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Published on: January 4, 2018
Removal of melatonin receptor type 1 induces insulin resistance in the mouse
Susana Contreras-Alcantara1, Kenkichi Baba, Gianluca Tosini
1Department of Pharmacology and Toxicology, Morehouse School of Medicine, Atlanta, Georgia, USA.
Abstract:
The incidence of obesity, insulin resistance, and type 2 diabetes (T2D) is increasing at an alarming rate worldwide. Emerging experimental evidence suggests that the hormone melatonin plays an important role in the regulation of glucose metabolisms. In this study, we report that removal of melatonin receptor type 1 (MT1) significantly impairs the ability of mice to metabolize glucose and such inability is probably due to an increased insulin resistance in these mice. Our data suggest that MT1 receptors are implicated in the pathogenesis of T2D and open the door for a detailed exploration on the mechanisms by which MT1 receptors signaling may affect glucose metabolism.
Insights
Melatonin receptor type 1 (MT1) is crucial for glucose metabolism. Mice lacking MT1 receptors show impaired glucose metabolism, likely due to increased insulin resistance, suggesting MT1
Area of Science:
- Metabolic disease research
- Endocrinology
- Molecular biology
Background:
- Global rise in obesity, insulin resistance, and type 2 diabetes (T2D).
- Emerging evidence implicates the hormone melatonin in glucose metabolism regulation.
Purpose of the Study:
- Investigate the role of melatonin receptor type 1 (MT1) in glucose metabolism.
- Determine if MT1 receptor deficiency affects insulin resistance and glucose tolerance.
Main Methods:
- Utilized a mouse model lacking the MT1 receptor.
- Assessed glucose metabolism and insulin resistance in these mice.
Main Results:
- Mice lacking MT1 receptors exhibited significantly impaired glucose metabolism.
- This impairment is likely associated with increased insulin resistance.
Conclusions:
- MT1 receptors play a significant role in maintaining normal glucose homeostasis.
- MT1 receptor signaling is implicated in the pathogenesis of type 2 diabetes.
- Further research into MT1 receptor mechanisms in glucose metabolism is warranted.
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