I found a new clue to obesity treatment...Increase energy consumption by promoting sympathetic nerves through hormones
Nov 18, 2025
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Professor Kim Ji-yoon and Lee Myung-sik, chair professor of the Medical Life Research Institute at Soonchunhyang University, led the study as corresponding authors, and the study was published in the 2025 edition of the International Journal of Life Sciences 'Experimental and Molecular Medicine' (IF 12.9, Nature sister journal), and the title of the paper is 'GDF15 regulations development and growth of sympathetic energy expansion and thermal genesis'.
Until now, GDF15 has been known as a hormone that suppresses appetite and stimulates sympathetic nerves to increase energy consumption. Simply put, in the body's energy consumption system, GDF15 was understood to serve as a 'accelerator (accelerator pedal)'.
However, in this study, Professor Kim Ji-yoon's team newly discovered that GDF15 does not just step on the accelerator, but promotes the growth and development of sympathetic neurons. Sympathetic nerves are neural networks that control our body's energy consumption and send signals to fat cells to generate heat ('thermal generation', thermal genesis) or to consume energy.
The research team proved through animal experiments that GDF15 increases energy consumption by increasing the density of sympathetic nerves in adipose tissue. Mice with overexpression of GDF15 increased sympathetic nerves in adipose tissue and improved body temperature maintenance. Conversely, mice lacking the GDF15 gene showed lower sympathetic nerve density and reduced energy consumption.
Furthermore, the research team found that the receptor (GFRAL) of GDF15 does not exist only in the brain as previously known, but also in the peripheral sympathetic ganglia. This is a finding that suggests a new pathway in which GDF15 can be directly involved in neural growth without going through the brain.
This study is of great academic significance in that it has extended the function of GDF15 from 'neural activation' to a new concept of 'neural growth and development control'. This means that GDF15 does not simply send a signal to use energy, but rather acts as a key factor in increasing long-term energy consumption efficiency by redesigning and expanding the neural structure itself that sends and receives the signal.
These findings suggest the potential to lead to the development of new treatments for not only obesity but also various metabolic diseases such as diabetic neuropathy and sympathetic nerve damage caused by aging. In particular, it is noteworthy that by newly identifying the GFRL receptor that also exists in the peripheral sympathetic nervous system, a new target strategy away from the 'brain-centered approach' was proposed when developing new drugs, and a new approach was proposed to correct the energy metabolism imbalance, the root cause of obesity, at the neural level.
Professor Lee Myung-sik said, "This study not only presents a new paradigm for obesity treatment, but also opens a new research direction: treatment of metabolic diseases through structural restoration of the nervous system."GDF15 could be a fundamental solution to conditions such as aging and diabetes if it could restore a damaged sympathetic neural network "
Professor Kim Ji-yoon said "Until now, GDF15 was thought to be simply the role of 'turn on' the energy consumption switch', but this study confirmed its function as an architect to strengthen the 'wiring' of the energy system."It could lead to the development of customized obesity treatments or nerve regeneration treatments based on GDF15 in the future."
Meanwhile, this study was conducted with the support of the National Research Foundation of Korea (NRF) and the Korea Health Industry Promotion Agency (KHIDI).
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This article was translated by Naver AI translator.
