title: PPARgamma gene polymorphism is associated with exercise-mediated changes of insulin resistance in healthy men.
abstract: Exercise training improves insulin sensitivity, but individual responses vary greatly. Peroxisome proliferator-activated receptor-gamma (PPARgamma) is a regulator of adipose cell differentiation and plays an important role in systemic insulin action. We investigated whether PPARgamma gene polymorphism affects insulin resistance in response to exercise in Japanese healthy men. The exercise program at an individual intensity of 50% of the maximal heart rate was performed for 20 to 60 min/d, and 2 to 3 days per week to attain a level of physical activity of 700 kcal/wk. The program was conducted for 3 months without any dietary intervention, and the clinical and metabolic characteristics were examined before and after the exercise program. Body mass index (BMI) did not change significantly after the exercise program, whereas percentage of body fat (% body fat), fasting plasma glucose (FPG), and serum leptin levels decreased significantly. Pro12Ala polymorphism in PPARgamma gene was performed on genomic DNA isolated from human leukocytes and examined with polymerase chain reaction (PCR) and subsequent restriction enzyme analysis using BstU-I. In this study, the Ala allele did not correlate with fasting immunoreactive insulin (IRI) and homeostasis model assessment-insulin resistance index (HOMA-R) at baseline, but did so with the changes in IRI and HOMA-R after exercise (DeltaIRI, Pro/Pro 0.55 +/- 3.49 microU/mL v Pro/Ala -2.83 +/- 1.47 microU/mL, P <.05; DeltaHOMA-R, Pro/Pro 0.09 +/- 0.86 v Pro/Ala -0.61 +/- 0.32, P <.05). This result suggests that the Ala allele is associated with improvement in insulin resistance after exercise. We conclude that PPARgamma gene polymorphism may be a reliable indicator of whether exercise will have a beneficial effect as part of the treatment of insulin resistance syndrome.
authors.affiliation: Department of Endocrinology and Metabolism, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
authors.forename: Toshio
authors.initials: T
authors.lastname: Kahara
authors.forename: Toshinari
authors.initials: T
authors.lastname: Takamura
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Hayakawa
authors.forename: Yukihiro
authors.initials: Y
authors.lastname: Nagai
authors.forename: Hiromi
authors.initials: H
authors.lastname: Yamaguchi
authors.forename: Tatsuo
authors.initials: T
authors.lastname: Katsuki
authors.forename: Ken-Ichi
authors.initials: K
authors.lastname: Katsuki
authors.forename: Michio
authors.initials: M
authors.lastname: Katsuki
authors.forename: Ken-Ichi
authors.initials: K
authors.lastname: Kobayashi
mesh_terms: D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000032:analysis; D015444:Exercise / Q000502:physiology*; D005215:Fasting / Q000097:blood; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D020738:Leptin / Q000097:blood; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic / Q000502:physiology*; D011446:Prospective Studies; D018160:Receptors, Cytoplasmic and Nuclear / Q000235:genetics*; D012016:Reference Values; D014157:Transcription Factors / Q000235:genetics*
chemical_list: D001786:Blood Glucose; D020738:Leptin; D018160:Receptors, Cytoplasmic and Nuclear; D014157:Transcription Factors