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.
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.
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DOI：
10.1016/j.ebiom.2014.11.001
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发表时间：
2014-11
期刊：
影响因子：
11.1
通讯作者：
Araki, Eiichi
中科院分区：
文献类型：
--
作者：
Kondo, Tatsuya;Ono, Kaoru;Kitano, Sayaka;Matsuyama, Rina;Goto, Rieko;Suico, Mary Ann;Kawasaki, Shuji;Igata, Motoyuki;Kawashima, Junji;Motoshima, Hiroyuki;Matsumura, Takeshi;Kai, Hirofumi;Araki, Eiichi
温和电刺激+热休克(MES+Hs)诱导热休克蛋白(HSP)72，改善小鼠内脏脂肪和胰岛素抵抗，可能有益于治疗代谢综合征(MS)或2型糖尿病(T2 DM)。使用开放标签交叉试验，40名患有MS或T2 DM的受试者使用计算机生成的随机数被随机分配到12周的治疗性MES+HHS，然后是12周的不治疗，反之亦然。干预期间进行生理生化指标检测。与不治疗相比，MES+HS治疗组内脏肥胖度显著降低(T2 DM组−为7.54亿cm~2(−=8.61%)，95%CI−为8.55至−为6.53(p=0.037)，−为19.73cm2(−为10.89%)，95%CI−为20.97至−为18.49(p=0.003)。空腹血糖在MS组和T2 DM组分别下降3.74g/dL(−=5.28%：95%CI−=4.37to−=3.09m g/dL，p=0.029)和14.97m g/dL(10.40%：95%CI−=15.79~14.15m g/dL，p<0.001)，胰岛素水平也分别下降10.39%和25.93%。糖化血红蛋白水平在MS组呈下降趋势(−为0.06%)，在T2 DM组下降−为0.43%(95%CI−为0.55至−为0.31%，p=0.009)。接受MES+HS治疗的T2 DM患者中，52.5%的患者HbA1c水平低于7.0%，而未治疗组的这一比例为15%。两组胰岛素抵抗指数、炎症细胞因子或脂肪因子，包括C-反应蛋白、脂联素和肿瘤坏死因子-α均有改善。在分离的单核细胞中，经MES+HS处理后，HSP72表达增加，细胞因子表达降低。T2 DM患者应用MES+HS后，餐耐量试验的血糖漂移明显降低。这种联合治疗对MS或T2 DM受试者的身体成分、代谢异常和炎症有有益的影响。MES+HS激活热休克反应可能为生活方式相关疾病的治疗提供一种新的方法。这项研究的资金由(日本文部科学省科学研究补助金)提供。我们报告使用温和的电刺激和热休克(MES+HHS)治疗代谢综合征或2型糖尿病。该疗法可改善内脏肥胖、葡萄糖稳态、胰岛素抵抗和慢性炎症状态。我们的发现表明，MES+HHS可能是这些生活方式相关疾病患者的有价值的治疗选择。
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). 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. Compared to no treatment, MES + HS treatment was associated with a significant decrease in visceral adiposity (− 7.54 cm2 (− 8.61%), 95% CI − 8.55 to − 6.53 (p = 0.037) in MS, − 19.73 cm2 (− 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-α, 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. 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 for this research was provided by (Grants-in-Aid for Scientific Research from Ministry of Education, Culture, Sports, Science and Technology, Japan). We report the use of mild electrical stimulation with heat shock (MES + HS) in treating metabolic syndrome or type 2 diabetes. The treatment improves visceral adiposity, glucose homeostasis, insulin resistance and chronic inflammatory status. Our findings suggest that MES + HS might be a valuable therapeutic option for patients with these lifestyle-related diseases.
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影响因子：
7.7
作者：
Kondo T;Sasaki K;Matsuyama R;Morino-Koga S;Adachi H;Suico MA;Kawashima J;Motoshima H;Furukawa N;Kai H;Araki E
通讯作者：
Araki E
影响因子：
3.7
作者：
Morino, Saori;Kondo, Tatsuya;Sasaki, Kazunari;Adachi, Hironori;Suico, Mary Ann;Sekimoto, Erika;Matsuda, Tomoko;Shuto, Tsuyoshi;Araki, Eiichi;Kai, Hirofumi
通讯作者：
Kai, Hirofumi
DOI：
10.1073/pnas.0705799105
发表时间：
2008-02-05
影响因子：
11.1
作者：
Chung, Jason;Nguyen, Anh-Khoi;Febbraio, Mark A.
通讯作者：
Febbraio, Mark A.
影响因子：
7.7
作者：
Kurucz, I;Morva, A;Koranyi, L
通讯作者：
Koranyi, L
影响因子：
3.5
作者：
Morino, Saori;Suico, Mary Ann;Kai, Hirofumi
通讯作者：
Kai, Hirofumi