A recent study conducted by researchers at Baylor College of Medicine and the University of Texas Health Science Center at Houston has shed light on brain circuits and chemical messengers involved in regulating meal initiation and food intake. Published in the journal Metabolism, this research could influence future therapies for managing obesity.
Dr. Yong Xu, professor of pediatrics – nutrition and associate director of basic sciences at the USDA/ARS Children’s Nutrition Research Center at Baylor, highlighted the role of serotonin in suppressing food intake. "It’s well known that serotonin, a neurotransmitter in the brain, can suppress food intake," Xu stated. However, he noted that drugs targeting serotonin have sometimes caused unwanted side effects, underscoring the need for better understanding to improve drug design.
The research team focused on serotonin-producing neurons located in the dorsal Raphe nucleus (DRN) within the midbrain. These neurons project to various regions including the arcuate nucleus of the hypothalamus (ARH). The study found that two neurotransmitters, GABA and dopamine, are integral to initiating meals by inhibiting these neurons when animals feel hungry.
"Working with animal models, we found that when the animals are hungry, serotonin-producing neurons in the DRN are inhibited by GABA and dopamine," explained Xu. This inhibition reduces serotonin levels allowing meal initiation. As feeding continues and satiety is reached, inhibitory signals decrease resulting in increased serotonin production which inhibits further feeding via projections to ARH.
Xu emphasized that "GABA and dopamine act synergistically – when both are present, serotonin neurons appear to be more inhibited than when only one of the neurotransmitters is present." This insight into how neurotransmitters manage body weight through feeding behavior could guide future development of obesity treatments.
Looking ahead, Xu expressed interest in exploring signals regulating other phases of feeding beyond meal initiation.
Contributors to this study include Kristine M. Conde, Huey Zhong Wong among others from Baylor College of Medicine or University of Texas Health Science Center at Houston. Funding was provided by USDA/CRIS grants 51000-064-01S and 3092-51000-062-04(B)S; National Institutes of Health grants R01DK120858 F32DK134121 R01DK131446; American Heart Association grant 23POST1030352.
