1: Identification of Diet and Gut Bacteria that Induce Beige Adipocytes / 2: Does Multiple Sclerosis Start in the Gut? — A New Immune Control Mechanism Mediated by the Small Intestine
Science of the Month - May 2026
1: Identification of Diet and Gut Bacteria that Induce Beige Adipocytes
Tanoue T, Nagayama M, Roochana AJA, Zimmerman S, Ashenberg O, Jain T, Igarashi R, Sasajima S, Takeshita K, Hetherington N, Okahashi N, Ueda M, Konishi M, Nakayama Y, Minoda A, Skelly AN, Minokoshi Y, Pucci N, Mende DR, Arita M, Yamamoto H, Watanabe S, Miura K, Behie SW, Suda W, Sato T, Atarashi K, Matsushita M, Kajimura S, Plichta DR, Saito M, Xavier RJ, Honda K.
The interaction between diet and gut bacteria has a fundamental impact on the host metabolic system, but many details of the mechanisms by which they regulate function remain unexplained. In particular, "browning"—the process where white adipose tissue, which stores energy, transforms into energy-consuming beige adipocytes—is attracting attention as a key to improving metabolism. When SPF (Specific pathogen-free) mice with normal gut microbiota were fed diets with varying compositions of macronutrients (carbohydrates, lipids, and proteins), it was discovered that a low-protein diet strongly induces beige cells in white adipose tissue. This phenomenon was significantly attenuated in germ-free mice, revealing that gut bacteria are essential. Next, bacteria capable of inducing browning were isolated, screened, and identified from the feces of SPF mice in which beige adipocytes were induced by a low-protein diet, as well as from humans whose high beige fat activity was confirmed by FDG-PET scans. For example, it was confirmed in mice that the colonization of four human-derived strains (Bilophila, Adlercreutzia, Eubacteriaceae, Romboutsia) combined with a low-protein diet reproduced the strong induction of beige cells. Regarding the mechanism, it was found that under low-protein conditions, these gut bacteria enhance FGF21 production in the liver and bile acid metabolism resulting from ammonia production, which is important for beige cell induction. In the future, the development of treatments for metabolic diseases such as obesity, diabetes, and fatty liver with fewer side effects is expected by combining specific diets with bacterial strains or their metabolites, or by mimicking the aforementioned pathways.
(Department of Microbiology and Immunology: Kenya Honda, Dai Tanoue)
2: Does Multiple Sclerosis Start in the Gut? — A New Immune Control Mechanism Mediated by the Small Intestine
Science Immunology.
2026 Mar 27;11(117):eaec1627. doi: 10.1126/sciimmunol.aec1627.
Shohei Suzuki, Kentaro Miyamoto, Anna Tojo, Yusuke Yoshimatsu, Toshiaki Teratani, Hitoshi Uchida, Yasuhiro Nemoto, Ryuichi Okamoto, Andreas Michael Sihombing, Toshiro Sato, Jin Nakahara, Takanori Kanai, Tomohisa Sujino
We have previously analyzed how the intestinal environment, centered on the gut microbiota, is involved in immune responses and pathogenesis in multiple sclerosis and its model diseases (Miyamoto K, et al., Cell Reports, 2023). In this study, we confirmed that inflammatory T cells (Th17 cells) are increased in the small intestine of patients with multiple sclerosis. Furthermore, mouse experiments revealed that these cells activated in the gut migrate to the spinal cord and cause autoimmune inflammation. Additionally, we discovered that small intestinal epithelial cells do not merely perform nutrient absorption and barrier functions, but also have the function of presenting antigens to immune cells and inducing inflammation. The disease was alleviated in mice lacking this function. In other words, a new concept was demonstrated (Figure) showing that distant organs—the gut and the brain—coordinate via immune cells to participate in the disease, and that the intestinal epithelium acts as a command center for immunity. Treatments targeting intestinal immunity may lead to new therapies for neurological diseases.
(The Sakaguchi Laboratory: Tomohisa Sujino)
Other Published Papers
2) Florzolotau (18F) retention is linked to neuropsychological performance in tauopathy.
Alzheimer's & Dementia.
Atsushi Shimizu, Yu Iwabuchi, Shogyoku Bun, Memi Watanabe, Masahito Kubota, Sho Shimohama, Toshiki Tezuka, Keisuke Takahata, Hajime Tabuchi, Morinobu Seki, Yuki Momota, Yasuharu Yamamoto, Ryo Shikimoto, Yu Mimura, Shin Kurose, Ryosuke Sakurai, Toshiki Takayama, Yuka Hoshino, Takayuki Hoshino, Natsumi Suzuki, Ayaka Morimoto, Azusa Osumi, Masaru Mimura, Masahiro Jinzaki, Daisuke Ito