逻辑错误

Studies addressing the association between EE and weight gain found a low resting energy expenditure (REE) to be a predictor of weight gain [23,24]. This finding fuelled a discussion about whether obesity is due to high EI or low EE [25,26]. As most obese subjects tended to have a high rather than a low EE [27], the focus of research had shifted from EE to EI as the major determinant of a positive energy balance and obesity [13,28]. The assessment of EI, however, is inaccurate and biased in overweight subjects [29,30].Mathematical modelling of energy balance revealed that pharmacological inhibition of sodium-glucose co-transporter 2 (SGLT2), used for metabolic control of patients with type 2 diabetes mellitus, led to an increase in EI whereas EE remained unchanged. This is in line with genetic studies showing that defects in the EI underlies all known causes of obesity. However, a second look at the SGLT2inhibition data, showed that the increase in EI was lesser than the energy losses, leading to an energy gap, resulting in an involuntary weight loss. The increase in EI could not match EE. EE, on the other hand, was kept constant suggesting that it is tightly controlled. This experience showed that there is no tight feedback control of EI by EE, giving credence to the idea that EE and not EI is under tight control and is therefore the major determinant of energy balance

针对EE和体重增加之间关系的研究发现，低静息能量消耗(REE)是体重增加的一个预测因素。这一发现引发了肥胖是由高EI还是低EE造成的讨 论。大多数肥胖受试者的EE倾向于较高而不是较低21,因此，研究的重点已经从EE转移到EI,将EI视为正能量平衡和肥胖的主要决定因素13.2。然，在超重的受试者中，对EI的评估是不准确且有偏倚的。能量平衡的数学模型显示，用于2型糖尿病患者的代谢控制的钠-葡萄糖共转运体2(SGLT2)的药理抑制可以导致EI的增加，而使EE保持不变。这与基因研究结果一致，即EI缺陷是所有已知肥胖原因的基础。然而，对SGLT2抑制数据的二次观察研究显示，EI的增加小于能量损失，从而导致体重减轻。EI的增加无法与EE的增加相匹配。而另一方面，EE则保持不变，表明其受到了严格的控制。这一经验表明，EE对EI没有严格的反馈控制，证明EE而非EI受到严格控制的观点，因此，EE是能量守恒的主要决定因素。

能量消耗（EE）保持不变，受严格控制，能量摄入（EI）并不受能量消耗（EE）的严格反馈控制，那肯定是能量摄入（EI）才是能量平衡的主要决定因素

修改：这一经验表明，EE未对EI严格反馈控制，证明只有EE（而非EI）受到了严格控制，因此EI是能量平衡的主要决定因素。