Obesity and its metabolic sequelae are implicated in dysfunction of the somatosensory, sympathetic, and hypothalamic systems. Since these systems contribute to integrative regulation of energy expenditure (EE) and energy intake (EI) in response to ambient temperature (T_a) changes, we hypothesized that diet-induced obesity (DIO) disrupts T_a-associated EE-EI coupling. C57BL/6N male mice were fed a high fat diet (HFD, 45% kcal) or low fat diet (LFD, 10% kcal) for ~9.5 wk; HFD mice were then split into body weight (BWT) quartiles (n=8 ea.) to study DIO-low gainers (Q1) vs. -high gainers (Q4). EI and indirect calorimetry (IC) were measured over 3 d each at 10°C, 20°C, and 30°C. Responses did not differ between LFD, Q1 and Q4: EI and BWT-adjusted EE increased rapidly when transitioning toward 20°C and 10°C. In all groups, EI at 30°C was not reduced despite lower EE, resulting in positive energy balance and respiratory exchange ratios consistent with increased de novo lipogenesis, energy storage, and relative hyperphagia. Conclusions: (1) systems controlling T_a-dependent acute EI/EE coupling remained intact in obese mice, and (2) Rapid coupling of EI/EE at cooler temperatures is an important adaptation to maintain energy stores and defend body temperature, but less critical at thermoneutrality. A post hoc analysis using digestible EI plus IC-calculated EE suggests that standard IC assumptions for EE calculation require further validation in the setting of DIO. The experimental paradigm provides a platform to query the hypothalamic, somatosensory, and sympathetic mechanisms that drive T_a-associated EI/EE coupling.

中文翻译：

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温度范围内能量摄入和能量消耗的耦合：饮食引起的肥胖对小鼠的影响。

肥胖及其代谢后遗症与躯体感觉、交感神经和下丘脑系统功能障碍有关。由于这些系统有助于响应环境温度 (T _a ) 变化对能量消耗 (EE) 和能量摄入 (EI) 的综合调节，我们假设饮食诱导的肥胖 (DIO) 会破坏 T _a-相关的EE-EI耦合。C57BL/6N 雄性小鼠喂食高脂肪饮食（HFD，45% kcal）或低脂肪饮食（LFD，10% kcal）约 9.5 周；然后将 HFD 小鼠分成体重 (BWT) 四分位数 (n = 8 个)，以研究 DIO 低增益者 (Q1) 与高增益者 (Q4)。EI 和间接量热法 (IC) 分别在 10°C、20°C 和 30°C 下测量超过 3 天。LFD、Q1 和 Q4 之间的响应没有差异：当向 20°C 和 10°C 过渡时，EI 和 BWT 调整后的 EE 迅速增加。在所有组中，尽管 EE 较低，但 30°C 下的 EI 并未降低，导致正能量平衡和呼吸交换比率与增加的脂肪新生、能量储存和相对摄食量一致。结论：(1) 控制 T _{a 的}系统依赖的急性 EI/EE 耦合在肥胖小鼠中保持完整，并且 (2) EI/EE 在较低温度下的快速耦合是维持能量储存和保护体温的重要适应，但在热中性方面不太重要。使用可消化 EI 加上 IC 计算的 EE 的事后分析表明，EE 计算的标准 IC 假设需要在 DIO 设置中进一步验证。实验范式提供了一个平台来查询驱动 T _a相关 EI/EE 耦合的下丘脑、体感和交感神经机制。