Gender-related long-term effects in adult rats by perinatal dietary ratio of n-6/n-3 fatty acids

Korotkova, Marina; Gabrielsson, Britt G.; Holmäng, Agneta; Larsson, Bo; Hanson, Lars Å.; Strandvik, Birgitta

doi:10.1152/ajpregu.00342.2004

Cited by 87 publications

(69 citation statements)

References 25 publications

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“…However, not all of these report an increase in offspring fat mass 25 and the fatty acid composition of the fat enriched diet appears critical, with excessive maternal saturated fat intake being key. 16,18 An influence of maternal obesity per se has been suggested by recent studies of Yamashita et al 26 and Lambin et al, 10 which have shown increased fat mass in adult wild-type progeny of obese and insulin resistant heterozygous leptin receptor-deficient (Lepr db/ϩ ) mice. Complex interactions between dietary and obesity related metabolic sequelae are therefore likely to set in train events leading to offspring obesity.…”

Section: Discussionmentioning

confidence: 99%

Diet-Induced Obesity in Female Mice Leads to Offspring Hyperphagia, Adiposity, Hypertension, and Insulin Resistance

et al. 2008

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Abstract-Maternal obesity is increasingly prevalent and may affect the long-term health of the child. We investigated the effects of maternal diet-induced obesity in mice on offspring metabolic and cardiovascular function. Female C57BL/6J mice were fed either a standard chow (3% fat, 7% sugar) or a palatable obesogenic diet (16% fat, 33% sugar) for 6 weeks before mating and throughout pregnancy and lactation. Offspring of control (OC) and obese dams (OO) were weaned onto standard chow and studied at 3 and 6 months of age. OO were hyperphagic from 4 to 6 weeks of age compared with OC and at 3 months locomotor activity was reduced and adiposity increased (abdominal fat pad mass; PϽ0.01). OO were heavier than OC at 6 months (body weight, PϽ0.05). OO abdominal obesity was associated with adipocyte hypertrophy and altered mRNA expression of ␤-adrenoceptor 2 and 3, 11␤HSD-1, and PPAR-␥ 2. OO showed resistance artery endothelial dysfunction at 3 months, and were hypertensive, as assessed by radiotelemetry (nighttime systolic blood pressure at 6 months [ Key Words: obesity Ⅲ pregnancy Ⅲ developmental programming Ⅲ metabolic syndrome Ⅲ appetite Ⅲ blood pressure Ⅲ mouse O besity among women of reproductive age is presenting a critical challenge to health care. 29% of USA women aged 20 to 39 years are reported to be clinically obese 1 and there is serious concern in many European countries over the increasing obesity among young women. 2 While obesity is associated with increased risk of almost every common complication of pregnancy, obesity in the mother may play a direct role in transmission of an obesogenic and diabetogenic trait from generation to generation. Increasing evidence suggests that children born of pregnancies complicated by either obesity or related gestational diabetes mellitus (GDM) are at increased risk of obesity, impaired glucose tolerance, and other facets of the metabolic syndrome. 3 Animal models have proven invaluable in interrogation of associations between maternal diet and body composition and offspring phenotype. 4 Those studies which have addressed effects of maternal calorific excess, including several from our laboratory, have generally fed rats diets rich in animal fat. 4 -7 Because young women of reproductive age often consume excessive amounts of sugars as well as fats, 8 the relevance of a diet rich in fat alone is limited. In this study, we induced obesity by feeding mice a highly palatable diet rich in sugars and animal fat, and addressed the hypothesis that diet-induced obesity during pregnancy can transmit a propensity for adiposity, glucose intolerance, and cardiovascular dysfunction to the offspring. Obesity was induced in female mice and offspring cardiovascular and metabolic function

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Section: Discussionmentioning

confidence: 99%

Diet-Induced Obesity in Female Mice Leads to Offspring Hyperphagia, Adiposity, Hypertension, and Insulin Resistance

et al. 2008

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“…The type of fat however may also be important as dams fed with diets high in essential fatty acids throughout late gestation and lactation produce offspring that eat less, are leaner and have improved insulin sensitivity as adults. 61 High carbohydrate diets are also protective and produce offspring that remain lighter in weight. 62 There is also evidence that the suckling period is critical in the developmental induction of obesity.…”

Section: The Developmental Origins Of Human Metabolic Diseasementioning

confidence: 99%

Epigenetic changes in early life and future risk of obesity

2010

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The rapid increase in incidence of obesity over the past two decades cannot be explained solely by genetic and adult lifestyle factors. There is now considerable evidence that the fetal and early postnatal environments also strongly influence the risk of developing obesity in later life. Initially, human studies showed that low birth weight was associated with an increased risk of obesity but increasingly there is evidence that overnutrition in the early life can also increase susceptibility to future obesity. These findings have now been replicated in animal models, which have shown that both maternal under-and overnutrition can induce persistent changes in gene expression and metabolism. The mechanism by which the maternal nutritional environment induces such changes is beginning to be understood and involves the altered epigenetic regulation of specific genes. In this review, we discuss the recent evidence that shows that early-life environment can induce altered epigenetic regulation leading to the induction of an altered phenotype. The demonstration of a role for altered epigenetic regulation of genes in the developmental induction of obesity opens the possibility that interventions, either through nutrition or specific drugs, may modify long-term obesity risk and combat this rapid rise in obesity.

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“…Despite this evidence, deficiency studies have not universally observed hypertension when different strains, 10 sexes of rats 11 or source of o-3/o-6 fatty acids 11 have been examined. Recent evidence suggests that many of the problems with replication may be related to dietary interactions with other nutrients including protein content.…”

Section: Introductionmentioning

confidence: 99%

Hypertension induced by ω-3 polyunsaturated fatty acid deficiency is alleviated by α-linolenic acid regardless of dietary source

et al. 2010

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X-3 polyunsaturated fatty acid deficiency, particularly during the prenatal period, can cause hypertension in later life. This study examined the effect of different sources of a-linolenic acid (canola oil or flaxseed oil) in the prevention of hypertension and other metabolic symptoms induced by an x-3 fatty acid-deficient diet. Dams were provided one of three experimental diets from 1 week before mating. Diets were either deficient (10% safflower oil-DEF) or sufficient (7% safflower oil+3% flaxseed oil-SUF-F; or 10% canola oil-SUF-C) in x-3 fatty acids. The male offspring were continued on the maternal diet from weaning for the duration of the study. Body weight, ingestive behaviors, blood pressure, body composition, metabolic rate, plasma leptin and brain fatty acids were all assessed. The DEF animals were hypertensive at 24 weeks of age compared with SUF-F or SUF-C animals; this was not evident at 12 weeks. These results suggest that different sources of ALA are effective in preventing hypertension related to x-3 fatty acid deficiency. However, there were other marked differences between the DEF and, in particular, the SUF-C phenotype including lowered body weight, adiposity, leptin and food intake in SUF-C animals. SUF-F animals also had lower, but less marked reductions in adiposity and leptin compared with DEF animals. The differences observed between DEF, SUF-F and SUF-C phenotypes indicate that body fat and leptin may be involved in x-3 fatty acid deficiency hypertension.

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Gender-related long-term effects in adult rats by perinatal dietary ratio of n-6/n-3 fatty acids

Cited by 87 publications

References 25 publications

Diet-Induced Obesity in Female Mice Leads to Offspring Hyperphagia, Adiposity, Hypertension, and Insulin Resistance

Diet-Induced Obesity in Female Mice Leads to Offspring Hyperphagia, Adiposity, Hypertension, and Insulin Resistance

Epigenetic changes in early life and future risk of obesity

Hypertension induced by ω-3 polyunsaturated fatty acid deficiency is alleviated by α-linolenic acid regardless of dietary source

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