Comparative evaluation of the therapeutic effect of metformin monotherapy with metformin and acupuncture combined therapy on weight loss and insulin sensitivity in diabetic patients

Abstract

Objective: Obesity induces insulin resistance (IR), the key etiologic defect of type 2 diabetes mellitus (T2DM). Therefore, an incidence of obesity-induced diabetes is expected to decrease if obesity is controlled. Although Metformin is currently one of the main treatment options for T2DM in obese patients, resulting in an average of 5% weight loss, adequate weight control in all patients cannot be achieved with Metformin alone. Thus, additional therapies with a weight loss effect, such as acupuncture, may improve the effectiveness of Metformin.Subjective:We designed this randomized clinical trial (RCT) to compare the effects of Metformin monotherapy with that of Metformin and acupuncture combined therapy on weight loss and insulin sensitivity among overweight/obese T2DM patients, to understand whether acupuncture plus Metformin is a better approach than Metformin only on treating diabetes. To understand whether acupuncture can be an insulin sensitizer and, if so, its therapeutic mechanism.

Results: Our results show that Metformin and acupuncture combined therapy significantly improves body weight, body mass index (BMI), fasting blood sugar (FBS), fasting insulin (FINS), homeostasis model assessment (HOMA) index, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), leptin, adiponectin, glucagon-like peptide-1 (GLP-1), resistin, serotonin, free fatty acids (FFAs), triglyceride (TG), low-density lipoprotein cholesterol (LDLc), high-density lipoprotein cholesterol (HDLc) and ceramides.

Conclusions: Consequently, Metformin and acupuncture combined therapy is more effective than Metformin only, proving that acupuncture is an insulin sensitizer and is able to improve insulin sensitivity possibly by reducing body weight and inflammation, while improving lipid metabolism and adipokines. As a result, electro-acupuncture (EA) might be useful in controlling the ongoing epidemics in obesity and T2DM.

Figure 1

Trial profile and design.

Figure 2

Effects of EA treatment on anthropometric and T2DM markers. (a) Body weight (±0.1 kg). (b) BMI (kg m⁻²). (c) Serum FBS concentration (mmol l⁻¹) by ELISA. (d) FINS concentration (μIU ml⁻¹) by ELISA. (e) HOMA index=FBS × FINS/22.5. Data were expressed as means±s.d., *P<0.01 vs Control, ^#P<0.01 vs First. Time point: First: at the beginning of treatment, 5th: at the fifth time, last: at the last time of treatment.

Figure 3

Effects of EA treatment on lipid profiles. (a) Serum TG (mmol l⁻¹). (b) Serum LDLc (mmol l⁻¹). (c) Serum ceramide (g dl⁻¹). (d) Serum HDLc (mmol l⁻¹). (e) Serum FFAs (mmol l⁻¹). All data by ELISA. Data were expressed as means±s.d., *P<0.01 vs Control, ^#P<0.01 vs First. Time point: First: at the beginning of treatment, 5th: at the fifth time, last: at the last time of treatment.

Figure 4

Effects of EA treatment on inflammatory markers. (a) Serum TNF-α (pg ml⁻¹). (b) Serum IL-6 (pg ml⁻¹). (c) Serum CRP (mg dl⁻¹). All data by ELISA. Data were expressed as means±s.d., *P<0.01 vs Control, ^#P<0.01 vs First. Time point: First: at the beginning of treatment, 5th: at the fifth time, last: at the last time of treatment.

Figure 5

Effects of EA treatment on adipokines. (a) Serum leptin (ng ml⁻¹). (b) Serum adiponectin (ng ml⁻¹). (c) Serum GLP-1 (mmol l⁻¹). (d) Serum serotonin (ng ml⁻¹). (e) Serum resistin (ng ml⁻¹). All data by ELISA. Data were expressed as means±s.d., *P<0.01 vs Control, ^#P<0.01 vs First. Time point: First: at the beginning of treatment, 5th: at the fifth time, last: at the last time of treatment.