scholarly journals Hypoxia-Induced Intrauterine Growth Restriction Increases the Susceptibility of Rats to High-Fat Diet-Induced Metabolic Syndrome

Diabetes ◽  
2011 ◽  
Vol 60 (2) ◽  
pp. 507-516 ◽  
Author(s):  
C. F. Rueda-Clausen ◽  
V. W. Dolinsky ◽  
J. S. Morton ◽  
S. D. Proctor ◽  
J. R. B. Dyck ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
High Fat Diet ◽  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
High Fat ◽  
Intrauterine Growth

scholarly journals Impact of diet on the persistence of early vascular remodeling and stiffening induced by intrauterine growth restriction and a maternal high-fat diet

2019 ◽  
Vol 317 (2) ◽  
pp. H424-H433 ◽  
Author(s):  
Thomas A. Miller ◽  
R. Blair Dodson ◽  
Anastasiya Mankouski ◽  
Kyle N. Powers ◽  
Yueqin Yang ◽  
...  
Keyword(s):  
Arterial Stiffness ◽  
High Fat Diet ◽  
Intrauterine Growth Restriction ◽  
Vascular Remodeling ◽  
Structural Changes ◽  
Growth Restriction ◽  
Female Rats ◽  
High Fat ◽  
Regular Diet ◽  
Intrauterine Growth

Intrauterine growth restriction (IUGR) and maternal high-fat diet (HFD) independently predispose offspring to hypertension. In a rat model, IUGR more so than maternal HFD increases arterial stiffness with vascular remodeling as early as postnatal day (PND) 21. The trajectory of such early vascular changes remains unknown. We hypothesized that IUGR would increase blood pressure (BP), arterial stiffness, and markers of ongoing detrimental vascular remodeling in adult rats exposed to a maternal HFD regardless of weaning diet. Adult female rats were fed either a regular diet (RD) or an HFD before mating through lactation. IUGR was induced by uterine artery ligation. Offspring were weaned to either a RD or HFD through PND 60. For both control and IUGR rats, this design resulted in the following three diet groups: offspring from RD dams weaned to a RD and offspring from HFD dams weaned to a RD or to an HFD (IHH). In both males and females, only IHH increased systolic BP, but IUGR and HFD both alone and in combination increased arterial stiffness. Aortas contained fewer but thicker elastin bands in IHH rats and IUGR offspring from dams fed an HFD and weaned to a regular diet. IHH increased aortic lysl oxidase protein. In summary, the PND 21 rat mediators of vascular remodeling from IUGR and maternal HFD normalize by PND 60 while changes in elastin and arterial stiffness persist. We speculate that the longer-term risk of hypertension from dietary mediators is augmented by underlying IUGR-induced structural changes to the extracellular matrix. NEW & NOTEWORTHY We report that a combined insult of intrauterine growth restriction and maternal high-fat diet increases the risk of early cardiovascular pathology both independently and in conjunction with a continued high-fat diet in offspring.

Intrauterine growth restriction combined with a maternal high-fat diet increased adiposity and serum corticosterone levels in adult rat offspring

2018 ◽  
Vol 9 (3) ◽  
pp. 315-328 ◽  
Author(s):  
E. K. Zinkhan ◽  
B. Yu ◽  
C. W. Callaway ◽  
R. A. McKnight
Keyword(s):  
High Fat Diet ◽  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Female Rats ◽  
Male Rats ◽  
High Fat ◽  
Serum Corticosterone ◽  
Regular Diet ◽  
Intrauterine Growth ◽  
Rat Offspring

AbstractIntrauterine growth restriction (IUGR) and fetal exposure to a maternal high-fat diet (HFD) independently increase the risk of developing obesity in adulthood. Excess glucocorticoids increase obesity. We hypothesized that surgically induced IUGR combined with an HFD would increase adiposity and glucocorticoids more than in non-IUGR offspring combined with the same HFD, findings that would persist despite weaning to a regular diet. Non-IUGR (N) and IUGR (I) rat offspring from dams fed either regular rat chow (R) or an HFD (H) were weaned to either a regular rat chow or an HFD. For non-IUGR and IUGR rats, this study design resulted in three diet groups: offspring from dams fed a regular diet and weaned to a regular diet (NRR and IRR), offspring rats from dams fed an HFD and weaned to a regular diet (NHR and IHR) and offspring from dams fed an HFD and weaned to an HFD (NHH and IHH). Magnetic resonance imaging or fasting visceral and subcutaneous adipose tissue collection occurred at postnatal day 60. IHH male rats had greater adiposity than NHH males, findings that were only partly normalized by weaning to a regular chow. IHH male rats had a 10-fold increase in serum corticosterone levels. IHH female rats had increased adiposity and serum triglycerides. We conclude that IUGR combined with an HFD throughout life increased adiposity, glucocorticoids and triglycerides in a sex-specific manner. Our data suggest that one mechanism through which the perinatal environment programs increased adiposity in IHH male rats may be via increased systemic glucocorticoids.

scholarly journals Intrauterine growth restriction influences vascular remodeling and stiffening in the weanling rat more than sex or diet

2017 ◽  
Vol 312 (2) ◽  
pp. H250-H264 ◽  
Author(s):  
R. Blair Dodson ◽  
Thomas A. Miller ◽  
Kyle Powers ◽  
Yueqin Yang ◽  
Baifeng Yu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
High Fat Diet ◽  
Intrauterine Growth Restriction ◽  
Vascular Remodeling ◽  
Growth Restriction ◽  
Female Rats ◽  
Matrix Metalloproteinase 2 ◽  
High Fat ◽  
Ecm Remodeling ◽  
Intrauterine Growth

Intrauterine growth restriction (IUGR) increases the incidence of adult cardiovascular disease (CVD). The sex-specific developmental mechanisms for IUGR-induced and Western high-fat diet (HFD) modification of CVD remain poorly understood. We hypothesized a maternal HFD in the Sprague-Dawley rat would augment IUGR-induced CVD in the offspring through decreased cardiac function and increased extracellular matrix (ECM) remodeling and stiffness in a sex-specific manner. HFD or regular diet (Reg) was given from 5 wk before mating through postnatal day (PND) 21. IUGR was induced by uterine artery ligation at embryonic day 19.5 (term = 21.5 days). At PND 21, echocardiographic assessments were made and carotid arteries tested for vascular compliance using pressure myography. Arterial samples were quantified for ECM constituents or fixed for histologic evaluation. The insult of IUGR (IUGR + Reg and IUGR + HFD) led to increased mechanical stiffness in both sexes ( P < 0.05). The combination of IUGR + HFD increased diastolic blood pressure 47% in males (M) and 35% in females (F) compared with the Con + Reg ( P < 0.05). ECM remodeling in IUGR + HFD caused fewer (M = −29%, F = −24%) but thicker elastin bands (M = 18%, F = 18%) and increased total collagen (M = 49%, F = 34%) compared with Con + Reg arteries. Remodeling in IUGR + HFD males increased medial collagen and soluble collagen ( P < 0.05). Remodeling in IUGR + HFD females increased adventitial collagen and wall thickness ( P < 0.05) and decreased matrix metalloproteinase 2 (MMP-2), advanced glycosylation end products (AGE), and receptor AGE (RAGE; P < 0.05). In summary, both IUGR + Reg and IUGR + HFD remodel ECM in PND 21 rats. While IUGR + HFD increases blood pressure, IUGR but not HFD increases vascular stiffness suggesting a specific mechanism of vascular remodeling that can be targeted to limit future disease. NEW & NOTEWORTHY We report intrauterine growth restriction (IUGR) increases vascular stiffening in both male and female rats through increased collagen content and altered elastin structure more than a high-fat diet (HFD) alone. Our study shows the importance of stiffness supporting the hypothesis that there are physiologic differences and potential windows for early intervention targeting vascular remodeling mechanisms.

scholarly journals Combination of intrauterine growth restriction and a high-fat diet impairs cholesterol elimination in rats

2014 ◽  
Vol 76 (5) ◽  
pp. 432-440 ◽  
Author(s):  
Erin K. Zinkhan ◽  
Jeanette R. Chin ◽  
Jennifer M. Zalla ◽  
Baifeng Yu ◽  
Ben Numpang ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
High Fat ◽  
Intrauterine Growth

Intrauterine Programming of Adult Disease: Identification of Cardinal Genes Associated with Hypertension, Obesity and Metabolic Syndrome

2021 ◽  
Vol 89 (1) ◽  
pp. 27-36
Author(s):  
Iván Acevedo Monterrosa ◽  
Damián A. Soria ◽  
Analía Tomat ◽  
Rosana Elesgaray ◽  
Cristina Arranz ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Intrauterine Growth Restriction ◽  
Adult Life ◽  
Treatment Strategies ◽  
Interaction Network ◽  
Growth Restriction ◽  
Adult Disease ◽  
Intrauterine Growth ◽  
Significant Gene ◽  
Obesity Hypertension

Background: Intrauterine growth restriction is an abnormal fetal development characterized by a fetal growth rate lower than the potential genetic growth for the gestational age. This condition represents a major burden for public health systems, as it increases short and long-term morbidity and mortality in the offspring, particularly because of its association with the development of cardiovascular and metabolic disease in adult life. Objectives: The aim of the present study was to identify possible cardinal genes involved in intrauterine growth restriction associated with the development of obesity, hypertension and metabolic syndrome using bioinformatics tools. Methods: A total of 343 genes involved in the phenotypes of interest were obtained and 20 genes were identified as significantly relevant in the interaction network analysis. Specifically, four of these identified genes encode for growth factors or their receptors, VEGFA, PDGFRB, IGF1R and EGFR. We also identified genes related to insulin and cardiovascular homeostasis as CTNNB1, APP, MYC and MDMD2. Cluster analysis provided the most significant gene ontology terms, including those related to the biological processes of proliferation and programmed cell death, intercellular communication, protein metabolism and development of the cardiovascular system. Conclusions: The genes found in this study could be useful as putative biomarkers for the presence of cardiovascular and metabolic disorders associated with intrauterine growth restriction, or as potential therapeutic targets for treatment strategies directed to the patient's genotype.

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