In the absence of UCP1-mediated diet-induced thermogenesis, obesity is augmented even in the obesity-resistant 129S mouse strain

Feb 27, 2019American journal of physiology. Endocrinology and metabolism

Lack of a key heat-producing protein increases obesity even in mice usually resistant to weight gain

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Abstract

UCP1 ablation led to increased obesity in high-fat diet- and cafeteria-fed 129S mice.

Absence of UCP1 resulted in greater weight gain, body fat mass, and fat depot size in mice, despite similar or lower food intake.
The increase in obesity was associated with decreased energy expenditure.
Wild-type mice on high-fat or cafeteria diets showed increased levels of UCP1 protein in brown adipose tissue.
High-fat and cafeteria diets also enhanced norepinephrine-induced oxygen consumption in wild-type mice.
A positive correlation was observed between body fat and total BAT UCP1 protein content.
No evidence of diet-induced thermogenesis was detected in UCP1-ablated mice.

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The attractive tenet that recruitment and activation of brown adipose tissue (BAT) and uncoupling protein 1 (UCP1) could counteract the development of obesity and its comorbidities in humans has been experimentally corroborated mainly by experiments demonstrating that UCP1-ablated mice on a C57Bl/6 background (exempt from thermal stress) become more obese when fed a high-fat diet. However, concerns may be raised that this outcome of UCP1 ablation is restricted to this very special inbred and particularly obesity-prone mouse strain. Therefore, we have examined to which degree UCP1 ablation has similar metabolic effects in a mouse strain known to be obesity resistant: the 129S strain. For this, male 129S2/sv or 129SV/Pas mice and corresponding UCP1-knockout mice were fed chow or a high-fat or a cafeteria diet for 4 wk. The absence of UCP1 augmented obesity (weight gain, body fat mass, %body fat, fat depot size) in high-fat diet- and cafeteria-fed mice, with a similar or lower food intake, indicating that, when present, UCP1 indeed decreases metabolic efficiency. The increased obesity was due to a decrease in energy expenditure. The consumption of a high-fat or cafeteria diet increased total BAT UCP1 protein levels in wild-type mice, and correspondingly, high-fat diet and cafeteria diet-fed mice demonstrated increased norepinephrine-induced oxygen consumption. There was a positive correlation between body fat and total BAT UCP1 protein content. No evidence for diet-induced adrenergic thermogenesis was found in UCP1-ablated mice. Thus, the obesity-reducing effect of UCP1 is not restricted to a particular, and perhaps not representative, mouse strain.

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In the absence of UCP1-mediated diet-induced thermogenesis, obesity is augmented even in the obesity-resistant 129S mouse strain

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