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Assessment of the Metabolic Effects of Isocaloric 2:1 Intermittent Fasting in Mice
Published on: November 27, 2019
Diet-induced obesity attenuates fasting-induced hyperphagia
1Department of Physiology, Monash University, Clayton, Victoria, Australia.
Journal of Neuroendocrinology
|April 27, 2011
Summary
Diet-induced obesity (DIO) impairs the brain
Area of Science:
- Neuroscience
- Metabolism
- Endocrinology
Background:
- Obesity is linked to impaired neuronal function in the arcuate nucleus (ARC).
- ARC neurons expressing neuropeptide Y (NPY) and agouti-related peptide (AgRP) are crucial for appetite regulation.
- These neurons normally respond to orexigenic hormones like ghrelin, but this response is blunted in obesity.
Purpose of the Study:
- To investigate how diet-induced obesity (DIO) affects feeding behavior and ARC neuronal activation.
- To examine the impact of DIO on hypothalamic NPY/AgRP mRNA expression after an overnight fast.
- To understand the mechanisms behind altered feeding responses in obese states.
Main Methods:
- Induction of diet-induced obesity (DIO) in mice using a high-fat diet for 9 weeks.
- Assessment of feeding behavior, specifically fasting-induced hyperphagia.
- Measurement of ARC neuronal activation and hypothalamic NPY/AgRP mRNA expression.
Main Results:
- Diet-induced obesity (DIO) significantly attenuated fasting-induced hyperphagia.
- High-fat feeding suppressed ARC neuronal activation in response to fasting.
- Hypothalamic NPY/AgRP mRNA expression was reduced following fasting in DIO mice.
Conclusions:
- Obesity impairs the ability of ARC neurons to recognize and respond to orexigenic cues during fasting.
- The diminished feeding response to fasting in DIO is not driven by homeostatic appetite control.
- Changes in the brain's reward circuitry may play a significant role in regulating appetite in obesity.
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