title: Effect of pioglitazone on muscle sympathetic nerve activity in type 2 diabetes mellitus with α-glucosidase inhibitor.
abstract: Activation of the sympathetic nervous system is augmented in patients with type 2 diabetes mellitus (DM). Pioglitazone, an anti-diabetic drug, improves insulin resistance, but its influence on sympathetic nerve activity is not clear. To identify the relationship between insulin resistance and sympathetic activity, we examined muscle sympathetic nerve activity (MSNA) in controlled type 2 DM patients with alpha-glucosidase inhibitor (GI). We measured MSNA and calculated homeostasis model assessment of insulin resistance index (HOMA-IR) in twelve DM patients treated with alpha-GI and thirteen age-matched healthy subjects. In DM patients with alpha-GI, all parameters were reexamined after three months of treatment with pioglitazone. MSNA and HOMA-IR were significantly greater in DM patients with alpha-GI compared to healthy subjects. Hemoglobin A1c did not differ in DM patients before and after pioglitazone. However, pioglitazone significantly decreased MSNA in DM patients compared with alpha-GI (21.7±5.2 vs. 32.0±6.8 burst/min, p<0.01). Furthermore, MSNA level in pioglitazone was similar to that in healthy subjects. HOMA-IR significantly decreased after pioglitazone, and a significant relationship was found between the absolute change in MSNA and HOMA-IR (r=0.65, p<0.05). These results suggest that improved insulin resistance with pioglitazone provides an additional effect on inhibition of sympathetic nerve activity.
authors.affiliation: Department of Disease Control and Homeostasis, Graduate School of Medical Science, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Ishikawa, Japan.
authors.forename: Daisuke
authors.initials: D
authors.lastname: Kobayashi
authors.forename: Masayuki
authors.initials: M
authors.lastname: Takamura
authors.forename: Hisayoshi
authors.initials: H
authors.lastname: Murai
authors.forename: Soichiro
authors.initials: S
authors.lastname: Usui
authors.forename: Tatsunori
authors.initials: T
authors.lastname: Ikeda
authors.forename: Jun-ichiro
authors.initials: J
authors.lastname: Inomata
authors.forename: Shin-ichiro
authors.initials: S
authors.lastname: Takashima
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kato
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Furusho
authors.forename: Yumie
authors.initials: Y
authors.lastname: Takeshita
authors.forename: Tsuguhito
authors.initials: T
authors.lastname: Ota
authors.forename: Toshinari
authors.initials: T
authors.lastname: Takamura
authors.forename: Shuichi
authors.initials: S
authors.lastname: Kaneko
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000368:Aged; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000201:enzymology* / Q000503:physiopathology; D005260:Female; D065089:Glycoside Hydrolase Inhibitors; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology / Q000627:therapeutic use; D007333:Insulin Resistance / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000098:blood supply / Q000201:enzymology / Q000294:innervation; D000077205:Pioglitazone; D017779:Sympathetic Fibers, Postganglionic / Q000187:drug effects* / Q000201:enzymology* / Q000503:physiopathology; D045162:Thiazolidinediones / Q000494:pharmacology* / Q000627:therapeutic use; D000520:alpha-Glucosidases / Q000502:physiology
chemical_list: D065089:Glycoside Hydrolase Inhibitors; D007004:Hypoglycemic Agents; D045162:Thiazolidinediones; D000520:alpha-Glucosidases; D000077205:Pioglitazone