"Protein of obesity"

Gastrokin-1 suspected of provoking obesity

Anastasia Kuznetsova, N+1

The researchers found that in the absence of the protein gastrokin-1, mice are more resistant to the appearance of excess body weight. In such animals, the number of Firmicutes bacteria involved in the development of obesity decreases. Scientists have hypothesized that gastrokin-1 acts as a link between the microbiome and metabolism. The study was published in Scientific Reports (Overstreet et al., Gastrokine-1, an anti-amyloidogenic protein secreted by the stomach, regulates diet-induced obesity).

Rosstat in 2018 conducted a study of the diet of Russians and calculated the proportion of obese patients. It turned out that 17.8% of men and 24.5% of women are obese, another 46.9% of men and 34.7% of women are overweight. The situation is not much better in the world: 11 percent of men and 15 percent of women are diagnosed with obesity, and 39 percent of men and 40 percent of women are overweight. Obesity is usually treated with diet and exercise, in some cases resorting to bariatric surgery. In the treatment of obesity, it is difficult to achieve a long-term effect, so the search for effective drugs is still relevant. To develop them, it is necessary to understand the physiological regulators underlying the occurrence of obesity.

Many organs are involved in the development of obesity and metabolic disorders: liver, adipose tissue, skeletal muscles, pancreas, intestines, and stomach. Scientists have noticed that gastric surgeries to treat obesity cause changes in the microbiome. When transplanting such a microbiome to mice, a decrease in their adipose tissue was observed, which indicates the important role of the stomach and its microbiota in the development of obesity. Gastrokin-1 is a protein specific exclusively to the stomach. It is secreted by mucocytes – cells that produce mucus. The physiological function of this protein is not yet clear. Scientists hypothesize that it can affect the microbiota and metabolism, as it is secreted into the stomach cavity.

American scientists led by David L. Boone from Indiana University decided to test how gastrokin-1 is associated with obesity. Scientists turned off this protein in mice and fed them food with a high fat content. Then their metabolic parameters, adipose tissue and liver mass were measured and the composition of microbiota in feces was analyzed. The data were compared with the indicators of mice in which the protein gastrokin-1 functioned. The Welch t-test was used for statistical analysis.

Mice with disabled gastrokin-1 were resistant to obesity. Their adipose tissue weight was on average 2.9 grams versus 10.3 grams in the control group (p < 0.005). The liver also weighed less than in mice with preserved protein: 1.1 grams and 1.3 grams, respectively (p < 0.05). Also, the number of Firmicutes bacteria involved in the development of obesity was reduced in their microbiome.

The researchers suggested that gastrokin-1 affects obesity by changing the composition of the microbiota. Bacteria are able to produce amyloids that form fibers on which microorganisms form biofilms. Gastrokin-1 can prevent the formation of such biofilms and thus affect the growth of bacteria – exactly how, remains to be seen.

Many molecular mechanisms of the development of obesity have not yet been discovered, but the relationship of obesity with the composition of the gut microbiome has been known for a long time. Scientists have even created a drug based on bacteria to improve carbohydrate metabolism in obese people.

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