title: Effects of maternal high-fat diet and statin treatment on bone marrow endothelial progenitor cells and cardiovascular risk factors in female mice offspring fed a similar diet.
abstract: OBJECTIVE
  The aim of this study was to prove that one possible statin-related protective mechanism in dams and offspring fed a high-fat diet (HFD) is the reduction in cardiovascular risk and impairment of the vasculogenic element of endothelial regeneration.
  
  
  METHODS
  To explore this, virgin C57 BL/6 mice (n = 8/group) were fed an HFD (fat: 45% kcal) or standard chow (C; fat: 21% kcal) from weaning and throughout their pregnancy and lactation. Half of the HFD group also was given the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor pravastatin (S) through their drinking water (5 mg/kg body weight per day) to create HF+S dam group (n = 8/group). Offspring from each group were fed HFD or C diet from weaning to adulthood, generating respective dam/offspring dietary groups (C/C, HF/HF, HF+S/HF; n = 8/group). Body weight, blood pressure, and serum lipid profile were measured in female offspring at age 24 wk, and bone marrow endothelial progenitor cells (EPCs) were cultured.
  
  
  RESULTS
  The results indicated that in the female offspring, the statin-fed (HF+S/HF) cohort had lower total and low-density lipoprotein cholesterol concentrations, were less obese and hypertensive, and had reduced C-reactive proteins (CRPs) compared with the HF/HF phenotype. The results also showed an increased bone marrow EPCs expressing colony numbers (P < 0.001) compared with the HF/HF phenotype.
  
  
  CONCLUSIONS
  Results from the present study demonstrated that statin administration in early life to dams fed on a HFD had a significant effect on their female offspring in terms of reduction in cardiovascular risk factors. Additionally, statin administration to female offspring on an HFD during early life was associated with reduction in circulating CRPs and an increased bone marrow EPC numbers and colony-forming characteristics.
authors.affiliation: Division of Cardiothoracic Surgery, Department of Surgery, Texas A & M Health Science Centre at Scott & White Memorial Hospital, Temple, Texas; Institute of Developmental Sciences, Developmental Origins of Health and Disease Division, University of Southampton, Southampton, United Kingdom.
authors.forename: Maqsood M
authors.initials: MM
authors.lastname: Elahi
authors.affiliation: Department of Clinical Quality, The Liverpool Heart & Chest Hospital NHS Foundation Trust, Liverpool, United Kingdom; Institute of Infection & Global Health, University of Liverpool, Liverpool, United Kingdom. Electronic address: Matata_bashir@hotmail.com.
authors.forename: Bashir Mnene
authors.initials: BM
authors.lastname: Matata
mesh_terms: D050154:Adiposity / Q000187:drug effects; D000818:Animals; D001794:Blood Pressure; D001835:Body Weight; D001853:Bone Marrow; D002097:C-Reactive Protein / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D059305:Diet, High-Fat / Q000009:adverse effects*; D066026:Endothelial Progenitor Cells / Q000187:drug effects*; D005260:Female; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D006937:Hypercholesterolemia / Q000097:blood; D006973:Hypertension / Q000209:etiology / Q000517:prevention & control*; D039382:Maternal Nutritional Physiological Phenomena; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000209:etiology / Q000517:prevention & control*; D011247:Pregnancy; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D014280:Triglycerides; D002097:C-Reactive Protein
keywords: Blood pressure; C-reactive proteins; Cardiovascular dysfunction; Developmental programming; Endothelial progenitor cells; HMG-CoA reductase inhibition