Eating in mice with gastric bypass surgery causes exaggerated activation of brainstem anorexia circuit

MB Mumphrey, Z Hao, RL Townsend… - International Journal of …, 2016 - nature.com
MB Mumphrey, Z Hao, RL Townsend, LM Patterson, H Münzberg, CD Morrison, J Ye…
International Journal of Obesity, 2016nature.com
Results: Voluntary ingestion of a meal 10 days after RYGB, but not after sham surgery,
strongly and selectively activates calcitonin gene-related peptide neurons in the external
lPBN as well as neurons in the nucleus tractus solitarius, area postrema and medial
amygdala. At 40 days after surgery, meal-induced activation in all these areas was greatly
diminished and did not reach statistical significance. Conclusions: The neural activation
pattern and dynamics suggest a role of the brainstem anorexia pathway in the early effects …
Results:
Voluntary ingestion of a meal 10 days after RYGB, but not after sham surgery, strongly and selectively activates calcitonin gene-related peptide neurons in the external lPBN as well as neurons in the nucleus tractus solitarius, area postrema and medial amygdala. At 40 days after surgery, meal-induced activation in all these areas was greatly diminished and did not reach statistical significance.
Conclusions:
The neural activation pattern and dynamics suggest a role of the brainstem anorexia pathway in the early effects of RYGB on meal size and food intake that may lead to adaptive neural and behavioral changes involved in the control of food intake and body weight at a lower level. However, selective inhibition of this pathway will be required for a more causal implication.
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