Plasma lipid levels and body weight altered by intrauterine growth restriction and postnatal fructose diet in adult rats

Malo, Elina; Saukko, Meiju; Santaniemi, Merja; Hietaniemi, Marianna; Lammentausta, Eveliina; Sequeiros, Roberto Blanco; Ukkola, Olavi; Kesäniemi, Y. Antero

doi:10.1038/pr.2012.173

Cited by 19 publications

(20 citation statements)

References 36 publications

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“…15,138,139 Following reduced in utero fetal growth, through global feed restriction, a postnatal high (60%)-fructose diet, from 1 month of age, evoked hypertriglyceridaemia and hyperinsulinaemia in both the sexes and decreased fasting glucose levels in female rats at 6 months of age. 140 Further, the postnatal fructose diet resulted in an increased lipid content percentage in the retroperitoneal and intra-abdominal adipose tissues in male rats. 140 In addition, fetal protein deprivation, as a means of inducing an adverse in utero environment, has been studied extensively in a number of animal models and results in metabolic changes later in life, often the result of epigenetic changes and insulin resistance phenotypes.…”

Section: Effects Of Fructose On Fetal and Offspring Physiologymentioning

confidence: 98%

“…140 Further, the postnatal fructose diet resulted in an increased lipid content percentage in the retroperitoneal and intra-abdominal adipose tissues in male rats. 140 In addition, fetal protein deprivation, as a means of inducing an adverse in utero environment, has been studied extensively in a number of animal models and results in metabolic changes later in life, often the result of epigenetic changes and insulin resistance phenotypes. 141,142 Furthermore, changes in the mRNA expression of some key hepatic gluconeogenic and glycolytic enzymes, such as fructose-1,6-bisphosphatase and pyruvate kinase, have been reported following a low-protein exposure in utero.…”

Section: Effects Of Fructose On Fetal and Offspring Physiologymentioning

confidence: 98%

“…This biochemical difference in structure and fructose concentration may result in different metabolic outcomes. Comparing the effects of sucrose or glucose and HFCS ingestion on acute metabolic and haemodynamic parameters demonstrates that the ingestion of 90,100,108,110,[112][113][114]133 10% v/v tap water GDM, altered placental vessel development, sex-specific weight effects and hypertriglyceridaemia 63% feed GDM and increased liver TAG Fetus 20% and 10% v/v in water Reductions in placental/birth weights 100,117 10%, 50% and 60% v/v in water Fetal hyperglycaemia and hypertriglyceridaemia and changes in fetal liver weight and genes 90,95,114,[131][132][133] Lactation~60% v/v drinking water Altered calcium metabolism 136 Offspring 10% and 20% v/v drinking water Sex effects, bodyweight, fat depot and hypothalamic changes 97,99,100,140 In utero environment modulation of growth prior to postnatal fructose exposure OR, odds ratio; GDM, gestational diabetes mellitus; TAG, triacylglycerol.…”

Section: Interactive Effects Of Fructose Sucrose and Fat In The Matementioning

confidence: 99%

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Fructose, pregnancy and later life impacts

Regnault

Gentili

Sarr

et al. 2013

Clin Exp Pharma Physio

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Fructose is an increasingly common constituent of the Westernized diet due to cost and production efficiencies. Although an integral component of our pre-industrial revolution diet, over the past two decades human and animal studies have highlighted that excessive fructose intake appears to be associated with adverse metabolic effects. Excessive intake of fructose is the combined result of increased total energy consumption and increased portion sizes of foods, which often incorporate the fructose-containing sugars sucrose and high-fructose corn-syrup (HFCS). The adverse metabolic effects following excessive fructose consumption have become a hot topic in mainstream media and there is now rigorous scientific debate regarding periods of exposure, dosage levels, interactive effects with other sugars and fats and mechanisms underlying the actions of fructose. There is still a degree of controversy regarding the extent to which sugars such as sucrose and HFCS have contributed to the current epidemic of obesity and diabetes. Furthermore, an increasing number of infants are being exposed to sugar-sweetened food and beverages before birth and during early postnatal life, highlighting the importance of determining the long-term effects of this perinatal exposure on the developing offspring. There are limited human observational and controlled studies identifying associations of excessive sweetened food and beverage consumption with poor pregnancy outcomes. Animal research has demonstrated an increased incidence of gestational diabetes as well as altered maternal, fetal and offspring metabolic function, although the long-term effects and the mechanism underlying these perturbations are ill defined. This review aims to understand the role of early life fructose exposure in modifying postnatal risk of disease in the offspring, focusing on fructose intake during pregnancy and in early postnatal life.

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Section: Effects Of Fructose On Fetal and Offspring Physiologymentioning

confidence: 98%

Section: Effects Of Fructose On Fetal and Offspring Physiologymentioning

confidence: 98%

Section: Interactive Effects Of Fructose Sucrose and Fat In The Matementioning

confidence: 99%

See 1 more Smart Citation

Fructose, pregnancy and later life impacts

Regnault

Gentili

Sarr

et al. 2013

Clin Exp Pharma Physio

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“…Studies from other groups also demonstrate a variety of sex-divergent responses in IUGR. Malo et al, for example, reported that IUGR females fed a fructose-rich diet maintained a milder phenotype with maintained insulin sensitivity and lower adipose tissue lipid content in comparison to IUGR males on the same diet [32]. Studies on hypertension have also reported that IUGR female animals do not develop as severe features of high blood pressure and vascular dysfunction as males [33,34].…”

Section: Discussionmentioning

confidence: 99%

Fatty Acid de Novo Synthesis in Adult Intrauterine Growth‐Restricted Offspring, and Adult Male Response to a High Fat Diet

Yee

Han

Vega

et al. 2016

Lipids

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Intrauterine growth restriction (IUGR) with rapid catch-up growth leads to adult obesity and insulin resistance. We have previously shown that IUGR male rats demonstrated increased de novo fatty acid synthesis in the subcutaneous (SC) fat, but not the visceral fat, during the nursing period prior to the onset of obesity. Young IUGR females do not exhibit the same increase. We further hypothesized that in male IUGR offspring, de novo synthesis is a programmed intrinsic effect that persists to adulthood and does not suppress in response to a high fat diet. We measured fatty acid de novo synthesis in IUGR adult males (6 months) using deuterium-enriched drinking water as a stable isotope tracer, then further studied the response after consumption of an isocaloric high fat diet. Baseline de novo synthesis in adult females was also studied at age 9 months. Males demonstrated increased baseline de novo synthesis in both SC fat and visceral fat. Correspondingly, SC and visceral fat protein expression of lipogenic enzymes acetyl-coA carboxylase-α (ACCα) and fatty acid synthase were upregulated. After the isocaloric high fat diet, de novo synthesis was suppressed such that no differences remained between the two groups, although, IUGR SC fat demonstrated persistently increased lipogenic protein expression. In contrast, de novo synthesis among adult females is not impacted in IUGR. In conclusion, enhancement of male IUGR SC fat de novo synthesis appears to be an early consequence of metabolic programming, whereas enhancement in visceral fat appears to be a later consequence.

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“…Alterations in fetal development and growth have been associated with lifelong adverse health problems (48). Intrauterine growth restriction increases low-density lipoprotein cholesterol in rats and the fructose diet which is used as an enhancer of metabolic syndrome causes hypertriglyceridemia and hyperinsulinemia and decreased fasting glucose levels in rats (49). In rats maternal fructose intake during pregnancy causes maternal hyperglycemia and up-regulates hepatic sterol regulatory element-binding protein-1c expression in fetuses and in dams; leading to defects in carbohydrate and lipid metabolism in the adult offspring (50).…”

Section: Fetal Protein Metabolismmentioning

confidence: 99%