Makoto Fukuda, Ph.D.
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Makoto Fukuda, Ph.D.
Associate Professor
Positions
- Associate Professor
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Pediatrics-Nutrition
Baylor College of Medicine
Houston, TX US
Addresses
- Children's Nutrition Research Center (Lab)
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Room: CNRC-8035
Houston, TX 77030
United States
fukuda@bcm.edu
- Children's Nutrition Research Center (Office)
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Room: CNRC-8035
Houston, TX 77030
United States
fukuda@bcm.edu
Education
- BS from Kyushu University
- Fukuoka, Japan
- PhD from University of Tokyo
- Tokyo, Japan
- Post-Doctoral Fellowship at Beth Israel Deaconess Medical Center
- Boston, MA United States
- Post-Doctoral Fellowship at University of Texas Southwestern Medical Center
- Dallas, TX United States
Professional Statement
The goal of our laboratory is to understand how and whether the brain mediates obesity and type 2 diabetes. The critical role of the central nervous system (CNS) in obesity and type 2 diabetes is increasingly clear, yet the neural processes mediating pathogenesis of obesity and type 2 diabetes are unclear. We are approaching this fundamental question in a unique fashion. First, using organotypic brain slice cultures that recapitulate key aspects of obesity-associated pathophysiology within the brain, we identify neural processes underlying the pathophysiological changes occurring during obesity. Then, their physiological relevance will be validated by employing various in vivo approaches including mouse genetics, optogenetics/chemogenetics, and in vivo tracer studies of glucose metabolism. Through our approach, we hope to discover novel CNS mechanisms responsible for obesity and type 2 diabetes, and to ultimately develop more effective therapies for these prevalent diseases by manipulating the neural pathways.We are currently focusing on the following two CNS pathways we have recently identified:
(1) A signal from the gut to the brain to promote obesity.
(2) A novel CNS pathway that may offer an antidiabetic effect.
Websites
Selected Publications
- Cordonier EL, Liu T, Saito K, Chen SS, Xu Y, Fukuda M. "Luciferase Reporter Mice for In Vivo Monitoring and Ex Vivo Assessment of Hypothalamic Signaling of Socs3 Expression.." J Endocr Soc.. 2019 Jul;3(7):1246-1260. Pubmed PMID: 31214662
- Kaneko K, Fu Y, Lin HY, Cordonier EL, Mo Q, Gao Y, Yao T, Naylor J, Howard V, Saito K, Xu P, Chen SS, Chen MH, Xu Y, Williams KW, Ravn P, Fukuda M "Gut-derived GIP activates central Rap1 to impair neural leptin sensitivity during overnutrition." J Clin Invest.. 2019 Aug;129(49):3786-3791. Pubmed PMID: 31403469
- Fu Y, Kaneko K, Lin HY, Mo Q, Xu Y, Suganami T, Ravn P, Fukuda M. "Gut Hormone GIP Induces Inflammation and Insulin Resistance in the Hypothalamus.." Endocrinology. 2020 Sep;161 Pubmed PMID: 32603429
Funding
- A Novel Neural Mechanism that Mediates the Therapeutic Effects of Metformin - #R01DK126655 (02/15/2021 - 11/30/2024) Grant funding from NIH/NIDDK
- Central Role of Gut Hormone GIP in Leptin Resistance and Obesity - #1R01DK104901-01A1 (09/23/2015 - 07/31/2021) Grant funding from NIH/NIDDK
- The Role of Leptin in Diet-Induced Obesity - #3092-51000-060-02 (04/01/2014 - 03/31/2019) Grant funding from USDA/CRIS
- The gut hormone GIP drives neural leptin resistance - #14BGIA20460080 (07/01/2014 - 06/30/2016) Grant funding from American Heart Association
- Secreted Signal that Causes Neuronal Leptin Resistance - #P30-DK079638 (11/01/2013 - 12/31/2014) Grant funding from NIH/NIDDK (DERC)
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