School of Food Science and Nutrition, Faculty of Environment, University of Leeds, Leeds, United Kingdom.
School of Psychology, Faculty of Medicine and Health, University of Leeds, Leeds, United Kingdom; Steno Diabetes Center Copenhagen, Gentofte, Denmark.
Can J Diabetes. 2020 Dec;44(8):768-774. doi: 10.1016/j.jcjd.2020.10.018. Epub 2020 Nov 4.
Hyperglycemia is the defining feature of type 1 diabetes (T1D) and type 2 diabetes (T2D) and results from deficient insulin production, impaired insulin-stimulated glucose uptake or both. It is now well established that hyperglycemia results in profound metabolic complications, but the effect of diabetes and its associated metabolic effects on homeostatic and hedonic appetite control has received less attention. Inappropriate food choices and excess food intake might promote weight gain, further exacerbating the metabolic consequences of T1D and T2D. The need to control blood glucose through diet, physical activity and/or medication as a consequence of impaired insulin secretion and/or sensitivity adds a further level of physiological and behavioural complexity to the processes underlying food choice and appetite control. Alterations in appetite-related processes have been noted in people with T2D, but the effect of T1D on appetite is largely unexplored. Peripheral neuroendocrine signalling appears disrupted in people with T2D, and brain regions involved in the central modulation of appetite might display central insulin resistance. However, it is difficult to isolate the consequences of T2D from those of obesity. Health-care policy advocates the use of physical activity as a means of preventing and treating T2D via the promotion of weight loss and its independent influence on insulin sensitivity. Exercise-induced perturbations to energy balance can elicit biological and behavioural compensation that attenuates weight loss, and diabetes pathophysiology might alter the strength of such compensation. However, the effect of exercise on appetite in people living with diabetes has yet to be fully explored.
高血糖是 1 型糖尿病（T1D）和 2 型糖尿病（T2D）的特征，是由胰岛素产生不足、胰岛素刺激的葡萄糖摄取受损或两者共同引起的。现在已经明确，高血糖会导致严重的代谢并发症，但糖尿病及其相关代谢效应对体内平衡和享乐性食欲控制的影响却没有得到太多关注。不适当的食物选择和过量进食可能会导致体重增加，进一步加剧 T1D 和 T2D 的代谢后果。由于胰岛素分泌和/或敏感性受损，需要通过饮食、体力活动和/或药物来控制血糖，这给食物选择和食欲控制的潜在过程增加了进一步的生理和行为复杂性。在 T2D 患者中已经注意到与食欲相关的过程发生了改变，但 T1D 对食欲的影响在很大程度上尚未得到探索。外周神经内分泌信号似乎在 T2D 患者中受到干扰，而参与食欲中枢调节的大脑区域可能显示出中枢胰岛素抵抗。然而，很难将 T2D 的后果与肥胖的后果分开。医疗保健政策提倡通过促进减肥和独立影响胰岛素敏感性来使用体力活动作为预防和治疗 T2D 的手段。运动引起的能量平衡波动会引起生物学和行为学补偿，从而减轻体重减轻，而糖尿病病理生理学可能会改变这种补偿的强度。然而，运动对糖尿病患者食欲的影响尚未得到充分探索。
