title: Adipogenic Impairment of Adipose Tissue-Derived Mesenchymal Stem Cells in Subjects With Metabolic Syndrome: Possible Protective Role of FGF2.
abstract: The decreased expansion capacity of adipose tissue plays a crucial role in the onset of disorders associated with metabolic syndrome.
  
  
  
  The aim of this study was to examine the state of adipose tissue-derived mesenchymal stem cells (ASCs) from obese subjects with different metabolic profiles.
  
  
  
  This was a 2-year study to enroll subjects who underwent bariatric surgery or cholecystectomy.
  
  
  
  University Hospital.
  
  
  
  Patients who underwent either bariatric surgery (20 morbidly obese) or cholecystectomy (40 subjects) participated in the study.
  
  
  
  ASCs were obtained from both visceral and subcutaneous adipose tissue. Adipogenic, fibrotic gene expression was quantified by quantitative polymerase chain reaction; Smad7 and fibroblast growth factor 2 were quantified by western blotting and enzyme-linked immunosorbent assay, respectively. The susceptibility of ASCs to apoptosis, their population doubling time, and their clonogenic potential were evaluated.
  
  
  
  The worsening metabolic profile of the patients was accompanied by a decrease in the intrinsic levels of adipogenic gene expression, reduced proliferation rate, clonogenic potential, and exportation of fibroblast growth factor 2 to the cell surface of the ASCs derived from both tissues. In addition, the ASCs from patients without metabolic syndrome showed differences in susceptibility to apoptosis and expression of TGFβ-signaling inhibitory protein Smad7 with respect to the ASCs from patients with metabolic syndrome.
  
  
  
  Our results suggest that the decrease in adipogenic-gene mRNA and clonogenic potential, as well as the accumulation of fibrotic proteins with metabolic alterations, could be a relevant mechanism controlling the number and size of neogenerated adipocytes and involved in alteration of adipose-tissue expansion.
authors.affiliation: Departments of Clinical Endocrinology and Nutrition, and.|CIBER Fisiopatología Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid 28029, Spain.
authors.forename: Wilfredo
authors.initials: W
authors.lastname: Oliva-Olivera
authors.affiliation: Departments of Clinical Endocrinology and Nutrition, and.|CIBER Fisiopatología Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid 28029, Spain.
authors.forename: Leticia
authors.initials: L
authors.lastname: Coín-Aragüez
authors.affiliation: Departments of Clinical Endocrinology and Nutrition, and.|CIBER Fisiopatología Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid 28029, Spain.
authors.forename: Said
authors.initials: S
authors.lastname: Lhamyani
authors.affiliation: Departments of Clinical Endocrinology and Nutrition, and.|CIBER Fisiopatología Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid 28029, Spain.
authors.forename: Mercedes
authors.initials: M
authors.lastname: Clemente-Postigo
authors.affiliation: Departments of Clinical Endocrinology and Nutrition, and.|CIBER Fisiopatología Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid 28029, Spain.
authors.forename: Juan Alcaide
authors.initials: JA
authors.lastname: Torres
authors.affiliation: Internal Medicine, Regional University Hospital of Málaga, Institute of Biomedical Research of Málaga, Hospital of Málaga (Virgen de la Victoria), University of Málaga, Málaga 29010, Spain; and.|CIBER Fisiopatología Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid 28029, Spain.
authors.forename: Maria Rosa
authors.initials: MR
authors.lastname: Bernal-López
authors.affiliation: Departments of Clinical Endocrinology and Nutrition, and.|CIBER Fisiopatología Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid 28029, Spain.
authors.forename: Rajaa
authors.initials: R
authors.lastname: El Bekay
authors.affiliation: Departments of Clinical Endocrinology and Nutrition, and.|CIBER Fisiopatología Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid 28029, Spain.
authors.forename: Francisco José
authors.initials: FJ
authors.lastname: Tinahones
mesh_terms: D050156:Adipogenesis / Q000235:genetics / Q000502:physiology*; D000273:Adipose Tissue / Q000378:metabolism / Q000473:pathology*; D000328:Adult; D000886:Anthropometry / Q000379:methods; D017209:Apoptosis / Q000502:physiology; D050110:Bariatric Surgery; D002454:Cell Differentiation / Q000502:physiology; D049109:Cell Proliferation; D002763:Cholecystectomy; D003114:Colony-Forming Units Assay; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism / Q000502:physiology*; D005786:Gene Expression Regulation / Q000502:physiology; D051275:Glucose Transporter Type 4 / Q000096:biosynthesis / Q000235:genetics; D006801:Humans; D059630:Mesenchymal Stem Cells / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D024821:Metabolic Syndrome / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D008875:Middle Aged; D009767:Obesity, Morbid / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D000070778:Perilipin-1 / Q000096:biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics
chemical_list: D051275:Glucose Transporter Type 4; C000602978:PLIN1 protein, human; D000070778:Perilipin-1; D012333:RNA, Messenger; C495692:SLC2A4 protein, human; D016222:Fibroblast Growth Factor 2