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Somatropin is a human growth hormone that helps children grow taller and adults add muscle mass. As the child ages, the body loses its ability to produce somatropins and the children’s body starts to lose muscle mass. People with obesity often experience these changes, and it is thought that the loss of muscle mass may be responsible for the development of the condition known as sarcopenia.

A new study, published in Cell Metabolism, shows that the activity of genes in the muscle and liver has an impact on obesity. Using the same genome-sequencing technique as the current study, scientists found that those with a gene known as SH2B18 (also known as SH1B18) had a higher weight gain than those who lacked this gene.

The new study suggests that this may be because the cells in the liver lack the gene, but since there’s no one specific gene that is associated with obesity, it may be common to have the other, lesser-known SH1B18.

« This may be a reason why people with obesity might have normal liver function. But in addition, the liver often isn’t metabolically active, » Dr. Aravind N, Suthanandam, M.L., and colleagues wrote.

The scientists also found that the lack of SH1B18 may increase insulin resistance. Insulin resistance, or glucose intolerance, is associated with diseases like diabetes and high blood pressure. When liver cells lack SH1B18, the cells have less sensitivity to insulin and insulin resistance can increase.

The researchers suspect that if they can figure out what exactly these genes are doing, they may be able to treat some of the health problems associated with obesity.

« We don’t want to overstate the significance of these results, » said Dr. N, Suthanandam. « But this study raises exciting questions. Specifically, do these results support the idea that SH1B18-deficient cells could provide a target for treatments that target insulin-sensitive cells that are critical for metabolic health? » he said.

« This study raises exciting questions, » Dr. Aravind N, Suthanandam, M.L., and colleagues wrote. « Specifically, do these results support the idea that SH1B18-deficient cells could provide a target for treatments that target insulin-sensitized cells that are critical for metabolic health? » he said.

Dr. Suthanandam added that while the next step is to figure out what specific genes in particular are responsible for these effects, « I

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