A Baptist University-led study found that a proteolytic enzyme called "membrane type 1 matrix metalloproteinase" (MT1-MMP) can affect the activation of satiety in the hindbrain. The team tried to reduce MT1 in a mouse model. -MMP, successfully reduced food intake by 10% and gained 50% less weight than the control group.
Dr. Wang Kailiang, Assistant Professor of Teaching and Research Department of HKBU School of Chinese Medicine, pointed out that this discovery provides a potential target for the development of innovative drugs for the treatment of obesity.
Wang Kailiang (left) believes that the research results provide a potential target for the development of innovative drugs for the treatment of obesity.
(Screenshot of the press conference)
A research team led by Assistant Professor Wang Kailiang of the Teaching and Research Department of HKBU's School of Chinese Medicine and Bian Zhaoxiang, Director of the Clinical Department and Professor of Clinical Research of Tsang Shiu-Tian Chinese Medicine, has identified a hydrolytic protease called MT1-MMP, which signals satiety in the human brain regulation in the mechanism.
Wang Kailiang explained that the satiety signal is generated through the binding of growth and differentiation factor 15 (GDF15) to a neuron receptor called "GDNF family receptor alpha-like" (GFRAL) located in the hindbrain, but MT1-MMP will GFRAL snips from the surface of brain neurons, preventing it from binding to GDF15, reducing the number of satiety signals.
Through a mouse model experiment, the team fed a high-fat diet to genetically modified mice lacking MT1-MMP and a control group. After 16 weeks, it was found that the MT1-MMP group of mice ate 10% less, and gained more weight. 50% lower control group (provided by Baptist University)
Through a mouse model experiment, the team fed a high-fat diet to genetically modified mice lacking MT1-MMP and a control group. After 16 weeks, it was found that the MT1-MMP group of mice ate 10% less, and gained more weight. 50% lower than the control group, and the levels of glucose and plasma insulin are also lower, reflecting that the lack of MT1-MMP can prevent the obesity caused by high-fat food in mice; the team also inhibited the activity of MT1-MMP in vivo through pharmacological methods, and found obesity Metabolic parameters, including food intake, glucose tolerance, and body weight, were significantly improved in the mice.
Wang Kailiang believes that the research results provide a potential target for the development of innovative drugs for the treatment of obesity. In addition, no obvious negative effects or adverse effects have been found in the mouse model in the current research. Drugs to inhibit MT1-MMP , is a feasible strategy to develop drugs that can effectively treat obesity. In addition to research in mouse models, the next step will be to conduct research in monkey models, and then conduct clinical research, hoping to develop more effective weight loss drugs to help Address obesity.
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