Following publication of the original article [1], the authors reported a misalignment error of the x-axis in Fig. 1b; in addition, there were two typos and two formatting errors. The revised Fig. 1b and revised text is indicated hereafter. The changes have been highlighted in bold typeface.
Fig. 1
a Difference between calculated and measured energy expenditure over time. b Percentage of patients in RQ groups (≤ 0.8 vs. > 0.8) between survivors and non-survivors
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The sentence currently reads:
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The metabolic profiles differed between survivors and non-survivors (Fig. 1a). Both groups had negative energy balance during fasting state. Survivors transitioned to a hypermetabolic state following feeding initiation, achieving positive energy balance. Non-survivors remained hypometabolic despite feeding.
The sentence should read:
The metabolic profiles differed between survivors and non-survivors (Fig. 1a). Both groups had negative energy balance during fasting state. Survivors transitioned to a hypermetabolic state following feeding initiation, achieving positive energy balance. Non-survivors remained hypometabolic despite feeding.
The sentence currently reads:
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Our study advances the understanding of energy balance and substrate utilization in sepsis. During fasting, low insulin with elevated counter-regulatory hormones promotes lipolysis; muscle glycogen is depleted at an exponential rate greater than athletes running marathons [4]. The predominant energy substrate switches from carbohydrates to lipids—the hallmark of fasting physiology. This explains the low RQ in early sepsis, when patients are preferentially utilizing lipids (RQ ≤ 0.8) during permissive underfeeding [5]. The hypermetabolic state and inability for non-survivors to transit to carbohydrate utilization suggest ongoing debilitating mitochondrial dysfunction, consistent with associated multi-organ failure [6]. However, whether adjusting the feeding types and regimen to alter these patterns and improve outcomes remain unknown.
The sentence should read:
Our study advances the understanding of energy balance and substrate utilization in sepsis. During fasting, low insulin with elevated counter-regulatory hormones promotes lipolysis; muscle glycogen is depleted at an exponential rate greater than athletes running marathons [4]. The predominant energy substrate switches from carbohydrates to lipids—the hallmark of fasting physiology. This explains the low RQ in early sepsis, when patients are preferentially utilizing lipids (RQ ≤ 0.8) during relative underfeeding [5]. The hypometabolic state and inability for non-survivors to transit to carbohydrate utilization suggest on-going debilitating mitochondrial dysfunction, consistent with associated multi-organ failure [6]. However, whether adjusting the feeding types and regimen to alter these patterns to improve outcomes remain unknown.
This has now been included in this correction article.
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