Worldwide obesity has more than doubled since 1980. In 2014, there were over 600 million people classified as obese, making up 13% of the global population. Researchers have long known that humans produce at least two types of fat tissue, white and brown. Each white fat cell stores energy in the form of a single large, oily droplet which is otherwise relatively inert. In contrast, brown fat cells contain many smaller droplets, as well as chestnut-colored molecular machines known as mitochondria that burn up the droplets to generate heat.
Therefore, much work has been done on how to incite the body to produce extra brown fat and/or stimulate existing brown fat, to convert a larger number of calories into heat, reducing unhealthy deposits of white fat in the process. Now, researchers at Université Catholique de Louvain have, for the first time, kick-started the natural process by which genetically predisposed obese mice gain weight, opening up a new potential approach to stave-off obesity. The team state that their findings suggest that impaired brown adipose tissue (BAT), otherwise known as ‘brown fat’, drives obesity, and by stimulating heat production in this fatty tissue, weight-management and glucose tolerance can be improved. The study was presented at The International Liver CongressTM.
Previous studies show that brown fat has proved difficult to study due to the fact it was so hard to find in adults. Also, the easiest way to stimulate brown fat is to expose people to low temperatures which can be unappealing. Now, several new methodologies can find and measure brown fat within the body, with several experiments able target brown fat and cool the body to burn calories. However, the holy grail is to develop ways to multiply the number of brown fat cells in the body or boost their activity; as well as transform white fat cells into tissue that behaves a lot like brown fat, ‘beige’ or ‘brite’ (brown in white) fat. The current study shows that stimulating energy consumption in brown fat, can improve weight-management and glucose control in a mouse model of metabolic syndrome.
The current study utilised male foz/foz mice which are prone to developing metabolic syndrome, characterised by obesity, high blood pressure and diabetes. The foz/foz mice were studied alongside wild-type mice, that do not have the same metabolic predisposition. Results show that metabolic syndrome in foz/foz mice was linked to impaired thermogenesis in brown adipose tissue in response to high fat diet feeding or to cold exposure. The lab hypothesize that this could contribute to lower energy expenditure and increase fat storage.
The group stimulated brown adipose tissue activity in the overweight foz/foz mice with intermittent cold exposure, β3-adrenergic agonist treatment and brown adipose tissue transplantation from wild type mice. Data findings show the foz/foz mice that had stimulated brown adipose tissue activity experienced decreased body weight gain and improved glucose tolerance compared to untreated foz/foz mice.
The team surmise their findings show that certain cellular impairments found in one’s metabolic make-up increases the likelihood of obesity and the associated issues, such as diabetes and high blood pressure. They go on to add that by intervening to reverse such impairments using a mouse model, they have shown effective therapeutic strategies could be developed to combat obesity and associated comorbidities. For the future, the researchers state that this data uncovers a smart approach that could help the global medical community develop effective interventions to address the global obesity epidemic.