Rutgers scientist describes GLP-1 as a brain circuit signal at Seoul conference

At the 2026 Good Brain Conference in Seoul on Sept. 3, Rutgers professor Fang Zhiping described GLP-1 as a neuromodulator that adjusts signaling in specific brain circuits, not only a gut hormone that suppresses appetite ^[1].

Fang, director of the Brain Metabolism Center at Rutgers Robert Wood Johnson Medical School in the United States, gave the keynote address at the conference, hosted by The Asia Business Daily at The Westin Chosun Hotel Seoul in Sogong-dong, Jung-gu, Seoul. His talk was titled "Glucagon-Like Peptide-1 (GLP-1): From a Metabolic Hormone to a Brain Circuit Signal," under the conference theme "Brain Revolution: The Future of Humanity Changed by GLP-1" ^[1].

GLP-1 is a hormone released from the gut after eating that lowers blood sugar and suppresses appetite, and all anti-obesity drugs currently sold worldwide are designed to mimic it ^[1]. Fang, who said he has spent nearly 20 years researching GLP-1 produced by the brain, argued that this description covers only part of the picture. "Understanding GLP-1 merely as an appetite-suppressing signal is only half the explanation," he said ^[1].

He described GLP-1 as a "manager" that adjusts how strongly signals travel inside the brain, rather than a messenger that only delivers feelings of fullness. "GLP-1 is not just a hormone, but a neuromodulator," he said. Hormones travel through the bloodstream and act across the body, while neuromodulators attach to specific neural circuits and amplify or reduce the signals moving through those paths, according to his talk ^[1].

His team's recent mouse experiments mapped those paths, he said. The researchers used genetically modified mice so that GLP-1-producing neurons and GLP-1-receiving neurons would express fluorescent proteins, allowing them to select those cells from among millions of neurons. They also used optogenetics, inserting light-sensitive proteins so that only targeted cells activate under blue light, then placed microelectrodes in the receiving neurons to measure signal strength directly ^[1].

"While the fact that GLP-1-based drugs lead to weight loss is well understood, the precise neural pathways within the brain responsible for this effect had not yet been elucidated," Fang said. "In this regard, we had the 'medicine,' but not the 'blueprint'" ^[1].

The presentation did not include structural or molecular detail of the receptor, and no clinical candidate, human trial data or development partner was disclosed. The work was described as laboratory research in mice ^[1].

Fang outlined two possible directions. First, knowing which circuit produces which effect could allow drugs that act on only those pathways. Current GLP-1-based drugs act on receptors throughout the body, which means that along with weight loss, side effects such as nausea or indigestion can occur ^[1]. Second, he said the breakdown of signal transmission between neurons is not unique to obesity. Mental illnesses such as depression, and neurodegenerative diseases such as Alzheimer's and Parkinson's, also involve disrupted communication between neurons, raising the possibility that drugs first developed for obesity could be repurposed for brain disorders ^[1].

"We are entering an era in which GLP-1 should be understood not merely as a metabolic disease treatment target, but as a powerful neuromodulatory system," he said. "GLP-1 and circuit-specific neuromodulators may hold the key to transforming brain disease treatment" ^[1].

Why it matters for patients

Nothing in the presentation changes how today's medicines work or how they are prescribed. For people taking semaglutide (Ozempic, Wegovy, Rybelsus) or tirzepatide (Mounjaro, Zepbound), the nausea and indigestion that can come with treatment reflect drug action on receptors throughout the body, not only in the brain, according to the account Fang gave ^[1].

The practical hope he described is separation: if researchers can learn which circuit drives which outcome, a drug could be built to hit the intended pathway and spare others, which might mean more benefit and fewer gut side effects ^[1]. That is a design goal, not a finding. No such drug was described, and no timeline for one was given.

The same caution applies to brain disease. Fang listed depression, Alzheimer's and Parkinson's as conditions rooted in disrupted neural communication and raised the idea of repurposing obesity drugs for them ^[1]. No trials in those conditions were reported in the session described, and it is not known whether effects seen in mouse circuits would carry over to people.

What happens next

No next steps, trial dates or development milestones were disclosed ^[1]. The talk was described as basic science with no clinical candidate attached ^[1].