Activation of heat shock response to treat obese subjects with type 2 diabetes: a prospective, frequency-escalating, randomized, open-label, triple-arm trial.

Tatsuya Kondo,Hirofumi Kai,Kaoru Ono,Mary Ann Suico,Miki Sato,Takeshi Matsumura,Sayaka Kitano,Hiroyuki Motoshima,Eiichi Araki,Junji Kawashima,Motoyuki Igata,Rieko Goto

doi:10.1038/srep35690

Tatsuya Kondo, Hirofumi Kai + Show 10 more

Open Access

https://doi.org/10.1038/srep35690

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Journal: Scientific Reports	Publication Date: Oct 19, 2016
Citations: 11	License type: CC BY 4.0

Affiliation: Kumamoto University

Abstract

Activation of heat shock response (HSR) improves accumulated visceral adiposity and metabolic abnormalities in type 2 diabetes. To identify the optimal intervention strategy of the activation of the HSR provided by mild electrical stimulation (MES) with heat shock (HS) in type 2 diabetes. This study was a prospective, frequency-escalating, randomized, open-label, triple-arm trial in Japan. A total of 60 obese type 2 diabetes patients were randomized into three groups receiving two, four, or seven treatments per week for 12 weeks. No adverse events were identified. MES + HS treatment (when all three groups were combined), significantly improved visceral adiposity, glycemic control, insulin resistance, systemic inflammation, renal function, hepatic steatosis and lipid profile compared to baseline. The reduction in HbA1c was significantly greater among those treated four times per week (−0.36%) or seven times per week (−0.65%) than among those treated two times per week (−0.10%). The relative HbA1c levels in seven times per week group was significantly decreased when adjusted by two times per week group (−0.55%. p = 0.001). This research provides the positive impact of MES + HS to treat obese patients with type 2 diabetes mellitus.

Highlights

Homeostasis, and inflammatory surrogate markers including tumor necrosis factor (TNF)-αand C-reactive protein (CRP)[6], which are quite similar to the effects observed in diabetic animal models treated with MES +HS7,9
For patients who are obese and have type 2 diabetes, a therapeutic strategy to modify the progression of the disease and complications beyond the control of glucose levels may provide additional long-term health benefits
The preferable metabolic effects of MES +HS treatment in obese patients with type 2 diabetes were regulated by the frequency of intervention

Summary

Introduction

Homeostasis, and inflammatory surrogate markers including tumor necrosis factor (TNF)-αand C-reactive protein (CRP)[6], which are quite similar to the effects observed in diabetic animal models treated with MES +HS7,9. The number of participants Age (years) Female (%) Diabetes history (years) Medications SU BG α-GI glinide TZD DPP-4 inhibitor SGLT2 inhibitor Adiposity Visceral Fat Area (cm2) SubQ Fat Area (cm2) total Fat Area (cm2) BMI (kg/m2) Wc (cm) Glucose control and insulin resistance Fasting plasma glucose (mg/dL) Fasting IRI (μIU/mL) HOMA-IR HbA1c (%) GA (%) Adiponectin (μg/mL) Blood pressure Systolic Blood Pressure (mmHg) Diastolic Blood Pressure (mmHg) Heart Rate (bpm) Systemic inflammation TNF-α (pg/mL) IL-6 (pg/mL) hs-CRP (ng/mL) WBC (/μL) Renal function eGFR (mL/min/1.73 m2) ACR (μg/gCre) L-FABP (mg/gCr) Hepatic steatosis and lipids AST/ALT UA (mg/dL) LDL-C (mg/dL) HDL-C (mg/dL) TG (mg/dL) FFA (μEq/L)

Results

Conclusion