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Updated: Aug 13, 2026
Real-time Analysis of Gut-brain Neural Communication: Cortex wide Calcium Dynamics in Response to Intestinal Glucose Stimulation
Published on: December 29, 2023
Central but not peripheral glucoprivation is impaired in monosodium glutamate-treated rats
Iracema Senna de Andrade1, João Carlos Gonzalez Gonzalez, Aparecida Emiko Hirata
1Department of Physiology, Division of Neurophysiology and Endocrine Physiology, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, SP 04023-060, Brazil.
Abstract:
In the present study, newborn male Wistar rats were injected, subcutaneously, five times, every other day, with monosodium glutamate (MSG, 4 g/kg bw) or saline (as control, C), during the neonatal period. MSG animals developed destruction of the arcuate nuclei (ARC) with absence of NPY-immunoreactive cell bodies, which impaired both the food intake (baseline) and the 2-deoxy-D-glucose (2DG) glucoprivic feeding response. Increases in the immunoreactivity of corticotropin-releasing hormone-cell bodies in the paraventricular nuclei might have developed to compensate for the atrophy of the pituitary in MSG-treated rats. After systemic 2DG injection, neither the C nor the MSG rats increased their food intake, but they showed similar hyperglycemic responses, whereas plasma free fatty acids (FFA) increased only in the C group. In other groups, 2DG, norepinephrine (NE), neostigmine (NEO) and saline were intracerebroventricularly (i.c.v.) administered. In this condition, impairment of the hyperglycemic and food intake responses, associated to a lower increase in plasma FFA levels, were observed. As opposed to this, the MSG treatment gives support to NE effects, enhancing food intake, as well as plasma glucose and FFA levels. After NEO, plasma glucose increased only in the MSG group, while plasma FFA levels were elevated in the C rats. Taken together, the results obtained after MSG treatment point to a separate neural control of the hyperglycemic response and of the lipid mobilization when stimulated by central 2DG, NE or NEO administration. It seems likely that the excitatory neural pathway that controls lipid metabolism and is present in C rats was destroyed by the MSG treatment.
Insights
Neonatal monosodium glutamate (MSG) exposure destroys arcuate nuclei, impairing feeding responses. MSG-treated rats show altered responses to central 2-deoxy-D-glucose (2DG), norepinephrine, and neostigmine, suggesting disrupted neural control of metabolism.
Area of Science:
- Neuroscience
- Endocrinology
- Metabolism
Background:
- Neonatal exposure to monosodium glutamate (MSG) is known to cause neurotoxicity, particularly affecting the hypothalamus.
- The arcuate nucleus (ARC) plays a critical role in regulating appetite and energy balance.
- Understanding the long-term metabolic consequences of neonatal MSG exposure is crucial for metabolic research.
Purpose of the Study:
- To investigate the effects of neonatal monosodium glutamate (MSG) administration on feeding behavior, glucose homeostasis, and lipid metabolism in adult rats.
- To determine the impact of MSG-induced ARC damage on the neural control of metabolic responses to various stimuli.
Main Methods:
- Newborn male Wistar rats were injected with MSG (4 g/kg) or saline subcutaneously every other day.
- Arcuate nuclei (ARC) integrity and NPY/CRH immunoreactivity were assessed.
- Baseline and 2-deoxy-D-glucose (2DG)-induced feeding and glycemic responses were measured.
- Intracerebroventricular (i.c.v.) administration of 2DG, norepinephrine (NE), or neostigmine (NEO) was performed to assess metabolic responses.
Main Results:
- MSG treatment resulted in ARC destruction and absence of NPY-immunoreactive cell bodies, impairing baseline and 2DG-induced feeding.
- MSG rats exhibited impaired hyperglycemic and feeding responses to central 2DG, NE, and NEO, with altered plasma free fatty acid (FFA) levels.
- MSG treatment enhanced NE-stimulated food intake, plasma glucose, and FFA levels, but only MSG rats showed a glucose increase after NEO.
- MSG rats failed to increase food intake after systemic 2DG, unlike controls.
Conclusions:
- Neonatal MSG exposure causes significant neurotoxicity in the ARC, disrupting central regulation of feeding and metabolism.
- The study reveals a dissociation in neural control of hyperglycemia and lipid mobilization following central stimulation in MSG-treated rats.
- MSG-induced destruction of neural pathways likely underlies the observed metabolic dysregulations, particularly affecting lipid metabolism control.
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