Effects of resistance training and turmeric supplementation on reactive species marker stress in diabetic rats

Abstract

Background: Type 1 diabetes mellitus (T1DM) is a metabolic disease characterized by hyperglycemia and excessive generation of reactive oxygen species caused by autoimmune destruction of beta-cells in the pancreas. Among the antioxidant compounds, Curcuma longa (CL) has potential antioxidant effects and may improve hyperglycemia in uncontrolled T1DM/TD1, as well as prevent its complications (higher costs for the maintenance of health per patient, functional disability, cardiovascular disease, and metabolic damage). In addition to the use of compounds to attenuate the effects triggered by diabetes, physical exercise is also essential for glycemic control and the maintenance of skeletal muscles. Our objective is to evaluate the effects of CL supplementation associated with moderate- to high-intensity resistance training on the parameters of body weight recovery, glycemic control, reactive species markers, and tissue damage in rats with T1DM/TD1.

Methods: Forty male 3-month-old Wistar rats (200-250 g) with alloxan-induced T1DM were divided into 4 groups (n = 7-10): sedentary diabetics (DC); diabetic rats that underwent a 4-week resistance training protocol (TD); CL-supplemented diabetic rats (200 mg/kg body weight, 3x a week) (SD); and supplemented diabetic rats under the same conditions as above and submitted to training (TSD). Body weight, blood glucose, and the following biochemical markers were analyzed: lipid profile, aspartate aminotransferase (AST), alanine aminotransferase (ALT), uric acid, creatine kinase (CK), lactate dehydrogenase (LDH), and thiobarbituric acid reactive substances (TBARS).

Results: Compared to the DC group, the TD group showed body weight gain (↑7.99%, p = 0.0153) and attenuated glycemia (↓23.14%, p = 0.0008) and total cholesterol (↓31.72%, p ≤ 0.0041) associated with diminished reactive species markers in pancreatic (↓45.53%, p < 0.0001) and cardiac tissues (↓51.85%, p < 0.0001). In addition, compared to DC, TSD promoted body weight recovery (↑15.44%, p ≤ 0.0001); attenuated glycemia (↓42.40%, p ≤ 0.0001), triglycerides (↓39.96%, p ≤ 0.001), and total cholesterol (↓28.61%, p ≤ 0.05); and attenuated the reactive species markers in the serum (↓26.92%, p ≤ 0.01), pancreas (↓46.22%, p ≤ 0.0001), cardiac (↓55.33%, p ≤ 0.001), and skeletal muscle (↓42.27%, p ≤ 0.001) tissues caused by T1DM.

Conclusion: Resistance training associated (and/or not) with the use of Curcuma longa attenuated weight loss, the hypoglycemic and hypolipidemic effects, reactive species markers, and T1DM-induced tissue injury.

Keywords: Diabetes mellitus; Resistance training; Turmeric.

Fig. 1

Analysis of body weight, fasting plasma glucose, aspartate aminotransferase, and alanine aminotransferase of the diabetic animals group (DC) (white bar); trained diabetics (TD) group submitted to resistance training for four weeks (light gray bar); supplemented diabetics (SD) group receiving 200 mg/kg body three times per week for four weeks (dark gray bar); and trained and supplemented diabetics (TSD) group submitted to Curcuma longa supplementation and the resistance training program simultaneously (black bar). Body weight (a), fasting plasma glucose (b), aspartate aminotransferase (AST) (c) and alanine aminotransferase (ALT) (d). Data represent the mean ± standard deviation of the mean. One-way analysis of variance (ANOVA one way) and post hoc de Bonferroni tests were used. Letters on the bars represent the significant difference by one-way ANOVA followed by Bonferroni’s test among the groups as follows: body weight (^**p ≤ 0.01 for DC vs. SD; ^***p ≤ 0.001 for DC vs. TSD), glucose (^#p ≤ 0.05 for DC vs. SD; ^###p ≤ 0.001 for DC vs. TSD), AST (p ≤ 0.05 for DC vs. TSD), and ALT (^●p ≤ 0.05 for DC vs. SD; ^●●●p ≤ 0.001 for DC vs. TSD). For the DC vs. TD and SD vs. TSD groups, Student’s t-test was used. ns = no significant difference. n = 7–8 in all experimental groups

Fig. 2

Analysis of lipid profile, lactate dehydrogenase, and creatine kinase of the diabetic animals group (DC) (white bar); trained diabetics (TD) group submitted to resistance training for four weeks (light gray bar); supplemented diabetics (SD) group receiving 200 mg/kg body three times per week for four weeks (dark gray bar); and trained and supplemented diabetics (TSD) group submitted to Curcuma longa supplementation and the resistance training program simultaneously (black bar). High-density lipoprotein (HDL) (a), uric acid (b), triglycerides (c), total cholesterol (d), lactate dehydrogenase (e), and creatine kinase (f). Data represent the mean ± standard deviation of the mean. Letters on the bars represent the significant difference by one-way ANOVA followed by Bonferroni’s test among groups as follows: high-density lipoprotein (HDL) (^**p ≤ 0.01 for SD vs. TD; ^***p ≤ 0.001 for DC vs. TSD), uric acid (^#p ≤ 0.01 for DC vs. SD; ^##p ≤ 0.001 for DC vs. TSD; ^###p ≤ 0.01 for TD vs. TSD), triglycerides (^°p ≤ 0.01 for DC vs. TSD; ^°°p ≤ 0.05 for TD vs. TSD), and creatine kinase (^§ ≤ 0.001 for TD vs. SD; ^§§ ≤ 0.001 for TD vs. TSD). The DC vs. TD and SD vs. TSD groups were analyzed using Student’s t-test. ns = no significant difference. n = 7–8 in all experimental groups

Fig. 3

Analysis of tissue damage markers of the diabetic animals group (DC) (white bar); trained diabetics (TD) group submitted to resistance training for four weeks (light gray bar); supplemented diabetics (SD) that received 200 mg/kg body three times per week for four weeks (dark gray bar); and trained and supplemented diabetics (TSD) group submitted to Curcuma longa supplementation and the resistance training program simultaneously (black bar). Plasma TBARS (a), liver tissue TBARS (b), pancreatic tissue TBARS (c), heart tissue TBARS (d), and muscle tissue TBARS (e). Data represent the mean ± standard deviation of the mean. Letters on the bars represent the significant difference by one-way ANOVA followed by Bonferroni’s test among groups as follows: plasma TBARS (^*p ≤ 0.01 for SD vs. TSD; ^**p ≤ 0.01 for TD vs. SD; ^***p ≤ 0.01 for TD vs. TSD), liver tissue TBARS (^#p ≤ 0.001 for TD vs. SD; ^##p ≤ 0.01 for TD vs. TSD), pancreatic tissue TBARS (^°p ≤ 0.001 for DC vs. SD; ^°°p ≤ 0.001 for DC vs. TSD), heart tissue TBARS (^●p ≤ 0.001 for DC vs. SD; ^●●p ≤ 0.001 for DC vs. TSD), and muscle tissue TBARS (^§ ≤ 0.001 for DC vs. SD; ^§§ ≤ 0.001 for DC vs. TSD; ^§§§ ≤ 0.001 for TD vs. SD; ^§§§§ ≤ 0.0010 for TD vs. TSD). The DC vs. TD and SD vs. TSD groups were analyzed using Student’s t-test. ns = no significant difference. n = 7–8 (in triplicate) in all experimental groups