Gene involved in learning may hold key to obesity treatment

Researchers have discovered that the regulation of a gene involved in brain functions such as memory and learning can also help treat or prevent development of obesity caused by consumption of high-fat diet.


“It’s well known that the brain is involved in the development of obesity, but how a high-fat diet changes the brain so it triggers the accumulation of body fat is still unclear,” says senior study author Dr. Makoto Fukuda, an assistant professor at the Baylor and Texas Childrens Hospital.

Fukudas team used a mouse model to study a gene called Rap1, which is expressed in a variety of tissues, including the brain where it is involved in functions such as memory and learning. However, the role of Rap1 in keeping energy balance was not revealed in previous studies.

The researchers used two groups of mice in their experiment “ the one which contained genetically engineered rodents to lack the Rap1 gene and the other which had a functional Rap 1 gene.


They fed the mice in both groups a high-fat diet in which 60 per cent of the calories came from fat. As expected, the control mice with a working Rap1 gene gained weight, but, in comparison, the mice that lacked Rap 1 had markedly reduced body weight and less body fat.

Interestingly, when both groups of mice were fed a normal diet, both showed similar weights and body fat.

“We observed that the mice lacking Rap1 were not more physically active. However, they ate less and burned more body fat than mice with Rap1,” says Dr. Fukuda.

“These observations were associated with the hypothalamus producing more of a hormone that reduces appetite, called POMC, and less of hormones that stimulate appetite, called NPY and AgRP,” the researcher adds. These mice also had lower levels of blood glucose and insulin than controls.

Dr. Fukudas team also studied whether leptin, the ‘satiety hormone’ produced by fatty tissue that helps regulate body weight by inhibiting appetite, changed in mice lacking Rap1.

It has been found that obese people do not respond to leptin’s signals of satiety, and the blood levels of leptin are higher than those in non-obese people. Leptin resistance is a hallmark of human obesity.

Significantly, the researchers found that mice that lacked Rap1 and ate a high-fat diet did not develop leptin resistance.

The study, published recently in the open-access journal Cell Reports, concluded that consuming a high-fat diet results in changes in the brain that increase Rap1 activity, which in turn leads to a decreased sensitivity to leptin, and this sets the body on a path to obesity.

The research work was supported by the Current Research Information System (CRIS), which provides data and reports on studies, education and extension activities undertaken by the National Institute of Food and Agriculture of the US.

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