Abbreviations ISI: insulin sensitivity index .MUFA: monounsaturated fatty acid . PGC-1: PPAR-γcoactivator-1 . PPAR: peroxisome proliferator-activatedreceptor . PUFA: polyunsaturated fatty acid . SNP: single-nucleotide polymorphismTo the Editor: Peroxisome proliferator-activated receptor(PPAR)-γ coactivator-1α (PGC-1α) is a metabolicallyrelevanttranscriptionalcoactivatorprotein.ThroughPPARsand nuclear respiratory factor-1, it enhances adaptivethermogenesis, oxidative phosphorylation, mitochondrialbiogenesis and β-oxidation in adipose tissue and skeletalmuscle [1]. Obese, insulin-resistant and type 2 diabeticstates reveal low muscle mitochondrial oxidative capacity,reduced expression of respiratory chain components, anddecreased expression of the gene encoding PGC-1α(PPARGC1A)[2, 3]. We have recently shown thatPPARGC1A expression in in vitro differentiated humanskeletal muscle cells (myotubes) is induced by commonunsaturated plasmaNEFAs, such aspalmitoleate,oleate andlinoleate, but is not influenced by common saturatedNEFAs, such as myristate, palmitate and stearate [4]. Inthe present study, we investigated (1) whether the basalexpression of PPARGC1A and the gene encoding its closehomologue, PGC-1β (PPARGC1B) in myotubes derivedfrom metabolically characterised white donors displaymarked individual variations, and, if so, (2) whether thesevariations are linked to in vivo metabolic features of thedonors, such as adiposity, insulin resistance, total NEFAconcentration, or concentration of individual plasmaNEFAs.We measured levels of PPARGC1A and PPARGC1BmRNAs in myotubes from 25 healthy subjects and per-formed linear regression analysis with the subjects’ anthro-pometricandmetabolicparameters.Thedonors(11women,14 men, age 26.6±4.9 years, body fat content 21.0±8.1%,WHR 0.81±0.07 [all means ± SD]) were participants in theTubingen family study for type 2 diabetes and gave writteninformedconsent tobeincludedinthe study. Thestudy wasapproved by the local ethics committee.Myoblasts were grown from satellite cells obtained frompercutaneous needle biopsies performed on the lateralportion of musculus quadriceps femoris and were differ-entiated into myotubes as described previously [4]. First-pass cells were used. RNA isolation was performed usingRNeasy silica-gel columns (Qiagen, Hilden, Germany).Total RNA treated with RNase-free DNase I was tran-scribed into cDNA using AMV reverse transcriptase andthe First-Strand cDNA Synthesis Kit from Roche Diag-nostics (Mannheim, Germany). Levels of PPARGC1A andPPARGC1B mRNAs were quantified using SYBR Green Idye and a LightCycler (Roche Diagnostics). The followingprimers were used: PPARGC1A forward 5′-TGTGCAACTCTCTGGAACTG-3′, reverse 5′-TGAGGACTTGCTGAGTGGTG-3′; PPARGC1B forward 5′-GCTCTCCTCCTTCTTCCTCA-3′, reverse 5′-ATAGAGCGTCTCCACCATCC-3′. PCR conditions were as follows: PPARGC1A:–65°Cannealing,45cycles,4mmol/lMgCl