Proteinuria in aging rats due to low-protein diet during mid-gestation

Joles, Jaap A.; Sculley, Dean V.; Langley‐Evans, Simon C.

doi:10.1017/s2040174409990183

Cited by 16 publications

(15 citation statements)

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“…Maternal protein restriction in rodent pregnancy is well established as a driver of metabolic and cardiovascular impairments in the resulting offspring as they age (Petry et al 2001; Bellinger et al 2006; Erhuma et al 2007 b ; Joles et al 2010). This nutritional programming of adult function is generally associated with evidence of altered, but not always impaired, fetal growth.…”

Section: Discussionmentioning

confidence: 99%

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Protein restriction in the pregnant mouse modifies fetal growth and pulmonary development: role of fetal exposure to β-hydroxybutyrate

Langley‐Evans¹,

Daniel²,

Wells³

et al. 2010

Experimental Physiology

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Maternal undernutrition during sensitive periods of pregnancy results in offspring predisposed towards the development of a number of diseases of adulthood, including hypertension and diabetes. In order to determine the nature of any gross alterations in fetal growth during early organogenesis, we supplied timed-mated pregnant mice with diets containing 6% protein (6%P), 9% protein (9%P) or 18% protein (18%P; control) from day 0 of pregnancy. At embryonic days 11 (E11), 12 (E12) and 13 (E13), females were killed and fetuses removed. Gross morphological analysis revealed that fetal limb growth was impaired between E11 and E12 in 6%P animals, but this recovered by E13. Likewise, fetal liver growth and lung branching morphogenesis were seen to exhibit an initial growth impairment at E12 followed by a rapid recovery by E13. Coincident with the observed changes in fetal growth, we noted an elevation in maternal hepatic triglyceride content, expression of the ketogenic 3-hydroxy-3-methylglutarylCoA synthase 2 (Hmgcs2) and circulating plasma β-hydroxybutyrate (BOHB). In addition, fetal liver Hmgcs2 expression was switched on by E13 in both 6%P-and 9%P-exposed animals. Exogenous BOHB did not influence branching morphogenesis in fetal lung explant cultures; however, we cannot rule out the possibility that this may occur in vivo. In conclusion, we find that disturbance of fetal growth by maternal dietary protein restriction is associated and therefore potentially indicated by changes in maternal and fetal ketone body metabolism.

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Section: Discussionmentioning

confidence: 99%

“…The effects of maternal protein restriction on organ structure can be clearly related to functional outcomes. Offspring from protein-restricted animals are hypertensive and develop proteinuria (Joles et al 2010) with ageing and are glucose intolerant (Petry et al 2001).…”

mentioning

confidence: 99%

Protein restriction in the pregnant mouse modifies fetal growth and pulmonary development: role of fetal exposure to β-hydroxybutyrate

Langley‐Evans¹,

Daniel²,

Wells³

et al. 2010

Experimental Physiology

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“…Rats at 5 weeks, 10 weeks, and 6 months of age were housed in metabolic cages for 24 hours and urine collected as previously described [21]. Urine concentrations of adrenaline, noradrenaline, and dopamine were determined using the DLD Diagnostika catecholamine ELISA kit (DLD Diagnostika GmbH, Hamburg, Germany), following the manufacturer's instructions.…”

Section: Methodsmentioning

confidence: 99%

The Effects of Prenatal Protein Restriction onβ-Adrenergic Signalling of the Adult Rat Heart during Ischaemia Reperfusion

Ryan

Elmes

Langley‐Evans

2012

Journal of Nutrition and Metabolism

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A maternal low-protein diet (MLP) fed during pregnancy leads to hypertension in adult rat offspring. Hypertension is a major risk factor for ischaemic heart disease. This study examined the capacity of hearts from MLP-exposed offspring to recover from myocardial ischaemia-reperfusion (IR) and related this to cardiac expression of β-adrenergic receptors (β-AR) and their associated G proteins. Pregnant rats were fed control (CON) or MLP diets (n = 12 each group) throughout pregnancy. When aged 6 months, hearts from offspring underwent Langendorff cannulation to assess contractile function during baseline perfusion, 30 min ischemia and 60 min reperfusion. CON male hearts demonstrated impaired recovery in left ventricular pressure (LVP) and dP/dt max (P < 0.01) during reperfusion when compared to MLP male hearts. Maternal diet had no effect on female hearts to recover from IR. MLP males exhibited greater membrane expression of β 2-AR following reperfusion and urinary excretion of noradrenaline and dopamine was lower in MLP and CON female rats versus CON males. In conclusion, the improved cardiac recovery in MLP male offspring following IR was attributed to greater membrane expression of β 2-AR and reduced noradrenaline and dopamine levels. In contrast, females exhibiting both decreased membrane expression of β 2-AR and catecholamine levels were protected from IR injury.

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“…However, studies by Woods et al also demonstrated that a moderate reduction in maternal protein during gestation did not alter BP in female low protein offspring [6]. Joles et al reported that, fetal exposure to low protein during gestation increased renal injury in the aging male kidney [81] (Figure 3). Yet, an additional study indicated that female offspring exposed to moderate maternal protein restriction during fetal life were protected against the accelerated development of renal injury [79].…”

Section: Introductionmentioning

confidence: 99%

Gender differences in developmental programming of cardiovascular diseases

2016

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Hypertension is a risk factor for cardiovascular disease, the leading cause of death worldwide. Although multiple factors contribute to the pathogenesis of hypertension, studies by Dr. David Barker reporting an inverse relationship between birth weight and blood pressure led to the hypothesis that slow growth during fetal life increases blood pressure and the risk for cardiovascular disease in later life. It is now recognized that growth during infancy and childhood in addition to exposure to adverse influences during fetal life contribute to the developmental programming of increased cardiovascular risk. Numerous epidemiological studies support the link between influences during early life with later cardiovascular health; experimental models provide proof of principle and indicate that numerous mechanisms contribute to the developmental origins of chronic disease. Sex impacts the severity of cardiovascular risk in experimental models of developmental insult. Yet, few studies examine the influence of sex on blood pressure and cardiovascular health in low birth weight men and women. Fewer still assess how aging impacts sex differences in programmed cardiovascular risk. Thus, the aim of this review is to highlight current data regarding sex differences in the developmental programming of blood pressure and cardiovascular disease.

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Proteinuria in aging rats due to low-protein diet during mid-gestation

Cited by 16 publications

References 50 publications

Protein restriction in the pregnant mouse modifies fetal growth and pulmonary development: role of fetal exposure to β-hydroxybutyrate

Protein restriction in the pregnant mouse modifies fetal growth and pulmonary development: role of fetal exposure to β-hydroxybutyrate

The Effects of Prenatal Protein Restriction onβ-Adrenergic Signalling of the Adult Rat Heart during Ischaemia Reperfusion

Gender differences in developmental programming of cardiovascular diseases

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