Impaired fetal growth and atherosclerosis of carotid and peripheral arteries

Martyn, Christopher; Galé, Catharine R.; Jespersen, S.; Sherriff, S B

doi:10.1016/s0140-6736(97)10404-4

Cited by 142 publications

(82 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Plasma LDL cholesterol levels at the age of 6 mo in both sexes were mostly affected by IUGR. In humans, similar results have been obtained (13,14). In previously reported studies on rats, there are differences between the experimental designs, and the results are difficult to compare.…”

Section: Discussionsupporting

confidence: 59%

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

et al. 2012

View full text Add to dashboard Cite

Background: Intrauterine growth restriction (IUGR) is known to affect the risk of adult diseases. consumption of lipogenic fructose is increasing, and it is used as an enhancer of metabolic syndrome in rat experiments. The effects of IUGR, postnatal fructose diet, and their interaction on the lipid profile and adiposity were studied in adult rats. Methods: IUGR was induced by providing pregnant rats with 50% of daily food intake. From 1 mo onward, half of the offspring received a fructose-rich diet and were then followed to the age of 1 and 6 mo, when plasma lipid, glucose, and insulin levels were measured. The adipose tissue was visualized by magnetic resonance imaging at the age of 6 mo. results: IUGR and fructose diet decreased body weight in adult rats. IUGR increased low-density lipoprotein cholesterol in 6-mo-old rats. The fructose diet evoked hypertriglyceridemia and hyperinsulinemia in both the sexes and decreased fasting glucose levels in female rats. Postnatal fructose diet increased lipid content percentage in the retroperitoneal and intra-abdominal adipose tissues in male rats. Interactions between IUGR and postnatal fructose diet were observed in adult weight in males. conclusion: These results demonstrate the importance of IUGR and fructose diet in adverse changes in lipid and glucose metabolism. t he terms "programming, " "fetal origins hypothesis, " and "metabolic imprinting" are used to describe the conditions in the uterus that can lead to possibly permanent or at least longterm changes in the systems involved in growth and metabolism (1,2). Epidemiological studies indicate that low birth weight is related to the risk of metabolic syndrome, type 2 diabetes, and atherosclerosis in adulthood. Poor fetal growth has also been linked to adult obesity, hypertension, and abnormal lipid metabolism (3).There is an interaction between the prenatal and postnatal environments on the health outcome of the offspring (3). Some, but not all, of the infants born small for gestational age show catch-up growth. Those experiencing early catch-up growth tend to have a higher BMI and fat mass as children (4), and according to some studies, they are at an increased risk for adult diseases as compared with those not showing catch-up growth (5). Therefore, it is interesting to elucidate the possible interactions between the prenatal growth and postnatal environment and their effects on the metabolic profile of the offspring.Fructose is a highly lipogenic sugar, and its consumption increases plasma triglyceride and low-density lipoprotein (LDL) cholesterol levels in humans (6). In rats, prolonged feeding of fructose induces moderate hypertension, glucose intolerance, insulin resistance, hyperinsulinemia, and hypertriglyceridemia, all of which are signs of metabolic syndrome (7,8). Therefore, fructose-fed rats are often used as a model of the metabolic syndrome (9).We performed a study of fetal growth restriction in rats. Initially, we aimed to determine if intrauterine growth restriction (IUGR) could affect plasma chole...

show abstract

Section: Discussionsupporting

confidence: 59%

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

et al. 2012

View full text Add to dashboard Cite

show abstract

“…These earlier studies have raised a common hypothesis, that programming of atherosclerosis in adults by suboptimal fetal nutrition (Martyn et al 1998) predisposes to coronary artery disease. However, interpretation of these earlier reports has been limited by their retrospective design.…”

Section: Historical Overviewmentioning

confidence: 99%

Endothelial dysfunction: role in obesity-related disorders and the early origins of CVD

Singhal¹

2005

Proc. Nutr. Soc.

View full text Add to dashboard Cite

Atherosclerotic CVD is the most common cause of death in the West. Yet, its pathogenesis and early development are only partially understood. Central to the early atherosclerotic process is impairment of vascular endothelial function. Endothelial dysfunction can be measured non-invasively and is evident in children before clinical manifestations of atherosclerosis in adulthood. Factors in early life, such as conventional cardiovascular risk factors, or programming by perinatal growth and nutrition strongly affect endothelial function and hence the development of atherosclerosis and CVD. For instance, low birth weight and faster growth early in infancy have a detrimental effect on vascular structure and function. Childhood obesity, a key independent risk factor for CVD, also adversely affects early vascular health. Obesity is associated with endothelial dysfunction and greater arterial stiffness from as early as the first decade of life, while weight loss is beneficial. This effect on vascular function is probably mediated in part by low-grade inflammation and insulin resistance associated with obesity or by the production by adipose tissue of cytokine-like molecules, collectively termed adipokines. A high leptin concentration, in particular, is found in obese individuals and is strongly associated with vascular changes related to early atherosclerosis. The present review focuses on the early origins of endothelial dysfunction, emphasising the role of obesity. It also considers the mechanisms by which obesity impairs endothelial function, understanding of which will be important to further scientific knowledge and to improve public health.

show abstract

“…[1][2][3] Being overweight or obese in adult life also increases the risk of these conditions 4,5 and there is accumulating evidence indicating that weight in pre-adult and early adult life also affect later adult-onset conditions. 6,7 However, among participants in the US Nurses Health Study body mass index, based on self-report of weight and height in a questionnaire when the participants were aged 30-55, was strongly associated with diabetes risk during eight years of follow-up, but body mass index when the nurses were 18 years of age (based on retrospective report of their earlier weight by the nurses at the baseline examination) was only weakly associated with future risk of diabetes, with this risk attenuating to the null with adjustment for later body mass index.…”

Section: Introductionmentioning

confidence: 99%

Lifecourse weight patterns and adult-onset diabetes: the Glasgow Alumni and British Women's Heart and Health studies

et al. 2005

View full text Add to dashboard Cite

Objective: To examine the association between body weight measures across the lifecourse and the risk of adult-onset diabetes. Methods: We analysed data from the Glasgow Alumni Cohort and the British Women's Heart and Health Study (BWHHS). The former included 5571 men and women who had height and weight measured at university, and reported birthweight, mid-and later-life weight in a postal questionnaire. The BWHHS analysis included 4280 women who had height and weight measured in later adulthood and recalled their birthweight and early adult height and weight. Adult-onset diabetes was defined as doctordiagnosed disease after age 30, either self-reported or abstracted from medical records. Results: Thirty nine women and 209 men (Glasgow Alumni study) and 314 women (BWHHS) had diabetes. Those with diabetes had lower mean birthweight than those without, although the differences were small. Individuals with diabetes were also shorter and heavier at all ages than those without diabetes. Being overweight during at least one time period in adult life was associated with an increased risk of diabetes, compared to those who were never overweight. While there was no age at which being overweight was particularly detrimental, the risk associated with being overweight was cumulative across the lifecourse. Conclusions: Being overweight at any point during life is associated with an increased risk of adult-onset diabetes. The cumulative nature of this association reinforces the need to prevent the development of excess weight at an early age to reduce diabetes prevalence in coming decades.

show abstract

Impaired fetal growth and atherosclerosis of carotid and peripheral arteries

Cited by 142 publications

References 20 publications

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

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

Endothelial dysfunction: role in obesity-related disorders and the early origins of CVD

Lifecourse weight patterns and adult-onset diabetes: the Glasgow Alumni and British Women's Heart and Health studies

Contact Info

Product

Resources

About