Maternal chocolate and sucrose soft drink intake induces hepatic steatosis in rat offspring associated with altered lipid gene expression profile

Kjærgaard, Magnus; Nilsson, Cecilia; Rosendal, Åsa; Nielsen, Mette Olaf; Raun, Kirsten

doi:10.1111/apha.12138

Cited by 41 publications

(38 citation statements)

References 49 publications

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“…*p < 0.05 versus oil treatment affect the prenatal differentiation of neurons in offspring and result in impaired ability for social interaction. Collectively, these observations agree with the previous findings that maternal factors, including health status and nutrition, can cause unfavorable outcomes in offspring (Leret et al 2009;Hussain et al 2013;Kjaergaard et al 2014;Pruis et al 2014a, b;Taylor et al 2014).…”

Section: Discussionsupporting

confidence: 92%

Maternal exposure to di-(2-ethylhexyl) phthalate exposure deregulates blood pressure, adiposity, cholesterol metabolism and social interaction in mouse offspring

et al. 2015

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Long-term exposure to di-(2-ethylhexyl) phthalate (DEHP) is highly associated with carcinogenicity, fetotoxicity, psychological disorders and metabolic diseases, but the detrimental effects and mechanisms are not fully understood. We investigated the effect of exposing mouse mothers to DEHP, and the underlying mechanism, on blood pressure, obesity and cholesterol metabolism as well as psychological and learning behaviors in offspring. Tail-cuff plethysmography was used for blood pressure measurement; Western blot used was for phosphorylation and expression of protein; hematoxylin and eosin staining, Nissl staining and Golgi staining were used for histological examination. The serum levels of cholesterol, triglycerides and glucose were measured by blood biochemical analysis. Hepatic cholesterol and triglyceride levels were assessed by colorimetric assay kits. Offspring behaviors were evaluated by open-field activity, elevated plus maze, social preference test and Morris water maze. Maternal DEHP exposure deregulated the phosphorylation of endothelial nitric oxide synthase and upregulated angiotensin type 1 receptor in offspring, which led to increased blood pressure. It led to obesity in offspring by increasing the size of adipocytes in white adipose tissue and number of adipocytes in brown adipose tissue. It increased the serum level of cholesterol in offspring by decreasing the hepatic capacity for cholesterol clearance. The impaired social interaction ability induced by maternal DEHP exposure might be due to abnormal neuronal development. Collectively, our findings provide new evidence that maternal exposure to DEHP has a lasting effect on the physiological functions of the vascular system, adipose tissue and nerve system in offspring.

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Section: Discussionsupporting

confidence: 92%

Maternal exposure to di-(2-ethylhexyl) phthalate exposure deregulates blood pressure, adiposity, cholesterol metabolism and social interaction in mouse offspring

et al. 2015

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“…Whether these physiological changes, seen in offspring prenatally exposed to western diet, are induced by elevated dietary fat content per se or are instead due to a change in dietary fatty acid composition was not addressed in this experimental design. Murine models have consistently described lipid abnormalities in offspring exposed to a high-fat diet during early phases of development (Bruce et al 2009, Elahi et al 2009, Gregorio et al 2010, Oben et al 2010, Ashino et al 2012, Kjaergaard et al 2013, Kruse et al 2013, Mouralidarane et al 2013. We here compared western-type diet (moderate fat and cholesterol) to matched semisynthetic control diet.…”

Section: Discussionmentioning

confidence: 99%

“…Very recently, several groups have described that gestational energy-rich diets can programme hepatic steatosis or even non-alcoholic steatohepatitis (NASH) in the offspring in rodent models (Bruce et al 2009, Elahi et al 2009, Gregorio et al 2010, Oben et al 2010, Ashino et al 2012, Kjaergaard et al 2013, Mouralidarane et al 2013. Often, these studies compare rodent chow with different diets based on lard as the main fat source (35, 45 or 60%), sometimes combined with high fructose intake or condensed milk.…”

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confidence: 99%

Maternal western diet primes non‐alcoholic fatty liver disease in adult mouse offspring

et al. 2013

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“…Alterations in plasma levels of HF-diet-fed newborn were observed (Franco et al, 2012;Troina et al, 2010;Tsuduki et al, 2013), but the mechanism remains unclear and may involve placental effects (Sabri et al, 2014). Previous studies have shown different results (Guarda et al, 2014;Kjaergaard, Nilsson, Rosendal, Nielsen, & Raun, 2014), suggesting that maternal nutritional status during pregnancy and lactation influences the methylation of genes related to lipid metabolism in the offspring (Aagaard-Tillery et al, 2008;Jousse et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Sex‐specific Alterations in Serology and the Expression of Liver FATP4 Protein in Offspring Exposed to High‐Fat Diet during Pregnancy and/or Lactation

Zhao

Yao

et al. 2018

Lipids

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Changes in dietary composition will have a significant impact on the nutritional status of the mother and the offspring. To examine the relevant hormone level changes during lactation and the expression of fatty acid transporters in the placenta and liver under the condition of a high-fat (HF) diet, we established HF animal models and conducted a cross-fostering program to mimic the shift in diet. On gestation day (GD)18, the weight of placenta in the HF group was significantly higher than that in the control group (p < 0.05). HF-fed male pups had a significantly lower serum insulin level, but the same phenomenon was not found in females. On the contrary, serum triacylglycerol (TAG) level presented a tendency to decrease only in female offspring. Oil red O staining showed lipid accumulation in the HF diet offspring livers. The mRNA levels of FATP4 in the placenta in the HF diet group were significantly upregulated compared to the control diet group (p < 0.05). High-fat diet (HFD) consumption also altered the liver mRNA levels of FATP4, SREBP-1, and SCD-1 in the male offspring, while the changes in protein levels of FATP4 were not observed in either sex. In conclusion, maternal HF diet has a profound impact on offspring growth, metabolism, and the risk of metabolic disorders, which would depend on the exposure period of pregnancy and lactation.

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Maternal chocolate and sucrose soft drink intake induces hepatic steatosis in rat offspring associated with altered lipid gene expression profile

Abstract: Our results suggest that supplementation of chocolate and soft drink during gestation and lactation contributes to early onset of hepatic steatosis associated with changes in hepatic gene expression and lipid handling.

Cited by 41 publications

References 49 publications

Maternal exposure to di-(2-ethylhexyl) phthalate exposure deregulates blood pressure, adiposity, cholesterol metabolism and social interaction in mouse offspring

Maternal exposure to di-(2-ethylhexyl) phthalate exposure deregulates blood pressure, adiposity, cholesterol metabolism and social interaction in mouse offspring

Maternal western diet primes non‐alcoholic fatty liver disease in adult mouse offspring

Sex‐specific Alterations in Serology and the Expression of Liver FATP4 Protein in Offspring Exposed to High‐Fat Diet during Pregnancy and/or Lactation

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