suggesting gender-mediated programming. This study further highlighted the role of postweaning diets in overriding the effects of maternal programming. fetal programming; plasma lipids; hepatic LDL-receptor; dietary fats; cardiovascular disease RECENT EVIDENCE BASED ON THE developmental origins of health and disease hypothesis suggests that early nutrition can be critical in determining the cardiovascular health of an individual (43, 44). According to this hypothesis, which was originally known as Barker's hypothesis, an adverse maternal nutrition during gestation can create a stressed environment for the developing fetus. The fetus responds to this nutritional stress by programming its own growth in a way that could increase its risk of developing metabolic disorders in later life (6 -8). Considering that a typical Western diet is rich in dietary fat content (17), especially saturated fatty acids (SFA), s...

show abstract

“…Although maternal nutrient deprivation has been well-characterised in this context, there is a relative paucity of data on how high-fat nutrition impacts on the subsequent generation. High fat consumption during pregnancy induces features of MetS including dyslipidaemia in adult offspring, independent of adult environmental factors (12)(13)(14) . A maternal high-fat diet (HFD) in nonhuman primates triggers lipid accumulation, inflammation and oxidative stress in the fetal liver (15) .…”

Section: Developmental Origin Of Adult Health and Diseasementioning

confidence: 99%

Nutritional developmental epigenomics: immediate and long-lasting effects

2010

View full text Add to dashboard Cite

The phenotype of an individual is the result of complex interactions between genome, epigenome and current, past and ancestral environment leading to a lifelong remodelling of the epigenomes. The genetic information expression contained in the genome is controlled by labile chromatin-associated epigenetic marks. Epigenetic misprogramming during development is widely thought to have a persistent effect on the health of the offspring and may even be transmitted to the next generation. The epigenome serves as an interface between the environment and the genome. Dietary factors, including folate involved in C 1 metabolism, and other social and lifestyle exposures have a profound effect on many aspects of health including ageing and do so, at least partly, through interactions with the genome, which result in altered gene expression with consequences for cell function and health throughout the life course. Depending on the nature and intensity of the environmental insult, the critical spatiotemporal windows and developmental or lifelong processes involved, epigenetic alterations can lead to permanent changes in tissue and organ structure and function or to phenotypic changes that can (or cannot) be reversed using appropriate epigenetic tools. Moreover, the flexibility of epigenetic marks may make it possible for environmental, nutritional and hormonal factors or endocrine disruptors to alter, during a particular spatiotemporal window in a sex-specific manner, the sex-specific methylation or demethylation of specific CpG and/or histone modifications underlying sex-specific expression of a substantial proportion of genes. Moreover, genetic factors, the environment and stochastic events change the epigenetic landscape during the lifetime of an individual. Epigenetic alterations leading to gene expression dysregulation accumulate during ageing and are important in tumorigenesis and age-related diseases. Several encouraging trials suggest that prevention and therapy of age-and lifestyle-related diseases by individualised tailoring to optimal epigenetic diets or drugs are conceivable. However, these interventions will require intense efforts to unravel the complexity of these epigenetic, genetic and environment interactions and to evaluate their potential reversibility with minimal side effects.

show abstract

High-fat feeding during pregnancy and lactation affects offspring metabolism in rats

Cited by 224 publications

References 30 publications

Established diet-induced obesity in female rats leads to offspring hyperphagia, adiposity and insulin resistance

Established diet-induced obesity in female rats leads to offspring hyperphagia, adiposity and insulin resistance

Developmental programming of lipid metabolism and aortic vascular function in C57BL/6 mice: a novel study suggesting an involvement of LDL-receptor

Nutritional developmental epigenomics: immediate and long-lasting effects

Contact Info

Product

Resources

About