Gender-Linked Hypertension in Offspring of Lard-Fed Pregnant Rats

Khan, Imran Y; Taylor, Paul D.; Dekou, Vasia; Seed, Paul; Lakasing, Lorin; Graham, Delyth; Dominiczak, Anna F.; Hanson, Mark A.; Poston, Lucilla

doi:10.1161/01.hyp.0000047511.97879.fc

Cited by 337 publications

(350 citation statements)

References 44 publications

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“…While we cannot categorically state that the difference in age did not contribute to the sex-related difference observed in insulin resistance, our recent report on the offspring of obese mice [42] also showed that glucose intolerance was predominantly observed in males. Moreover, we have also previously shown a male predominance of insulin resistance in adult offspring of rats fed a lard-rich diet [49]. Also, there was a marginally significant difference in insulin resistance in males, but not in females at 3 months.…”

Section: Discussionsupporting

confidence: 53%

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

et al. 2009

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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.

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Section: Discussionsupporting

confidence: 53%

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

et al. 2009

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“…On the contrary, feeding a diet rich in lard to pregnant rats also affected systolic blood pressure in adult offspring, even if fed a normal diet, but the female offspring were more sensitive than the male to this foetal nutrition-induced hypertension. 12 These results could be related to the saturated/polyunsaturated fatty acid ratio in endothelium, since it was shown that a saturated diet in rat increases catecholamine sensitivity and decreases endothelium-dependent relaxation mesenteric arteries. 13 Some epidemiological studies including a 'saturated fat' arm have focused on cholesterol, circulating lipids, atherosclerosis, coronaropathies and stroke, but not on blood pressure.…”

Section: Hypertension and Sfamentioning

confidence: 99%

Hypertension prevention: from nutrients to (fortified) foods to dietary patterns. Focus on fatty acids

Grynberg

2005

J Hum Hypertens

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A Grynberg INRA-Paris 11 UMR1154, Nutrition Lipidique et Re´gulation Fonctionnelle du Coeur et des Vaisseaux, Facultede Pharmacie, Châtenay-Malabry, FranceDiet affects significantly the incidence and severity of cardiovascular diseases and fatty acid intake, in its qualitative as well as quantitative aspects, and influences several risk factors including cholesterol (total, LDL and HDL), triglycerides, platelet aggregation and blood pressure, as evidenced in the 2001 WHO report. This review focuses on the qualitative concern of lipid intake, the various classes of fatty acids of the lipid fraction of the diet, saturated, monounsaturated and polyunsaturated, and their effects on blood pressure. Saturated fat have a bad file and several experimental studies in the rat showed a progressive increase in blood pressure in response to a highly saturated diet. Moreover, a highly saturated diet during gestation led to offspring which, when adults, presented a genderrelated hypertension. The mechanism of this effect may be related to the polyunsaturated/saturated ratio (p/s). During the past 20 years, trans fatty acids have been suspected of deleterious health effects, but the investigations have shown that these fatty acids display a biological behaviour close to that of saturated fatty acids (SFA). Moreover, epidemiological investigations did not confirm the relationship between trans fatty acids and cardiovascular pathology. Polyunsaturated fatty acids have been shown to exert a positive action on hypertension. This effect could be attributed to the alteration of the p/s, but mainly to the x3 polyunsaturated fatty acids (PUFAs). The comparison of several animal models led to the conclusion that long-chain x3 PUFAs (eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)) can prevent the increase in blood pressure and reduce established hypertension, but the efficient dose remains an object of discussion. Moreover, the two long-chain x3 PUFAs, EPA and DHA, display specific effects, which vary with the aetiology of hypertension, because their mechanism of action is different. DHA acts on both blood pressure and heart function (heart rate and ECG) and interferes with the adrenergic function. Conversely, EPA, which is not incorporated in cardiac phospholipids, has no effect on the heart and its mechanism of action is largely unknown. Although it is accepted by the scientific community that the intake of EPA and DHA needs to be increased, we will have to discover new ways to do it, since marine products are the main source of these fatty acids, and this source is not inexhaustible.

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“…Premenopausal women have lower arterial blood pressure than men matched for age and post-menopausal women, suggesting a role of ovarian hormones in blood pressure regulation [71]. In rats, feeding a diet rich in lard to pregnant females leads to gender-related cardiovascular dysfunction in normally fed offspring as blood pressure was found to be high in the female but not in the male offspring [72]. A maternal low-protein diet (LPD) during pregnancy and lactation modifies the growth and metabolism of the progeny (F2) of the female offspring (F1) [73,74].…”

Section: Sexual Dimorphism In Consequences On Offspringmentioning

confidence: 99%

Sexual dimorphism in environmental epigenetic programming

Gabory

Attig

Junien

2009

Molecular and Cellular Endocrinology

249

196

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The phenotype of an individual is the result of complex interactions between genotype and current, past and ancestral environment leading to a lifelong remodelling of our epigenomes. The vast majority of common diseases, including atherosclerosis, diabetes, osteoporosis, asthma, neuropsychological and autoimmune diseases, which often take root in early development, display some degree of sex bias, very marked in some cases. This bias could be explained by the role of sex chromosomes, the different regulatory pathways underlying sexual development of most organs and finally, lifelong fluctuating impact of sex hormones. A substantial proportion of dimorphic genes expression might be under the control of sex-specific epigenetic marks. Environmental factors such as social behaviour, nutrition or chemical compounds can influence, in a gender-related manner, these flexible epigenetic marks during particular spatiotemporal windows of life. Thus, finely tuned developmental program aspects, for each sex, may be more sensitive to specific environmental challenges, particularly during developmental programming and gametogenesis, but also throughout the individual's life under the influence of sex steroid hormones and/or sex chromosomes. An unfavourable programming could thus lead to various defects and different susceptibility to diseases between males and females. Recent studies suggest that this epigenetic programming could be sometimes transmitted to subsequent generations in a sex specific manner and lead to transgenerational effects (TGEs).This review summarizes the current understanding in the field of epigenetic programming and highlights the importance of studying both sexes in epidemiological protocols or dietary interventions both in humans and in experimental animal models.

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Gender-Linked Hypertension in Offspring of Lard-Fed Pregnant Rats

Cited by 337 publications

References 44 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

Hypertension prevention: from nutrients to (fortified) foods to dietary patterns. Focus on fatty acids

Sexual dimorphism in environmental epigenetic programming

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