PMID- 26137510
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20150703
LR  - 20181113
IS  - 2352-3964 (Print)
IS  - 2352-3964 (Electronic)
IS  - 2352-3964 (Linking)
VI  - 1
IP  - 1
DP  - 2014 Nov
TI  - Mild Electrical Stimulation with Heat Shock Reduces Visceral Adiposity and 
      Improves Metabolic Abnormalities in Subjects with Metabolic Syndrome or Type 2 
      Diabetes: Randomized Crossover Trials.
PG  - 80-9
LID - 10.1016/j.ebiom.2014.11.001 [doi]
AB  - BACKGROUND: The induction of heat shock protein (HSP) 72 by mild electrical 
      stimulation with heat shock (MES + HS), which improves visceral adiposity and 
      insulin resistance in mice, may be beneficial in treating metabolic syndrome (MS) 
      or type 2 diabetes mellitus (T2DM). METHODS: Using open-label crossover trials, 
      40 subjects with MS or T2DM were randomly assigned using computer-generated 
      random numbers to 12 weeks of therapeutic MES + HS followed by 12 weeks of no 
      treatment, or vice versa. During the intervention period, physical and 
      biochemical markers were measured. FINDINGS: Compared to no treatment, MES + HS 
      treatment was associated with a significant decrease in visceral adiposity 
      (- 7.54 cm(2) (- 8.61%), 95% CI - 8.55 to - 6.53 (p = 0.037) in MS, - 19.73 cm(2) 
      (- 10.89%), 95% CI - 20.97 to - 18.49 (p = 0.003) in T2DM). Fasting plasma 
      glucose levels were decreased by 3.74 mg/dL (- 5.28%: 95% CI - 4.37 to 
      - 3.09 mg/dL, p = 0.029) in MS and by 14.97 mg/dL (10.40%: 95% CI - 15.79 to 
      14.15 mg/dL, p < 0.001) in T2DM, and insulin levels were also reduced by 10.39% 
      and 25.93%, respectively. HbA1c levels showed a trend toward reduction (- 0.06%) 
      in MS, and was significantly declined by - 0.43% (95% CI - 0.55 to - 0.31%, 
      p = 0.009) in T2DM. HbA1c level of less than 7.0% was achieved in 52.5% of the 
      MES + HS-treated T2DM patients in contrast to 15% of the non-treated period. 
      Several insulin resistance indices, inflammatory cytokines or adipokines, 
      including C-reactive protein, adiponectin, and tumor necrosis factor-alpha, were all 
      improved in both groups. In isolated monocytes, HSP72 expression was increased 
      and cytokine expression was reduced following MES + HS treatment. Glucose 
      excursions on meal tolerance test were lower after using MES + HS in T2DM. 
      INTERPRETATION: This combination therapy has beneficial impacts on body 
      composition, metabolic abnormalities, and inflammation in subjects with MS or 
      T2DM. Activation of the heat shock response by MES + HS may provide a novel 
      approach for the treatment of lifestyle-related diseases. FUNDING: Funding for 
      this research was provided by MEXT KAKENHI (Grants-in-Aid for Scientific Research 
      from Ministry of Education, Culture, Sports, Science and Technology, Japan).
FAU - Kondo, Tatsuya
AU  - Kondo T
AD  - Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 
      Kumamoto, Japan.
FAU - Ono, Kaoru
AU  - Ono K
AD  - Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 
      Kumamoto, Japan.
FAU - Kitano, Sayaka
AU  - Kitano S
AD  - Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 
      Kumamoto, Japan.
FAU - Matsuyama, Rina
AU  - Matsuyama R
AD  - Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 
      Kumamoto, Japan.
FAU - Goto, Rieko
AU  - Goto R
AD  - Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 
      Kumamoto, Japan.
FAU - Suico, Mary Ann
AU  - Suico MA
AD  - Department of Molecular Medicine, Faculty of Life Sciences, Kumamoto University, 
      Kumamoto, Japan.
FAU - Kawasaki, Shuji
AU  - Kawasaki S
AD  - Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 
      Kumamoto, Japan.
FAU - Igata, Motoyuki
AU  - Igata M
AD  - Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 
      Kumamoto, Japan.
FAU - Kawashima, Junji
AU  - Kawashima J
AD  - Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 
      Kumamoto, Japan.
FAU - Motoshima, Hiroyuki
AU  - Motoshima H
AD  - Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 
      Kumamoto, Japan.
FAU - Matsumura, Takeshi
AU  - Matsumura T
AD  - Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 
      Kumamoto, Japan.
FAU - Kai, Hirofumi
AU  - Kai H
AD  - Department of Molecular Medicine, Faculty of Life Sciences, Kumamoto University, 
      Kumamoto, Japan.
FAU - Araki, Eiichi
AU  - Araki E
AD  - Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 
      Kumamoto, Japan.
LA  - eng
PT  - Journal Article
DEP - 20141111
PL  - Netherlands
TA  - EBioMedicine
JT  - EBioMedicine
JID - 101647039
PMC - PMC4457350
OTO - NOTNLM
OT  - Chronic inflammation
OT  - Heat shock response
OT  - Insulin resistance
OT  - Metabolic syndrome
OT  - Type 2 diabetes
EDAT- 2015/07/03 06:00
MHDA- 2015/07/03 06:01
PMCR- 2014/11/11
CRDT- 2015/07/03 06:00
PHST- 2014/09/17 00:00 [received]
PHST- 2014/11/04 00:00 [revised]
PHST- 2014/11/04 00:00 [accepted]
PHST- 2015/07/03 06:00 [entrez]
PHST- 2015/07/03 06:00 [pubmed]
PHST- 2015/07/03 06:01 [medline]
PHST- 2014/11/11 00:00 [pmc-release]
AID - S2352-3964(14)00025-5 [pii]
AID - 10.1016/j.ebiom.2014.11.001 [doi]
PST - epublish
SO  - EBioMedicine. 2014 Nov 11;1(1):80-9. doi: 10.1016/j.ebiom.2014.11.001. 
      eCollection 2014 Nov.