title: Regulation and function of C1Q/TNF-related protein-5 (CTRP-5) in the context of adipocyte biology.
abstract: OBJECTIVE
  The C1q/TNF-related protein (CTRP) family represents a growing family of adiponectin paralogous proteins. CTRP-5 was detected in adipose tissue of mice and plays a role in the context of the metabolic syndrome. It was the aim to investigate the detailed expression profile of CTRP-5 in a variety of adipocytic cells and to determine whether CTRP-5 circulates in human serum. Moreover, regulation and function of CTRP-5 was studied in the context of adipocyte biology.
  
  
  METHODS
  CTRP-5 serum levels were measured in 50 healthy subjects by ELISA. Genotype analysis was performed by direct sequencing in 200 probands. CTRP-5 mRNA and protein expression was analyzed by RT-PCR, real-time RT-PCR and Western blot. Recombinant CTRP-5 and fatty acids were used for stimulation experiments in 3T3-L1 adipocytes. siRNA-mediated knockdown of CTRP-3 was performed during adipocyte differentiation.
  
  
  RESULTS
  CTRP-5 mRNA and protein was strongly expressed in a wide variety of human and murine adipocytic cells and was induced during adipocyte differentiation. Saturated fatty acids increased CTRP-5 expression in adipocytes. siRNA-mediated cellular knockdown of CTRP-3 in adipocytes resulted in an upregulation of CTRP-5 expression. CTRP-5 inhibited the release of resistin and adiponectin dose-dependently. CTRP-5 circulates abundantly in human sera with a broad interindividual variation. The SNP 1014 T/A was not associated with type 2 diabetes mellitus in 200 Caucasian probands.
  
  
  CONCLUSIONS
  CTRP-5 might be a novel adipokine that circulates abundantly in human sera. CTRP-5 is functionally involved in adipocyte biology and there might exist a counter-regulatory connection with its family member, CTRP-3.
authors: Department of Internal Medicine I, Regensburg University Hospital, Germany.
authors: A
authors: A
authors: Schmid
authors: A
authors: A
authors: Kopp
authors: C
authors: C
authors: Aslanidis
authors: M
authors: M
authors: Wabitsch
authors: M
authors: M
authors: Müller
authors: A
authors: A
authors: Schäffler
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology*; D050156:Adipogenesis / Q000187:drug effects / Q000235:genetics; D000328:Adult; D000818:Animals; D016022:Case-Control Studies; D002478:Cells, Cultured; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology / Q000235:genetics / Q000473:pathology; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D005787:Gene Frequency; D006801:Humans; D008297:Male; D008565:Membrane Proteins / Q000097:blood / Q000235:genetics* / Q000378:metabolism / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide / Q000502:physiology; D034741:RNA, Small Interfering / Q000494:pharmacology; D055815:Young Adult
chemical_list: C516596:CTRP5 protein, mouse; D008565:Membrane Proteins; D034741:RNA, Small Interfering