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Brain and Hormone Interplay for Regulating Intake and Metabolism of Foods and Nutrients: Impact of Food Ingredients and Diet

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: 15 December 2025 | Viewed by 2314

Special Issue Editor


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Guest Editor
1. Department of Diabetes, Endocrinology and Metabolism, Gifu University Graduate School of Medicine, 2N12(2N18), Yanagido 1-1, Gifu 501-1194, Japan
2. Center for Integrative Physiology, Kansai Electric Power Medical Research Institute, Nakagyo-ku, Kyoto 604-8436, Japan
Interests: feeding center; gut hormone; obesity; anorexia; frailty; rare sugar; Japanese kampo medicine; diet; diabetes
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Special Issue Information

Dear Colleagues,

Foods and nutrients regulate the metabolism and functions of the body. In this process, the food/nutrient-driven endocrine system talks to the brain. Subsequently, the brain and hormones cooperate to signal to the peripheral organs for the utilization of foods/nutrients and to regulate the intake of foods/nutrients.

Hormones secreted in response to the intake of foods/nutrients inform the brain via the tanycyte and blood–brain barrier (BBB) pathways. The brain controls nutrient metabolism, feeding, and circadian behaviors.

Brain and hormone interplay plays a crucial role in the physiological regulation of eating behavior and metabolism. Furthermore, its disorder leads to metabolic diseases, including type 2 diabetes, obesity, cardiovascular disease, anorexia, and dementia, some of which suffer from a shortage of effective treatments.

Recently, new types of medicines, such as herbal medicines, and a variety of foods, including cacao and rare sugars, have been shown to ameliorate some metabolic diseases. However, the underlying mechanisms are often obscure, which has limited their use for treating diseases. The mechanisms potentially involve brain–hormone interplay.

This Special Issue of Nutrients deals with the brain–hormone Interplay regulating the intake and metabolism of foods/nutrients and the impacts of diets, foods, and natural active ingredients on them. Basic to clinical studies at the molecular to systemic level in all species are welcome.

Prof. Dr. Toshihiko Yada
Guest Editor

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Keywords

  • feeding center
  • gut hormone
  • obesity
  • diabetes
  • anorexia
  • frailty
  • memory
  • rare sugar
  • herbal medicine
  • tanycyte
  • blood–brain barrier
  • vagal afferent

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Published Papers (2 papers)

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Research

15 pages, 3413 KiB  
Article
Glucagon-like Peptide-2 Acts Partially Through Central GLP-2R and MC4R in Mobilizing Stored Lipids from the Intestine
by Kundanika Mukherjee, Muhammad Saad Abdullah Khan, John G. Howland and Changting Xiao
Nutrients 2025, 17(9), 1416; https://doi.org/10.3390/nu17091416 - 23 Apr 2025
Viewed by 607
Abstract
Background: Glucagon-like peptide-2 (GLP-2) is a gut hormone secreted in response to nutrient intake and regulates lipid metabolism in the gut. The present study aims to elucidate the underlying mechanism of GLP-2 in stimulating gut lipid secretion in the fasted state by testing [...] Read more.
Background: Glucagon-like peptide-2 (GLP-2) is a gut hormone secreted in response to nutrient intake and regulates lipid metabolism in the gut. The present study aims to elucidate the underlying mechanism of GLP-2 in stimulating gut lipid secretion in the fasted state by testing whether GLP-2 signals through the brain’s GLP-2 receptor and melanocortin 4 receptor (MC4R). Methods: Sprague-Dawley rats were implanted with a mesenteric lymph duct cannula for measuring gut lipid secretion and an intracerebroventricular cannula for infusion of a GLP-2R antagonist (GLP-2(11-33)), an MC4R antagonist (SHU9119), or saline as a control. The rat received a lipid infusion into the small intestine and a peritoneal injection of GLP-2 five hours later. Results: Brain administration of a GLP-2R antagonist or an MC4R antagonist attenuated the stimulatory effects of peripheral GLP-2 on lymph triglyceride output. These effects were associated with differential changes in the expression of key genes in jejunal endothelial cells, smooth muscle cells, and neuronal cells. Conclusions: These results support the involvement of central GLP-2R and MC4R in a neural pathway for GLP-2 to mobilize lipids stored in the gut during the post-absorptive state. Full article
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13 pages, 2617 KiB  
Article
Abilities of Rare Sugar Members to Release Glucagon-like Peptide-1 and Suppress Food Intake in Mice
by Yuta Masuda, Kento Ohbayashi, Kengo Iba, Rika Kitano, Tomonori Kimura, Takako Yamada, Tohru Hira, Toshihiko Yada and Yusaku Iwasaki
Nutrients 2025, 17(7), 1221; https://doi.org/10.3390/nu17071221 - 31 Mar 2025
Viewed by 1514
Abstract
Background/Objectives: Rare sugars, which naturally exist in small quantities, have gained attention as next-generation functional sugars due to their sweetness and low calorie content. Some of them have already been commercialized. Rare sugar-containing syrups, produced through alkaline isomerization of high-fructose corn syrup, are [...] Read more.
Background/Objectives: Rare sugars, which naturally exist in small quantities, have gained attention as next-generation functional sugars due to their sweetness and low calorie content. Some of them have already been commercialized. Rare sugar-containing syrups, produced through alkaline isomerization of high-fructose corn syrup, are effective in preventing obesity and type 2 diabetes. However, the mechanisms underlying these effects remain incompletely understood. Recently, D-allulose has been found to improve hyperphagic obesity by stimulating the secretion of the intestinal hormone glucagon-like peptide-1 (GLP-1). The present study aimed to determine the comparative effects of aldohexoses (D-glucose, D-allose) and ketohexoses (D-fructose, D-allulose, D-tagatose, D-sorbose) on GLP-1 secretion and food intake in male mice. Method and Results: Single peroral administration of four ketohexoses at 1 and 3 g/kg, but not aldohexoses at 1 and 3 g/kg, significantly increased plasma GLP-1 concentrations with comparable efficacy. Moreover, these ketohexoses at 1 g/kg suppressed food intake in the short term, an effect blunted by GLP-1 receptor antagonism. In contrast, zero-calorie D-allose at 3 g/kg suppressed feeding without raising plasma GLP-1 levels. Conclusions: These results demonstrate that D-allulose, D-tagatose, and D-sorbose, which are low-calorie rare sugars classified as ketohexoses, suppress food intake through promoting GLP-1 secretion, showing their potential to prevent and/or ameliorate type 2 diabetes, obesity and related diseases. Full article
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