Influence of Aging and Menopause on Lipids and Lipoproteins in Women

Kolovou, Genovefa; Bilianou, Helen

doi:10.1177/0003319708319645

Cited by 48 publications

(30 citation statements)

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“…38 Similarly, increasing age is associated with glucose intolerance due to a reduction in insulin sensitivity 39 and abnormal lipid profile with increased triglycerides and cholesterol. 40 We found that Black women are at increased risk of early-PE and that both Black and South Asian women have increased risk for late-PE. Racial differences are also observed in nonpregnant subjects both in terms of metabolic profiles and susceptibility to different types of cardiovascular disease.…”

Section: Discussionmentioning

confidence: 62%

Maternal risk factors for hypertensive disorders in pregnancy: a multivariate approach

et al. 2009

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The study aimed to develop prediction algorithms for hypertensive disorders based on multivariate analysis of factors from the maternal history and compare the estimated performance of such algorithms in the prediction of early preeclampsia (PE), late-PE and gestational hypertension (GH) with that recommended by the National Institute for Clinical Excellence (NICE). Logistic regression analysis was used to determine which of the maternal characteristics and history had significant contribution in predicting early-PE, late-PE and GH. There were 37 cases with early-PE, 128 with late-PE, 140 with GH and 8061 cases that were unaffected by PE or GH. Predictors of early-PE were Black race, chronic hypertension, prior PE and use of ovulation drugs. Predictors of late-PE and GH were increased maternal age and body mass index, and family history or history of PE. Additionally, late-PE was more common in Black, Indian and Pakistani women. The detection rates of early-PE, late-PE and GH in screening by maternal factors were 37.0, 28.9 and 20.7%, respectively, for a 5% false positive rate. Screening as suggested by NICE would have resulted in a false positive rate of 64.1% with detection rates of 89.2, 93.0 and 85.0% for early-PE, late-PE and GH, respectively. Meaningful screening for hypertensive disorders in pregnancy by maternal history necessitates the use of algorithms derived by logistic regression analysis.

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Section: Discussionmentioning

confidence: 62%

Maternal risk factors for hypertensive disorders in pregnancy: a multivariate approach

et al. 2009

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“…The women studied by Bantle et al were leaner and younger than the women in the present study and of mixed menopausal status. Body fat (19), age (20), and menopausal status (21,22) have all been shown to affect postprandial TG responses in women.…”

Section: Figurementioning

confidence: 99%

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans

et al. 2009

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Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose-or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults. IntroductionStudies investigating the effects of fructose consumption in humans and animals have been comprehensively reviewed (1-4), and while strong evidence exists that consumption of diets high in fructose results in increased de novo lipogenesis (DNL), dyslipidemia, insulin resistance, and obesity in animals, direct experimental evidence that consumption of fructose promotes DNL, dyslipidemia, insulin resistance, glucose intolerance, and obesity in humans is lacking. Thus, we have investigated and compared the biological effects of the 2 major simple sugars in the diet, glucose and fructose, on BW and regional fat deposition and on indices of lipid and carbohydrate metabolism in older, overweight and obese men and women.We sought to answer the following questions: (a) Does consumption of fructose with an ad libitum diet promote greater BW gain and have differential effects on regional adipose deposition and adipose gene expression compared with consumption of glucose with an ad libitum diet? (b) Does consumption of fructose induce dyslipidemia compared with consumption of glucose? (c) Is fructose-induced hypertriglyceridemia the result of increased rates

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“…However, this increase is more evident in aging women (women's peak cholesterol level is in the sixth decade, whereas in men it is in the fifth decade of their life) [17,18]. In advanced aging (octogenarians, nonagenarians) total cholesterol, LDL-C and triglyceride levels are decreased in both sexes [19].…”

Section: Lipid Profile In Aging Womenmentioning

confidence: 99%