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首页> 外文期刊>Medical hypotheses >Obesity and inactivity, not hyperglycemia, cause exercise intolerance in individuals with type 2 diabetes: Solving the obesity and inactivity versus hyperglycemia causality dilemma
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Obesity and inactivity, not hyperglycemia, cause exercise intolerance in individuals with type 2 diabetes: Solving the obesity and inactivity versus hyperglycemia causality dilemma

机译：肥胖和不活动，而不是高血糖，导致2型糖尿病的个体中的运动不耐受：解决肥胖和不活跃与高血糖因果关系困境

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Obesity, a sedentary lifestyle and type 2 diabetes are intricately linked conditions contributing to reduced exercise tolerance, significant morbidity, and premature deaths. It is unknown whether the reported exercise intolerance associated with type 2 diabetes is a direct result of the hyperglycemia, the impact of a relatively sedentary lifestyle, or increased adiposity. We hypothesize that obesity and inactivity, not hyperglycemia, cause exercise intolerance in individuals with type 2 diabetes. An analysis of the literature and results from the Goto-Kakizaki (GK) rat model of type 2 diabetes strongly support this hypothesis. GK rats were not sedentary or obese when compared with Wistar control rats and did not have exercise intolerance. Specifically, despite being hyperglycemic, GK rats demonstrated a longer treadmill run time to exhaustion (150.6 +/- 9.0 vs. 77.2 +/- 12,9 min), further distance run (1506 +/- 90 vs. 772 +/- 129 m), more work performed per gram muscle (44.0 +/- 2.8 vs. 21.9 +/- 3.8 kg*m/g) and a small increase in total vertical work performed when accounting for body mass (116.8 +/- 6.3 versus 98.9 +/- 15.2 kg*m). These results document preserved exercise tolerance in the non-obese, non-sedentary GK rat supporting the hypothesis that the reported exercise intolerance in models of type 2 diabetes is dependent on obesity and inactivity. Solving the obesity and inactivity versus hyperglycemia causality dilemma is important in understanding the development of type 2 diabetes and implications for future pharmacological and life style interventions.
机译：肥胖症，久坐不动的生活方式和2型糖尿病是凭证有思想的有助于减少运动耐受性，显着发病率和过早死亡的条件。尚不清楚是否报告的与2型糖尿病相关的运动不耐受是高血糖的直接结果，对相对久坐的生活方式的影响或增加的肥胖。我们假设肥胖症和不活动，而不是高血糖，导致2型糖尿病的个体中的运动不耐受。对2型糖尿病的Goto-Kakizaki（GK）大鼠模型的文献和结果的分析强烈支持这一假设。与Wistar对照大鼠相比，GK大鼠并不沉重或肥胖，并且没有运动不耐受。具体而言，尽管是高血糖，但GK大鼠展示了更长的跑步机运行时间来耗尽（150.6 +/- 9.0与77.2 +/- 12,90分钟），进一步距离运行（1506 +/- 90与772 +/- 129 m），每克肌肉进行的更多工作（44.0 +/- 2.8与21.9 +/- 3.8 kg * m / g），并且在核算体重时，在核算体重时的总垂直工作的小幅增加（116.8 +/- 6.3与98.9 +/- 15.2 kg * m）。这些结果证明了在非肥胖，非久坐的GK大鼠中的运动耐受性，支持的假设，即2型糖尿病模型中报告的运动不耐受依赖于肥胖症和不活动。解决肥胖和不活跃与高血糖因果关系困境对于了解2型糖尿病的发展和对未来药理学和生活方式干预措施的影响很重要。

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