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A Hypothalamic Phosphatase Switch Coordinates Energy Expenditure with Feeding
Garron T Dodd1, Zane B Andrews2, Stephanie E Simonds2
1Metabolic Disease and Obesity Program, Biomedicine Discovery Institute, Monash University, Victoria 3800, Australia; Department of Biochemistry and Molecular Biology, Monash University, Victoria 3800, Australia.
Cell Metabolism
|August 3, 2017
Summary
Researchers discovered a hypothalamic switch regulating energy expenditure. This switch, involving TCPTP phosphatase, controls beige adipocyte plasticity and responds to feeding, impacting weight management and obesity.
Area of Science:
- Metabolism and Endocrinology
- Cellular Plasticity
- Neuroscience
Background:
- Beige adipocytes exhibit plasticity, interconverting between energy storage and expenditure states.
- This plasticity is crucial for regulating energy expenditure in response to feeding cues.
Purpose of the Study:
- To investigate the role of hypothalamic TCPTP in coordinating beige adipocyte plasticity and energy expenditure with feeding behavior.
- To elucidate the mechanism by which TCPTP influences insulin signaling in AgRP/NPY neurons and white adipose tissue browning.
Main Methods:
- Utilized mouse models with genetic manipulation of TCPTP in AgRP/NPY neurons.
- Investigated the effects of fasting, feeding, and obesity on hypothalamic TCPTP levels and beige adipocyte activity.
- Assessed insulin signaling, white adipose tissue browning, and energy expenditure.
Main Results:
- Fasting increased hypothalamic TCPTP, inhibiting insulin signaling and decreasing energy expenditure.
- Feeding reduced TCPTP, enhancing insulin signaling, promoting white adipose tissue browning, and increasing energy expenditure.
- Defective TCPTP repression in obesity led to impaired feeding-induced browning; TCPTP deletion in AgRP/NPY neurons conferred resistance to diet-induced obesity.
Conclusions:
- Hypothalamic TCPTP acts as a crucial switch coordinating energy expenditure with feeding status.
- Modulating hypothalamic TCPTP can restore feeding-induced browning and increase energy expenditure, offering a potential therapeutic strategy for obesity.
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