Exposure to maternal overnutrition and a high-fat diet during early postnatal development increases susceptibility to renal and metabolic injury later in life

Jackson, Colette M.; Alexander, Barbara T.; Roach, Lauren A.; Haggerty, Deani; Marbury, David C.; Hutchens, Zachary M.; Flynn, Elizabeth R.; Maric‐Bilkan, Christine

doi:10.1152/ajprenal.00491.2011

Cited by 50 publications

(52 citation statements)

References 32 publications

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“…Similar to the observation that pups from fructose alone fed pregnancies are hyperinsulinaemic, 90 exposure to a highfat and high-fructose diet in utero and postnatally resulted in a 140% increase in plasma insulin levels compared with control offspring at 12 weeks of life and also increased blood glucose levels, although not significantly. 150 Fructose and saturated fatty acid (30% fructose, 9.9% coconut fat and 0.5% cholesterol) intake prior to pregnancy, throughout gestation and during lactation also results in increased fasting insulin and homeostatic model assessment (HOMA) levels in 3-month-old offspring fed a control diet from weaning. 79 This maternal hyperinsulinaemia and insulin insensitivity occurred without the development of obesity and, interestingly, epididymal and retroperitoneal fat depots were significantly smaller (18% and 44%, respectively) compared with control offspring.…”

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

confidence: 99%

“…101,150 Providing a highfat diet with water containing 10% w/v fructose throughout pregnancy and lactation, followed by continuation of the diet in postnatal life, resulted in increased bodyweight and visceral fat, elevated blood glucose levels, glucose intolerance, a greater than twofold increase in urine albumin excretion and 60% increase in glomerulosclerosis in adult offspring compared with controls at 17 weeks of age. 101 Finally, it has been observed that a maternal 'junk-food' diet impacts the expression of key components of the mesolimbic reward pathway in the offspring of rat dams at 6 weeks and 3 months of age, with higher fat intake from weaning until at least 3 month of age.…”

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: Interactive Effects Of Fructose Sucrose and Fat In The Matementioning

confidence: 99%

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

confidence: 99%

Fructose, pregnancy and later life impacts

Regnault

Gentili

Sarr

et al. 2013

Clin Exp Pharma Physio

View full text Add to dashboard Cite

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“…The offspring were fed their respective diets for 12 wk after weaning, making them 17 wk of age at the time of being euthanized. This time point was chosen based on our previous study in the male offspring (14).…”

Section: Experimental Designmentioning

confidence: 99%

“…However, the impact of postnatal overnutrition on adult renal function has not been fully examined. A study from our laboratory has recently shown that combined exposure to a high-fat/fructose diet during fetal and 17 wk of postnatal development potentiate the susceptibility of renal and metabolic disturbances later in life of the male offspring (14).…”

mentioning

confidence: 99%

High-fat/fructose feeding during prenatal and postnatal development in female rats increases susceptibility to renal and metabolic injury later in life

Flynn¹,

Alexander

Hutchens³

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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Accumulating evidence suggests that both an adverse prenatal and early postnatal environment increase susceptibility to renal and metabolic dysfunction later in life; however, whether exposure to adverse conditions during both prenatal and postnatal development act synergistically to potentiate the severity of renal and metabolic injury remains unknown. Sprague-Dawley rats were fed either a standard diet or a diet high in fat/fructose throughout pregnancy and lactation. After being weaned, female offspring were randomized to either standard diet or the high-fat/high-fructose diet, resulting in the following treatment groups: NF-NF, offspring of mothers fed a standard diet and fed a standard diet postnatally; NF-HF, offspring of mothers fed a standard diet and fed a high-fat/fructose diet postnatally; HF-NF, offspring of mothers fed a high-fat/fructose diet and fed a standard diet postnatally; HF-HF, offspring of mothers fed a high-fat/fructose diet and fed a high-fat/fructose diet postnatally. At the time of euthanasia (17 wk of age), HF-HF offspring weighed 30% more and had 110% more visceral fat than NF-NF offspring. The HF-HF offspring also had elevated blood glucose levels, glucose intolerance, 286% increase in urine albumin excretion, and 60% increase in glomerulosclerosis compared with NF-NF. In addition, HF-HF offspring exhibited a 100% increase in transforming growth factor-β protein expression and 116% increase in the abundance of infiltrated macrophages compared with the NF-NF offspring. These observations suggest that high-fat/fructose feeding during prenatal and throughout postnatal life increases the susceptibility to renal and metabolic injury later in life.

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“…Several rodent studies have taken a longer-term approach to determine the effects of overnutrition prior to, during gestation and during lactation on long-term kidney health. Feeding rats a high fat/high fructose diet from 6 weeks prior to mating, throughout pregnancy and subsequent lactation, resulted in offspring that developed albuminuria, which was exacerbated by postnatal overnutrition causing tubulointerstitial fibrosis and increased TGF-β expression (Jackson et al, 2012). In a separate study, inducing obesity in rats 5 weeks prior to mating results in the programming of increased adiposity in offspring, hyperleptinemia and hypertension in offspring in association with increased renal norepinephrine and increased renal renin expression (Samuelsson et al, 2010).…”

Section: Suboptimal Maternal Nutritionmentioning

confidence: 99%

Gestational hypoxia and programming of disease

Walton¹

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Fetal hypoxia remains the most common complication throughout pregnancy and has a wide aetiology including, but not limited to, placental insufficiency, high altitude living and maternal factors such as smoking and pulmonary disease. Intrauterine growth restriction and subsequent low birth weight are common features of pregnancies complicated by reduced oxygenation. Suboptimal organ development may arise, thereby substantially increasing vulnerability to cardiovascular and renal diseases in adulthood. Recently it has been established that prenatally programmed vulnerability to disease may be exacerbated by a postnatal 'second-hit', such as a high salt diet or ageing. The primary aim of this thesis was to investigate the effects of maternal hypoxia on the programming of cardiovascular and renal disease in mice, and secondly whether excess dietary salt intake throughout life may exacerbate disease outcomes.Pregnant CD1 mice were housed in a hypoxia chamber set to 12% oxygen throughout the last five days of pregnancy, from embryonic day (E) 14.5 until birth (P0). Control animals remained in normoxic room conditions (21% oxygen) throughout pregnancy. Upon littering, animals were removed from the hypoxia chamber and raised in normoxic room conditions. A subset of mice was fed a high salt diet from 10 weeks of age until post-mortem. Mice were housed in metabolic cages for 24 hours to assess renal function under basal conditions, and in response to a 24 hour water deprivation challenge, at 4 and 12 months of age. Blood pressure and microvascular function and structure were assessed in offspring at 12 months of age.Kidneys, hearts and aortas were collected for stereological and histological analyses.Prenatal hypoxia reduced nephron number in the kidneys of male offspring, leading to glomerular hypertrophy, renal fibrosis and mild albuminuria by 12 months of age. However, female offspring exposed to the same hypoxic insult in utero presented with normal number of glomeruli and renal pathology equivalent to control animals by 12 months of age. Both male and female hypoxia-exposed offspring had elevated mean arterial pressure at 12 months of age. A high salt diet throughout adult life increased cardiac tissue fibrosis, particularly in male hypoxia-exposed offspring, and exacerbated renal pathology in male hypoxia-exposed offspring only. Pressurized myography was performed at the time of post-mortem to assess functional, structural and mechanical properties of mesenteric resistance arteries at 12 months of age. Both male and female offspring exposed to maternal hypoxia had significantly 3 impaired endothelial function, which was not exacerbated by the high salt diet. The combination of prenatal hypoxia and a postnatal high salt diet caused marked stiffening of the microvasculature as well as loss of elastin integrity and increased collagen content in the aorta, consistent with vascular stiffness. This suggests that kidneys from female offspring are somehow protected from the in utero insult; however, this protection...

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Exposure to maternal overnutrition and a high-fat diet during early postnatal development increases susceptibility to renal and metabolic injury later in life

Cited by 50 publications

References 32 publications

Fructose, pregnancy and later life impacts

Fructose, pregnancy and later life impacts

High-fat/fructose feeding during prenatal and postnatal development in female rats increases susceptibility to renal and metabolic injury later in life

Gestational hypoxia and programming of disease

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