A model of poorly controlled type 1 diabetes mellitus and its treatment with aerobic exercise training

Melling, C.W. James; Grisé, Kenneth N.; Hasilo, Craig; Fier, B.; Milne, Kevin; Karmazyn, Morris; Noble, Earl G.

doi:10.1016/j.diabet.2013.02.004

Cited by 26 publications

(30 citation statements)

References 60 publications

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“…After the confirmation of two consecutive blood glucose measures of Ն18 mmol/l, rats received a surgically implanted subcutaneous insulin pellet (release rate 1 IU/12 h, Linplant, Linshin, Toronto, Ontraio, Canada). Each week, pellet size was adjusted (increased or decreased) to maintain moderate hyperglycemia (fedstate blood glucose obtained during dark cycle ϳ14.5 mmol/l) (44).…”

Section: Studymentioning

confidence: 99%

Exercise training enhances insulin-stimulated nerve arterial vasodilation in rats with insulin-treated experimental diabetes

Olver

McDonald

Grisé

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Insulin stimulates nerve arterial vasodilation through a nitric oxide (NO) synthase (NOS) mechanism. Experimental diabetes reduces vasa nervorum NO reactivity. Studies investigating hyperglycemia and nerve arterial vasodilation typically omit insulin treatment and use sedentary rats resulting in severe hyperglycemia. We tested the hypotheses that 1) insulin-treated experimental diabetes and inactivity (DS rats) will attenuate insulin-mediated nerve arterial vasodilation, and 2) deficits in vasodilation in DS rats will be overcome by concurrent exercise training (DX rats; 75-85% VO2 max, 1 h/day, 5 days/wk, for 10 wk). The baseline index of vascular conductance values (VCi = nerve blood flow velocity/mean arterial blood pressure) were similar (P ≥ 0.68), but peak VCi and the area under the curve (AUCi) for the VCi during a euglycemic hyperinsulinemic clamp (EHC; 10 mU·kg(-1)·min(-1)) were lower in DS rats versus control sedentary (CS) rats and DX rats (P ≤ 0.01). Motor nerve conduction velocity (MNCV) was lower in DS rats versus CS rats and DX rats (P ≤ 0.01). When compared with DS rats, DX rats expressed greater nerve endothelial NOS (eNOS) protein content (P = 0.04). In a separate analysis, we examined the impact of diabetes in exercise-trained rats alone. When compared with exercise-trained control rats (CX), DX rats had a lower AUCi during the EHC, lower MNCV values, and lower sciatic nerve eNOS protein content (P ≤ 0.03). Therefore, vasa nervorum and motor nerve function are impaired in DS rats. Such deficits in rats with diabetes can be overcome by concurrent exercise training. However, in exercise-trained rats (CX and DX groups), moderate hyperglycemia lowers vasa nervorum and nerve function.

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Section: Studymentioning

confidence: 99%

Exercise training enhances insulin-stimulated nerve arterial vasodilation in rats with insulin-treated experimental diabetes

Olver

McDonald

Grisé

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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“…It is believed that the model of induction to type 1 diabetes, with massive destruction of pancreatic beta cells, requires other stimuli beyond the application of moderate physical exercise to mobilize a greater amount of glucose in the body 24 . Furthermore, the fact that the animals had free access to ration intake may have contributed to the maintenance of above-normal glucose levels and, thus, contributed to the maintenance of the evaluated clinical signs.…”

mentioning

confidence: 99%

Previous physical exercise slows down the complications from experimental diabetes in the calcaneal tendon

et al. 2016

MLTJ

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SummaryBackground: the complications caused by diabetes increase fragility in the muscle-tendon system, resulting in degeneration and easier rupture. To avoid this issue, therapies that increase the metabolism of glucose by the body, with physical activity, have been used after the confirmation of diabetes. We evaluate the biomechanical behavior of the calcaneal tendon and the metabolic parameters in rats induced to experimental diabetes and submitted to pre-and post-induction exercise. Methods: 54-male-Wistar rats were randomly divided into four groups: Control Group (CG), Swimming Group (SG), Diabetic Group (DG), and Diabetic Swimming Group (DSG). The trained groups were submitted to swimming exercise, while unexercised groups remained restricted to the cages. Metabolic and biomechanical parameters were assessed. Results: the clinical parameters of DSG showed no change due to exercise protocol. The tendon analysis of the DSG showed increased values for the elastic modulus (p<0.01) and maximum tension (p<0.001) and lowest value for transverse area (p<0.001) when compared to the SG, however it showed no difference when compared to DG. Conclusion:the homogeneous values presented by the tendons of the DG and DSG show that physical exercise applied in the pre-and post-induction wasn't enough to promote a protective effect against the tendinopathy process, but prevent the progress of degeneration.

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“…In relation to the clinical signs evaluated, such as polyuria, polydipsia, and polyphagia (striking features in diabetic patients), which were observed three days after diabetes induction, showed no return to normal at the end of the experiment in this preventive and continuous protocol of exercise. It is believed that the model of induction to type 1 diabetes, with massive destruction of pancreatic beta cells, requires other stimuli beyond the application of moderate physical exercise to mobilize a greater amount of glucose in the body 24 . Furthermore, the fact that the animals had free access to ration intake may have contributed to the maintenance of above-normal glucose levels and, thus, contributed to the maintenance of the evaluated clinical signs.…”

Section: Discussionmentioning

confidence: 99%

Previous physical exercise slows down the complications from experimental diabetes in the calcaneal tendon

Bezerra

Nery

Silveira

et al. 2019

Muscle Ligaments and Tendons J

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Background: the complications caused by diabetes increase fragility in the muscle-tendon system, resulting in degeneration and easier rupture. To avoid this issue, therapies that increase the metabolism of glucose by the body, with physical activity, have been used after the confirmation of diabetes. We evaluate the biomechanical behavior of the calcaneal tendon and the metabolic parameters in rats induced to experimental diabetes and submitted to pre-and post-induction exercise. Methods: 54-male-Wistar rats were randomly divided into four groups: Control Group (CG), Swimming Group (SG), Diabetic Group (DG), and Diabetic Swimming Group (DSG). The trained groups were submitted to swimming exercise, while unexercised groups remained restricted to the cages. Metabolic and biomechanical parameters were assessed. Results: the clinical parameters of DSG showed no change due to exercise protocol. The tendon analysis of the DSG showed increased values for the elastic modulus (p<0.01) and maximum tension (p<0.001) and lowest value for transverse area (p<0.001) when compared to the SG, however it showed no difference when compared to DG.Conclusion: the homogeneous values presented by the tendons of the DG and DSG show that physical exercise applied in the pre-and post-induction wasn't enough to promote a protective effect against the tendinopathy process, but prevent the progress of degeneration.

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A model of poorly controlled type 1 diabetes mellitus and its treatment with aerobic exercise training

Cited by 26 publications

References 60 publications

Exercise training enhances insulin-stimulated nerve arterial vasodilation in rats with insulin-treated experimental diabetes

Exercise training enhances insulin-stimulated nerve arterial vasodilation in rats with insulin-treated experimental diabetes

Previous physical exercise slows down the complications from experimental diabetes in the calcaneal tendon

Previous physical exercise slows down the complications from experimental diabetes in the calcaneal tendon

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