title: Regulation of skeletal muscle peroxisome proliferator-activated receptor gamma expression by exercise and angiotensin-converting enzyme inhibition in fructose-fed hypertensive rats.
abstract: The purpose of this study was to examine the effects of chronic exercise training and angiotensin-converting enzyme (ACE) inhibition on peroxisome proliferator-activated receptor gamma (PPAR gamma) expression in fat and skeletal muscle in fructose-fed spontaneously hypertensive rats (SHR). SHR were fed a fructose-rich diet over 16 weeks of either exercise training (Ex group: 20 m/min, 0% grade, 60 min/day, 5 days/week), ACE inhibitor administration (TM group: temocapril, 10 mg/kg/day), or a combination of both treatments (TM+Ex group). The systolic blood pressure was reduced exclusively in the temocapril-treated groups. Serum leptin level was positively correlated with the ratio of epididymal fat weight to body weight (p<0.001). Exercise training significantly upregulated the PPARgamma expression in all tissues, which was attenuated by temocapril. PPARgamma expression was significantly upregulated in skeletal muscles in the Ex group, and temocapril administration attenuated this effect in the Ex+TM group. The level of PPARgamma protein was significantly higher in the extensor digitorum longus muscle than in the soleus muscle. Both TM and Ex prevented the fructose diet-induced transitions of fiber type. These data suggested that PPARgamma expression is tissue-specific, and that alterations in PPARgamma expression in the skeletal muscle induced by either or both treatments may have contributed to reducing the fat mass via the regulation of metabolic homeostasis. Changes in muscle morphology were independent of PPARgamma expression, and the higher proportion of type I fiber might also explain some of the beneficial impact of exercise and ACE inhibition on energy metabolism.
authors.affiliation: Department of Internal Medicine and Rehabilitation Science, Tohoku University Graduate School of Medicine, Sendai, Japan.
authors.forename: Takayuki
authors.initials: T
authors.lastname: Kawamura
authors.forename: Kazunori
authors.initials: K
authors.lastname: Yoshida
authors.forename: Akira
authors.initials: A
authors.lastname: Sugawara
authors.forename: Makoto
authors.initials: M
authors.lastname: Nagasaka
authors.forename: Nobuyoshi
authors.initials: N
authors.lastname: Mori
authors.forename: Kazuhisa
authors.initials: K
authors.lastname: Takeuchi
authors.forename: Masahiro
authors.initials: M
authors.lastname: Kohzuki
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D004822:Epididymis; D005632:Fructose / Q000494:pharmacology; D006321:Heart / Q000033:anatomy & histology; D007333:Insulin Resistance; D008297:Male; D018657:Muscle Fibers, Slow-Twitch / Q000166:cytology / Q000378:metabolism; D018482:Muscle, Skeletal / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D009929:Organ Size; D005082:Physical Exertion / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism*; D013841:Thiazepines / Q000494:pharmacology*; D014157:Transcription Factors / Q000378:metabolism*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D018160:Receptors, Cytoplasmic and Nuclear; D013841:Thiazepines; D014157:Transcription Factors; D005632:Fructose; C055603:temocapril hydrochloride