Restricted fetal growth and the response to dietary cholesterol in the guinea pig

Epidemiological studies suggest that retarded growth before birth is associated with increased plasma total and low-density lipoprotein (LDL) cholesterol concentrations in adult life. Thus perturbations of prenatal growth may permanently alter cholesterol metabolism. To determine directly whether restriction of prenatal nutrition and growth alters postnatal cholesterol homeostasis, the plasma cholesterol response to cholesterol feeding (0.25% cholesterol) was examined in adult guinea pig offspring of ad libitum-fed or moderately undernourished mothers. Maternal undernutrition (85% ad libitum intake throughout pregnancy) reduced birth weight (−13%). Plasma total cholesterol was higher prior to and following 6 wk cholesterol feeding in male offspring of undernourished mothers compared with male offspring of ad libitum-fed mothers ( P< 0.05). The influence of birth weight on cholesterol metabolism was examined by dividing the offspring into those whose birth weight was above (high) or below (low) the median birth weight. Plasma total cholesterol concentrations prior to cholesterol feeding did not differ with size at birth, but plasma total and LDL cholesterol were 31 and 34% higher, respectively, following cholesterol feeding in low- compared with high-birth weight males ( P < 0.02). The response to cholesterol feeding in female offspring was not altered by variable maternal nutrition or size at birth. Covariate analysis showed that the effect of maternal undernutrition on adult cholesterol metabolism could be partly accounted for by alterations in prenatal growth. In conclusion, maternal undernutrition and small size at birth permanently alter postnatal cholesterol homeostasis in the male guinea pig.

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Effect of maternal feed restriction during pregnancy on glucose tolerance in the adult guinea pig

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00587.2001 ◽

2003 ◽

Vol 284 (1) ◽

pp. R140-R152 ◽

Cited By ~ 72

Author(s):

Karen L. Kind ◽

Peter M. Clifton ◽

Patricia A. Grant ◽

Phillip C. Owens ◽

Annica Sohlstrom ◽

...

Keyword(s):

Insulin Resistance ◽

Birth Weight ◽

Young Adult ◽

Glucose Tolerance ◽

Guinea Pig ◽

Male Offspring ◽

Feed Restriction ◽

Glucose Ratio ◽

Ad Libitum ◽

Ad Libitum Intake

Maternal nutrient restriction and impaired fetal growth are associated with postnatal insulin resistance, hyperinsulinemia, and glucose intolerance in humans but not consistently in other species, such as the rat or sheep. We therefore determined the effect of mild (85% ad libitum intake/kg body wt) or moderate (70% ad libitum intake/kg body wt) maternal feed restriction throughout pregnancy on glucose and insulin responses to an intravenous glucose tolerance test (IVGTT) in the young adult guinea pig. Maternal feed restriction reduced birth weight (mild and moderate: both P < 0.02) in male offspring. Moderate restriction increased plasma glucose area under the curve ( P < 0.04) and decreased the glucose tolerance index ( K G) ( P < 0.02) during the IVGTT in male offspring compared with those of mildly restricted but not of ad libitum-fed mothers. Moderate restriction increased fasting plasma insulin ( P < 0.04, adjusted for litter size) and the insulin response to IVGTT ( P < 0.001), and both moderate and mild restriction increased the insulin-to-glucose ratio during the IVGTT ( P < 0.003 and P < 0.02) in male offspring. When offspring were classed into tertiles according to birth weight, glucose tolerance was not altered, but fasting insulin concentrations were increased in low compared with medium birth weight males ( P < 0.03). The insulin-to-glucose ratio throughout the IVGTT was increased in low compared with medium ( P < 0.01) or high ( P < 0.05) birth weight males. Thus maternal feed restriction in the guinea pig restricts fetal growth and causes hyperinsulinemia in young adult male offspring, suggestive of insulin resistance. These findings suggest that mild to moderate prenatal perturbation programs postnatal glucose homeostasis adversely in the guinea pig, as in the human.

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Sex-specific Alterations in Hepatic Cholesterol Metabolism in Young Uteroplacental Insufficiency-induced Low Birth Weight Adult Guinea Pig Offspring

10.1101/2020.11.12.379891 ◽

2020 ◽

Author(s):

Ousseynou Sarr ◽

Katherine E. Mathers ◽

Christina Vanderboor ◽

Aditya Devgan ◽

Daniel B. Hardy ◽

...

Keyword(s):

Risk Factor ◽

Birth Weight ◽

Young Adult ◽

Low Birth Weight ◽

Guinea Pig ◽

Guinea Pigs ◽

Cholesterol Metabolism ◽

Later Life ◽

Male Offspring ◽

Hepatic Cholesterol

AbstractBackgroundIntrauterine growth restriction (IUGR) and low birth weight (LBW) have been widely reported as an independent risk factor for hypercholesterolemia and increased hepatic cholesterol underlying liver dysfunction in adulthood. However, the specific impact of uteroplacental insufficiency (UPI), a leading cause of LBW in developed world, on hepatic cholesterol metabolism in later life, is ill defined and is clinically relevant in understanding later life liver metabolic health trajectories.MethodsHepatic cholesterol metabolism pathways were studied in uterine artery ablation-induced LBW and normal birth weight (NBW) male and female guinea pig offspring at postnatal day 150.ResultsHepatic free and total cholesterol were increased in LBW versus NBW males. Transcriptome analysis of LBW versus NBW livers revealed that “Cholesterol metabolism” was an enriched pathway in LBW males but not females. Microsomal triglyceride transfer protein and cytochrome P450 7A1 protein, involved in hepatic cholesterol efflux and catabolism, respectively, and catalase activity were decreased in LBW male livers. Superoxide dismutase activity was reduced in LBW males but increased in LBW females.ConclusionsUPI environment is associated with a later life programed hepatic cholesterol accumulation via impaired cholesterol elimination, in a sex-specific manner. These programmed alterations could underlie later life cholesterol-induced hepatic lipotoxicity in LBW male offspring.Impact StatementLow birth weight (LBW) is a risk factor for adult hypercholesterolemia and increased hepatic cholesterol.Uteroplacental insufficiency (UPI) resulting in LBW increased hepatic cholesterol content, altered hepatic expression of cholesterol metabolism-related genes in young adult guinea pigs.UPI-induced LBW was also associated with markers of a compromised hepatic cholesterol elimination process and failing antioxidant system in young adult guinea pigs.These changes, at the current age studied, were sex-specific, only being observed in LBW males and not LBW females.These programmed alterations could lead to further hepatic damage and greater predisposition to liver diseases in UPI-induced LBW male offspring as they age.

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Effect of maternal undernutrition in early gestation on the development of fetal myofibres in the guinea-pig

Reproduction Fertility and Development ◽

10.1071/rd9951285 ◽

1995 ◽

Vol 7 (5) ◽

pp. 1285 ◽

Cited By ~ 47

Author(s):

CM Dwyer ◽

AJ Madgwick ◽

SS Ward ◽

NC Stickland

Keyword(s):

Guinea Pig ◽

Muscle Fibre ◽

Guinea Pigs ◽

Biceps Brachii ◽

Fetal Weight ◽

Early Gestation ◽

Maternal Undernutrition ◽

Short Period ◽

Fibre Number ◽

Ad Libitum

A 40% restriction in maternal feed intake throughout gestation in the guinea-pig results in a 35% reduction in fetal body weight at term and a 20-25% reduction in muscle fibre number. To investigate the effect of maternal undernutrition in early gestation, four nutritional treatments were used: controls-pregnant females fed ad libitum throughout gestation; TR-fed 60% ad libitum intake throughout gestation; ER-fed 60% ad libitum for the first third of gestation (until Day 25), then ad libitum to term; LR-fed ad libitum for the first 25 days, then 60% of ad libitum to term. The LR group were complicated by a high degree of fetal resorption and early littering of viable litters. The biceps brachii and soleus muscles were removed from neonates and total muscle fibre numbers determined. In a second experiment a further 8 pregnant guinea-pigs were fed 60% ad libitum until Day 15 of gestation only, and then rehabilitated onto an ad libitum diet (VER). Of these, 5 guinea-pigs were killed at term and the remaining 3 at 45 days gestation. Fetuses and placentae were obtained from all VER animals and compared with TR and controls of a similar age. Body weights were reduced in all restricted groups at term when compared with controls (P < 0.05) by 12, 40 and 50% for VER = ER, TR and LR groups, respectively. Biceps fibre number was reduced (P < 0.05) in ER, TR and LR groups by 28, 20 and 25%, respectively, but was not affected in the VER group. Soleus fibre number was not significantly affected by any nutritional treatment. Restriction for 15 days in early gestation caused a significant 20% increase in fetal weight at 45 days' gestation compared with controls, but muscle and placental weights were not affected. Analysis of placental components at Days 45 and 65 suggested that underfeeding in early gestation and subsequent refeeding caused some placental adaptations to increase the exchange-surface area. A short period of maternal undernutrition in the first third of gestation alone (ER), therefore, resulted in a biceps brachii fibre number deficit similar to that caused by restriction throughout gestation only if the period of restriction extended as far as Day 25. Furthermore, fetal weight at term was impaired by short-term nutritional restriction in early gestation. Restriction in the last two-thirds of gestation, following an ad libitum diet in the first third, caused a reduction in biceps fibre number and had a severe effect on the maintenance of pregnancy. It is probable that undernutrition in early gestation had an indirect effect on muscle fibre number by affecting the development of the placenta. This could be avoided by nutritional rehabilitation before Day 25 of gestation, but appeared to be permanent thereafter. Undernutrition after Day 25 may have had a direct effect on the development of secondary fibres.

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MO019MATERNAL UNDERNUTRITION AMELIORATES CYST GROWTH IN ADPKD MODEL MICE*

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfab081.001 ◽

2021 ◽

Vol 36 (Supplement_1) ◽

Author(s):

Junpei Yoshikawa ◽

Nishio Saori ◽

Fumihiko Hattanda ◽

Daigo Nakazawa ◽

Tatsuya Atsumi

Keyword(s):

Body Weight ◽

Birth Weight ◽

Food Restriction ◽

Mapk Pathway ◽

Weight Ratio ◽

Mtor Pathway ◽

Nutrient Restriction ◽

Body Weight Ratio ◽

Maternal Undernutrition ◽

Ad Libitum

Abstract Background and Aims Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the progressive development of kidney and liver cysts. The major factors predicting disease progression in ADPKD are total kidney volume, genotype, age, sex. Recently, several studies have suggested that dietary intervention might be a potential treatment to prevent ADPKD progression. On the other hand, it has been reported that low-birth weight infants because of maternal global nutrient restriction are at increased risk for hypertension, type 2 diabetes, and metabolic syndrome and chronic kidney disease. However, little has been reported on relationship between maternal undernutrition and cyst formation in ADPKD. Therefore the purpose of this study is to clarify whether maternal undernutrition is associated with progression in ADPKD. Method We used Pkd1 conditional knockout mice (Pkd1flox/flox･Mx1-Cre mice). The offspring of dams given food ad libitum (control(CON)) and those subjected to nutrient restriction throughout pregnancy (food restriction (FR)) were examined. In FR, nutrient-restricted mothers were given about half amount of food by control mice during pregnancy. After delivery, food for children was given ad libitum. Mice were injected with polyinosinic-polycytidylic acid for 6 consecutive days from postnatal day 5 (P5) to P10 to inactivate Pkd1. We analyzed the phenotype of cystic kidneys by kidney/body weight ratio (2KW/BW), and cystic index (CI) which was defined as the percentage of areas occupied by cysts at P20, 35, 56. We carried out a series of analyses by kidney/body weight ratio, liver /body weight ratio or cystic index (CI) which was defined as the percentage of areas occupied by cysts. Elastica-Masson staining was performed for analyzing tissue fibrosis. The fibrotic index (FI) was expressed as the (fibrotic area/ total non-cystic area) ×100 (%). For evaluation of glomerular hypertrophy, glomerular area was measured in PAS-stained kidney sections using Image J software. The assay of renal function was performed by using UN-ML kit. We also performed western blotting of signaling pathway of proliferation by using whole kidneys. Data are shown as mean ± SEM. Two-tailed Student’s t-test was performed for comparing two groups. Results Food restriction of pregnant dams reduced birth weight. (FR 1.26±0.16 g vs CON 1.55±0.11g). However, FR showed rapid gain weight. There was no significant difference after P20. There were no difference between two groups in 2KW/BW, serum blood urea nitrogen (BUN) levels, CI of kidney and liver until P35. At P56, 2KW/BW was significantly greater in FR (4.59±0.52%) than in CON mice (2.91±0.98%; p＜0.01). CI of both kidney and liver was significantly higher in FR than in CON (Kidney : FR58.1±2.04% vs CON46.3±3.04%; p＜0.05) (Liver : FR11.1±1.41% vs CON 4.89±0.61%; p＜0.001). BUN levels elevated in FR (FR 58.1±5.76mg/dL vs CON 46.3±5.11mg/dL; p＜0.05) .FR showed glomerular sclerosis with PAS staining. Mean Glomerular volume was significantly increased in FR compared with CON (P35: FR 5625±419μm2 vs CON 3255±433μm2; p＜0.001, P56: FR 5780±1195μm2 vs CON 3756±266μm2; p＜0.001) . FR group showed significantly greater fibrosis in kidney (P35: FI 15.3±2.04% vs CON 11.1±1.41%; p＜0.01,P56: FI 42.1±3.2% vs CON 30.8±3.89%; p＜0.001). In western blotting analysis, MAPK pathway and mTOR pathway were suppressed in FR compared with CON at P20. In contrast, MAPK pathway and mTOR pathway were upregulated in FR compared with CON at P56. Conclusion Maternal undernutrition accelerates disease progression via kidney fibrosis, MAPK and mTOR pathway.

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Abnormal brain cholesterol homeostasis in Alzheimer’s disease—a targeted metabolomic and transcriptomic study

npj Aging and Mechanisms of Disease ◽

10.1038/s41514-021-00064-9 ◽

2021 ◽

Vol 7 (1) ◽

Author(s):

Vijay R. Varma ◽

H. Büşra Lüleci ◽

Anup M. Oommen ◽

Sudhir Varma ◽

Chad T. Blackshear ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Brain Tissue ◽

Cholesterol Metabolism ◽

Cholesterol Biosynthesis ◽

Cholesterol Homeostasis ◽

Transcriptomic Data ◽

Brain Cholesterol ◽

Cholesterol Levels

AbstractThe role of brain cholesterol metabolism in Alzheimer’s disease (AD) remains unclear. Peripheral and brain cholesterol levels are largely independent due to the impermeability of the blood brain barrier (BBB), highlighting the importance of studying the role of brain cholesterol homeostasis in AD. We first tested whether metabolite markers of brain cholesterol biosynthesis and catabolism were altered in AD and associated with AD pathology using linear mixed-effects models in two brain autopsy samples from the Baltimore Longitudinal Study of Aging (BLSA) and the Religious Orders Study (ROS). We next tested whether genetic regulators of brain cholesterol biosynthesis and catabolism were altered in AD using the ANOVA test in publicly available brain tissue transcriptomic datasets. Finally, using regional brain transcriptomic data, we performed genome-scale metabolic network modeling to assess alterations in cholesterol biosynthesis and catabolism reactions in AD. We show that AD is associated with pervasive abnormalities in cholesterol biosynthesis and catabolism. Using transcriptomic data from Parkinson’s disease (PD) brain tissue samples, we found that gene expression alterations identified in AD were not observed in PD, suggesting that these changes may be specific to AD. Our results suggest that reduced de novo cholesterol biosynthesis may occur in response to impaired enzymatic cholesterol catabolism and efflux to maintain brain cholesterol levels in AD. This is accompanied by the accumulation of nonenzymatically generated cytotoxic oxysterols. Our results set the stage for experimental studies to address whether abnormalities in cholesterol metabolism are plausible therapeutic targets in AD.

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Neurotrophins as Key Regulators of Cell Metabolism: Implications for Cholesterol Homeostasis

International Journal of Molecular Sciences ◽

10.3390/ijms22115692 ◽

2021 ◽

Vol 22 (11) ◽

pp. 5692

Author(s):

Mayra Colardo ◽

Noemi Martella ◽

Daniele Pensabene ◽

Silvia Siteni ◽

Sabrina Di Bartolomeo ◽

...

Keyword(s):

Growth Factors ◽

Cholesterol Metabolism ◽

System Development ◽

Cell Metabolism ◽

Redox Balance ◽

Nervous System Development ◽

Cholesterol Homeostasis ◽

Signaling Cascades ◽

Target Cells ◽

The Impact

Neurotrophins constitute a family of growth factors initially characterized as predominant mediators of nervous system development, neuronal survival, regeneration and plasticity. Their biological activity is promoted by the binding of two different types of receptors, leading to the generation of multiple and variegated signaling cascades in the target cells. Increasing evidence indicates that neurotrophins are also emerging as crucial regulators of metabolic processes in both neuronal and non-neuronal cells. In this context, it has been reported that neurotrophins affect redox balance, autophagy, glucose homeostasis and energy expenditure. Additionally, the trophic support provided by these secreted factors may involve the regulation of cholesterol metabolism. In this review, we examine the neurotrophins’ signaling pathways and their effects on metabolism by critically discussing the most up-to-date information. In particular, we gather experimental evidence demonstrating the impact of these growth factors on cholesterol metabolism.

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The Impact of Anthocyanins and Iridoids on Transcription Factors Crucial for Lipid and Cholesterol Homeostasis

International Journal of Molecular Sciences ◽

10.3390/ijms22116074 ◽

2021 ◽

Vol 22 (11) ◽

pp. 6074

Author(s):

Maciej Danielewski ◽

Agnieszka Matuszewska ◽

Adam Szeląg ◽

Tomasz Sozański

Keyword(s):

Transcription Factors ◽

Cholesterol Metabolism ◽

Binding Protein ◽

Regulatory Element ◽

Cholesterol Homeostasis ◽

Lipid Lowering ◽

Peroxisome Proliferator ◽

Peroxisome Proliferator Activated Receptor ◽

Cell Functions ◽

The Impact

Nutrition determines our health, both directly and indirectly. Consumed foods affect the functioning of individual organs as well as entire systems, e.g., the cardiovascular system. There are many different diets, but universal guidelines for proper nutrition are provided in the WHO healthy eating pyramid. According to the latest version, plant products should form the basis of our diet. Many groups of plant compounds with a beneficial effect on human health have been described. Such groups include anthocyanins and iridoids, for which it has been proven that their consumption may lead to, inter alia, antioxidant, cholesterol and lipid-lowering, anti-obesity and anti-diabetic effects. Transcription factors directly affect a number of parameters of cell functions and cellular metabolism. In the context of lipid and cholesterol metabolism, five particularly important transcription factors can be distinguished: liver X receptor (LXR), peroxisome proliferator-activated receptor-α (PPAR-α), peroxisome proliferator-activated receptor-γ (PPAR-γ), CCAAT/enhancer binding protein α (C/EBPα) and sterol regulatory element-binding protein 1c (SREBP-1c). Both anthocyanins and iridoids may alter the expression of these transcription factors. The aim of this review is to collect and systematize knowledge about the impact of anthocyanins and iridoids on transcription factors crucial for lipid and cholesterol homeostasis.

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Impact of size at birth and postnatal growth on metabolic and neurocognitive outcomes in prematurely born school-age children

Scientific Reports ◽

10.1038/s41598-021-86292-1 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Yoo Jinie Kim ◽

Seung Han Shin ◽

Eun Sun Lee ◽

Young Hwa Jung ◽

Young Ah Lee ◽

...

Keyword(s):

Birth Weight ◽

Preterm Infants ◽

Gestational Age ◽

Growth Velocity ◽

Postnatal Growth ◽

School Age ◽

Z Score ◽

Neurodevelopmental Outcomes ◽

Neurocognitive Outcomes ◽

Size At Birth

AbstractPrematurity, size at birth, and postnatal growth are important factors that determine cardiometabolic and neurodevelopmental outcomes later in life. In the present study, we aimed to investigate the associations between the size at birth and growth velocity after birth with cardiometabolic and neurodevelopmental outcomes in preterm infants. Fifty-six preterm infants born at < 32 weeks of gestation or having a birth weight of < 1500 g were enrolled and categorized into small for gestational age (SGA) and appropriate for gestational age (AGA) groups. Anthropometric and cardiometabolic parameters were assessed at school-age, and the Korean Wechsler Intelligence Scale for Children, fourth edition (K-WISC-IV) was used for assessing the intellectual abilities. The growth velocity was calculated by changes in the weight z-score at each time period. Multivariate analysis was conducted to investigate the associations of growth velocity at different periods with cardiometabolic and neurodevelopmental outcomes. Forty-two (75%) were classified as AGA and 25% as SGA. At school-age, despite the SGA children showing significantly lower body weight, lean mass index, and body mass index, there were no differences in the cardiometabolic parameters between SGA and AGA groups. After adjusting for gestational age, birth weight z-score, weight z-score change from birth to discharge and sex, change in weight z-score beyond 12 months were associated with a higher systolic blood pressure, waist circumference, and insulin resistance. Full-scale intelligent quotient (β = 0.314, p = 0.036) and perceptional reasoning index (β = 0.456, p = 0.003) of K-WISC-IV were positively correlated with postnatal weight gain in the neonatal intensive care unit. Although cardiometabolic outcomes were comparable in preterm SGA and AGA infants, the growth velocity at different time periods resulted in different cardiometabolic and neurocognitive outcomes. Thus, ensuring an optimal growth velocity at early neonatal period could promote good neurocognitive outcomes, while adequate growth after 1 year could prevent adverse cardiometabolic outcomes in preterm infants.

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Regulation of Bile Acid and Cholesterol Metabolism by PPARs

PPAR Research ◽

10.1155/2009/501739 ◽

2009 ◽

Vol 2009 ◽

pp. 1-15 ◽

Cited By ~ 65

Author(s):

Tiangang Li ◽

John Y. L. Chiang

Keyword(s):

Bile Acid ◽

Bile Acids ◽

Cholesterol Metabolism ◽

Acid Synthesis ◽

Bile Acid Synthesis ◽

Cholesterol Homeostasis ◽

Acid Oxidation ◽

Peroxisome Proliferator ◽

Major Pathway ◽

Therapeutic Implications

Bile acids are amphipathic molecules synthesized from cholesterol in the liver. Bile acid synthesis is a major pathway for hepatic cholesterol catabolism. Bile acid synthesis generates bile flow which is important for biliary secretion of free cholesterol, endogenous metabolites, and xenobiotics. Bile acids are biological detergents that facilitate intestinal absorption of lipids and fat-soluble vitamins. Recent studies suggest that bile acids are important metabolic regulators of lipid, glucose, and energy homeostasis. Agonists of peroxisome proliferator-activated receptors (PPARα, PPARγ, PPARδ) regulate lipoprotein metabolism, fatty acid oxidation, glucose homeostasis and inflammation, and therefore are used as anti-diabetic drugs for treatment of dyslipidemia and insulin insistence. Recent studies have shown that activation of PPARαalters bile acid synthesis, conjugation, and transport, and also cholesterol synthesis, absorption and reverse cholesterol transport. This review will focus on the roles of PPARs in the regulation of pathways in bile acid and cholesterol homeostasis, and the therapeutic implications of using PPAR agonists for the treatment of metabolic syndrome.

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A note on purebred performance of Belgian Piétrain pigs

Animal Science ◽

10.1017/s0003356100039477 ◽

1977 ◽

Vol 25 (2) ◽

pp. 255-258 ◽

Cited By ~ 2

Author(s):

A. N. Howard ◽

W. C. Smith

Keyword(s):

Cross Section ◽

Litter Size ◽

Live Weight ◽

Muscle Quality ◽

Feed Conversion ◽

Feeding Regime ◽

Weight Range ◽

Breed Difference ◽

Ad Libitum ◽

Size At Birth

SUMMARYIn an analysis of data from 211 litters in a Pietrain herd, litter size at birth and at weaning was lower than is generally found in indigenous breeds. Mortality in growing and breeding pigs was high with circulatory failure accounting for 23% and 95% of deaths respectively. Pietrains, fed ad libitum over the live-weight range 27 to 87 kg, grew more slowly by 130 g/day than contemporary Large Whites on the same feeding regime, had higher killing-out percentages (by 3 to 4 units) and larger eye muscles in cross-section (by 9·9 cm2) but tended to have higher feed conversion ratios. There was no breed difference in backfat measurements but Pietrain carcasses were shorter by 83 mm and their muscle quality was markedly inferior to that of the Large Whites.

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