Related Experiment Videos
Duodenal loading with glucose induces fos expression in rat brain: selective blockade by devazepide
1Center for Ulcer Research and Education/Digestive Disease Research Center, West Los Angeles Veterans Affairs Medical Center, Department of Medicine and Brain Research Institute, University of California, Los Angeles, CA 90073, USA.
The American Journal of Physiology
|September 14, 1999
Summary
Dietary glucose in the intestine activates brain neurons. Cholecystokinin-A (CCK-A) receptors mediate this activation in the nucleus of the solitary tract (NTS) and area postrema (AP).
Area of Science:
- Neuroscience
- Gastroenterology
- Endocrinology
Background:
- Dietary carbohydrates trigger physiological responses.
- The gut-brain axis plays a crucial role in nutrient sensing.
- Cholecystokinin (CCK) is implicated in satiety and nutrient signaling.
Purpose of the Study:
- To investigate the role of CCK in mediating brain neuronal activation by duodenal glucose.
- To determine which brain regions' activation by glucose is CCK-dependent.
Main Methods:
- Adult male Sprague-Dawley rats received a duodenal glucose infusion.
- Fos immunoreactivity was measured to detect neuronal activation.
- The CCK-A receptor antagonist devazepide was administered to assess CCK's role.
Main Results:
- Duodenal glucose induced Fos expression in the NTS, AP, CeAL, and LPBE.
- Devazepide significantly attenuated Fos expression in the NTS (81%) and AP (78%).
- Devazepide did not affect Fos expression in the CeAL or LPBE.
Conclusions:
- Central neuronal activation occurs in response to luminal glucose.
- Activation of NTS and AP neurons by glucose is mediated by CCK-A receptors.
- CCK-A receptor-independent pathways mediate glucose-induced activation in the amygdala and parabrachial nucleus.