Maternal Fat Feeding Augments Offspring Nephron Endowment in Mice

Hokke, Stacey; Puelles, Victor G.; Armitage, James A.; Fong, Karen; Bertram, John F.; Cullen‐McEwen, Luise A.

doi:10.1371/journal.pone.0161578

Cited by 19 publications

(15 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although most studies were performed in rats, similar results were published in mice [46,47] In rats, maternal high-fat diet during gestation and lactation was associated with persisting upregulation of the renin-angiotensin system in adipose and renal tissue, increased oxidative stress markers, dysregulation of sodium transporters and circadian clock markers, and the development of arterial hypertension in adult life [56][57][58]. Perinatally, high-fat offspring presented with increased glomerular number which was no longer retraceable at 9 months of age [59]. Exposure to a modified high-fat diet rich in lipids containing saturated, mono-unsaturated, and n-6 polyunsaturated fatty acids in utero and until weaning resulted in vascular dysfunction, reduced renal Na+,K+-ATPase and reduced renin activity at 6 to 12 months of age.…”

Section: Proteinsupporting

confidence: 72%

Impact of early-life diet on long-term renal health

et al. 2020

View full text Add to dashboard Cite

In the last years, great advances have been made in the effort to understand how nutritional influences can affect long-term renal health. Evidence has accumulated that maternal nutrition before and during pregnancy and lactation as well as early postnatal nutrition is of special significance. In this review, we summarize epidemiologic and experimental data on the renal effects of perinatal exposure to energy restriction, low-protein diet, high-fat diet, high-fructose diet, and high- and low-salt diet as well as micronutrient deficiencies. Interestingly, different modifications during early-life diet may end up with similar sequelae for the offspring. On the other hand, molecular pathways can be influenced in opposite directions by different dietary interventions during early life. Importantly, postnatal nutrition significantly modifies the phenotype induced by maternal diet. Sequelae of altered macro- or micronutrient intakes include altered nephron count, blood pressure dysregulation, altered sodium handling, endothelial dysfunction, inflammation, mitochondrial dysfunction, and oxidative stress. In addition, renal prostaglandin metabolism as well as renal AMPK, mTOR, and PPAR signaling can be affected and the renin-angiotensin-aldosterone system may be dysregulated. Lately, the influence of early-life diet on gut microbiota leading to altered short chain fatty acid profiles has been discussed in the etiology of arterial hypertension. Against this background, the preventive and therapeutic potential of perinatal nutritional interventions regarding kidney disease is an emerging field of research. Especially individuals at risk (e.g., newborns from mothers who suffered from malnutrition during gestation) could disproportionately benefit from well-targeted dietary interventions.

show abstract

Section: Proteinsupporting

confidence: 72%

Impact of early-life diet on long-term renal health

et al. 2020

View full text Add to dashboard Cite

show abstract

“…On the other hand, nephron endowment can be unaltered [ 46 ], or even increased in response to renal programming [ 47 , 48 ]. Thus, low nephron endowment, per se, does not appear to mediate all programmed processes related to the development of kidney disease.…”

Section: Animal Models Of Renal Programmingmentioning

confidence: 99%

Developmental Origins of Chronic Kidney Disease: Should We Focus on Early Life?

Tain

Hsu

2017

IJMS

103

View full text Add to dashboard Cite

Chronic kidney disease (CKD) is becoming a global burden, despite recent advances in management. CKD can begin in early life by so-called “developmental programming” or “developmental origins of health and disease” (DOHaD). Early-life insults cause structural and functional changes in the developing kidney, which is called renal programming. Epidemiological and experimental evidence supports the proposition that early-life adverse events lead to renal programming and make subjects vulnerable to developing CKD and its comorbidities in later life. In addition to low nephron endowment, several mechanisms have been proposed for renal programming. The DOHaD concept opens a new window to offset the programming process in early life to prevent the development of adult kidney disease, namely reprogramming. Here, we review the key themes on the developmental origins of CKD. We have particularly focused on the following areas: evidence from human studies support fetal programming of kidney disease; insight from animal models of renal programming; hypothetical mechanisms of renal programming; alterations of renal transcriptome in response to early-life insults; and the application of reprogramming interventions to prevent the programming of kidney disease.

show abstract

“…In contrast, the effect of a HFD during IU/L on kidney development and the renal RAAS is not clear. Interestingly, it was shown that offspring of mice exposed to HFD during IU/L had higher kidney volume and increased nephron numbers at embryonic day 18.5 [56]. However, no long-term renal health problems were observed in this study.…”

Section: Discussionmentioning

confidence: 52%

A High Fat Diet During Pregnancy and Lactation Induces Cardiac and Renal Abnormalities in GLUT4 +/- Male Mice

Kruse¹,

Fiallo²,

Jiang³

et al. 2017

Kidney Blood Press Res

View full text Add to dashboard Cite

Background/Aims: Altered nutrients during the in utero (IU) and/or lactation (L) period predispose offspring to cardio-renal diseases in adulthood. This study investigates the effect of a high fat diet (HFD) fed to female mice during IU/L on gene expression patterns associated with heart and kidney failure and hypertension in male offspring. Methods: Female wild type (WT) mice were fed either a HFD or control chow (C) prior to mating with males with a genetic heterozygous deletion of GLUT4 (G4+/-, a model of peripheral insulin resistance and hypertension) and throughout IU/L. After weaning male offspring were placed on a standard rodent chow until 24 weeks of age. Results: All offspring exposed to a maternal HFD showed increased heart and kidney weight and reduced cardiac insulin responsiveness. G4+/- offspring on a HFD displayed early hypertension associated with increased renal gene expression of renin and the AT₁- receptors compared to G4+/- on a C diet. This group showed decreased cardiac expression of key genes involved in fatty acid oxidation compared to WT on a C diet. Conclusions: These results indicate an interaction between a HFD diet and genotype during early life development that can enhance susceptibility to cardio-renal diseases later in life.

show abstract

Maternal Fat Feeding Augments Offspring Nephron Endowment in Mice

Cited by 19 publications

References 56 publications

Impact of early-life diet on long-term renal health

Impact of early-life diet on long-term renal health

Developmental Origins of Chronic Kidney Disease: Should We Focus on Early Life?

A High Fat Diet During Pregnancy and Lactation Induces Cardiac and Renal Abnormalities in GLUT4 +/- Male Mice

Contact Info

Product

Resources

About