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Publication
Coupling of energy intake and energy expenditure across a temperature spectrum:
impact of diet-induced obesity in mice.
Authors Ono-Moore KD, Rutkowsky JM, Pearson NA, Williams DK, Grobe JL, Tolentino T,
Lloyd KCK, Adams SH
Submitted By Submitted Externally on 12/3/2021
Status Published
Journal American journal of physiology. Endocrinology and metabolism
Year 2020
Date Published 9/1/2020
Volume : Pages 319 : E472 - E484
PubMed Reference 32691631
Abstract Obesity and its metabolic sequelae are implicated in dysfunction of the
somatosensory, sympathetic, and hypothalamic systems. Because these systems
contribute to integrative regulation of energy expenditure (EE) and energy
intake (EI) in response to ambient temperature (Ta) changes, we hypothesized
that diet-induced obesity (DIO) disrupts Ta-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 each) to study DIO-low gainers (Q1) versus -high gainers (Q4). EI and
indirect calorimetry (IC) were measured over 3 days 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. We conclude that 1) systems
controlling Ta-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
Ta-associated EI/EE coupling.




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