Researchers have identified a previously unknown signaling network between the gut and brain that detects protein shortages and shifts feeding preferences toward essential amino acids.
A team led by Director SUH Seong-Bae at the Institute for Basic Science, along with colleagues from Seoul National University and Ewha Womans University, mapped the mechanism in fruit flies and confirmed similar behavior in mice. The work was published in the journal Science on May 21.
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Researchers at APC Microbiome Ireland at University College Cork report that early-life exposure to a high-fat, high-sugar diet altered feeding behavior and appetite-related brain pathways in mice into adulthood, even after the animals returned to a standard diet and normal body weight. The team also found that a specific Bifidobacterium strain and a prebiotic fiber mix helped mitigate some of these long-term effects.
A team led by David Julius, the 2021 Nobel Prize winner in Medicine, has described the molecular mechanism by which intestinal tuft cells signal the brain to suppress appetite during parasitic infections. Published today in Nature, the study identifies communication via acetylcholine and serotonin that activates the vagus nerve. The finding could aid treatments for conditions like irritable bowel syndrome.
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University of Oklahoma scientists report that the hormone FGF21 reduces body weight in obese mice by acting on a hindbrain pathway—centered on the nucleus of the solitary tract and area postrema—that relays signals to the parabrachial nucleus. The team says the mechanism overlaps anatomically with brain regions implicated in GLP-1 drugs, but appears to promote weight loss mainly by increasing metabolic rate rather than primarily suppressing food intake.
A year-long observational study in Japan suggests that people with type 2 diabetes who tend to overeat in response to tempting food cues such as sight and smell may see greater weight loss—and possibly better blood-sugar improvement—after starting GLP-1 receptor agonists, while those with primarily emotional eating patterns show less consistent links to long-term outcomes.
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Researchers at the University of Colorado Boulder have pinpointed a brain region called the caudal granular insular cortex, or CGIC, that acts as a switch turning acute pain into chronic pain. In animal studies, disabling this circuit prevented chronic pain from developing or reversed it once established. The findings, published in the Journal of Neuroscience, open paths to new treatments beyond opioids.