In a recent study published within the journal Philosophical Transactions of the Royal Society B, researchers discuss diet-induced thermogenesis and determine whether reduced uncoupled protein 1 (UCP1) activity in brown adipose tissue could cause obesity.

Study: Brown adipose tissue: can it keep us slim? A discussion of the evidence for and against the existence of diet-induced thermogenesis in mice and men. Image Credit: Lightspring / Shutterstock.com

Background

Brown adipose tissue uses food or stored energy to generate heat, a process which will occur even when there is no such thing as a need for thermoregulation. This phenomenon, otherwise generally known as diet-induced thermogenesis, has led many researchers to analyze how this process will be manipulated to combat the present obesity epidemic.

Previous research indicates that obesity may arise as a result of reduced brown adipose, which can also be indicative of low diet-induced thermogenesis. Despite these observations, many researchers have questioned the existence of diet-induced thermogenesis, because it is contrary to the thought of maximizing energy efficiency.

The commonly accepted hypothesis is that this process would facilitate survival on a eating regimen low in proteins; nevertheless, this has not been proven experimentally. The truth is, high-fat diets contain sufficient protein and still induce diet-induced thermogenesis, which raises the likelihood that this phenomenon may arise to counter increased adiposity.

Exploring the phenomenon of diet-induced thermogenesis in mice is difficult, as many animals produce a thermogenic response to eating throughout the digestion of food and the transfer of energy into lipids. As in comparison with this natural process, the notion of diet-induced thermogenesis as an evolutionary response to forestall obesity must occur only when needed and when an organism consumes excess energy.   

Metabolic experiments in mice

In mice fed a high-fat eating regimen, the increased obligatory diet-induced thermogenic response is higher than in chow diet-fed mice. Although each mouse models consumed similar quantities of food, the high-fat eating regimen comprised a much higher ratio of fats than the carbohydrate-rich chow eating regimen, with fats related to lower obligatory thermogenesis.

Thermogenesis, which is a direct response to feeding, appears to rely on the presence of UCP1. For instance, wild-type mice exhibit an increased thermogenic response in comparison with the absence of this response in UCP1 knockout mice.

Although there’s a positive correlation between obesity, the recruitment of brown adipose tissue, and increased amounts of UCP1, UCP1 is just partly efficient in regulating energy levels under homeostatic control. Furthermore, studies in mice haven’t indicated that the absence of UCP1 led to obesity. 

Moreover, researchers have neither found evidence of spontaneous obesity in UCP1 knockout mice on different diets and under various genetic backgrounds nor obesity-protecting effects of UCP1 ablation in wild-type mice.

Brown adipose tissue-mediated diet-induced thermogenesis in humans

In humans, previous studies have observed a low amount of brown adipose tissue in obese people. Studies using radioactive oxygen have confirmed the meal-induced activation of human brown adipose tissue. In humans, glucose uptake in brown adipose tissue can also be influenced by insulin stimulation, thus indicating a possible false negative correlation between brown adipose tissue activity and obesity in humans.

Thus far, no genome-wide association study (GWAS) for obesity-related issues has identified the UCP1 gene in humans. Although the A3826G polymorphism within the upstream region of the UCP1 gene has been related to higher expression of UCP1, its observed effects have been inconsistent.

Likewise, researchers haven’t identified a UCP1 knockout gene in humans. The metabolic consequence of mutations within the UCP1 gene also stays unclear.

Conclusions

Food plan-induced thermogenesis in mice could also be observable under certain conditions, as demonstrated by the absence of brown adipose tissue contributing to obesity in UCP1 knockout mice.

Previous studies have estimated that total thermogenesis from brown adipose tissue in a mean adult man corresponds to a body weight change of as much as 10 kilograms (kg) every year. Thus, diet-induced brown-fat-derived thermogenesis likely occurs in humans and affects a person’s risk of obesity, provided that other risk aspects for obesity are also present.

Future studies are needed to analyze the obesity-inducing effects of alterations in UCP1 levels in murine models. Likewise, future human studies are required to find out the causation between obesity and reduced brown adipose tissue activity.