The vagal nerves—Important connectors of the gut and brain for energy balance
| Autor: | Karl-Heinz Herzig, Ghulam Shere Raza |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
obesity Physiology Efferent Hyperphagia 030204 cardiovascular system & hematology Weight Gain 03 medical and health sciences Parasympathetic nervous system 0302 clinical medicine fat Afferent Regular Paper medicine Humans Medulla post‐ingestive business.industry digestive oral and skin physiology Entire abdominal cavity Brain Vagus Nerve Anatomy Metabolism and Nutritional Physiology 030104 developmental biology medicine.anatomical_structure palatability nervous system sugar Sugars business circulatory and respiratory physiology |
| Zdroj: | Acta Physiologica (Oxford, England) |
| ISSN: | 1748-1716 1748-1708 |
| Popis: | Aim The tools that have been used to assess the function of the vagus nerve lack specificity. This could explain discrepancies about the role of vagal gut‐brain signalling in long‐term control of energy balance. Here we use a validated approach to selectively ablate sensory vagal neurones that innervate the gut to determine the role of vagal gut‐brain signalling in the control of food intake, energy expenditure and glucose homoeostasis in response to different diets. Methods Rat nodose ganglia were injected bilaterally with either the neurotoxin saporin conjugated to the gastrointestinal hormone cholecystokinin (CCK), or unconjugated saporin as a control. Food intake, body weight, glucose tolerance and energy expenditure were measured in both groups in response to chow or high‐fat high‐sugar (HFHS) diet. Willingness to work for fat or sugar was assessed by progressive ratio for orally administered solutions, while post‐ingestive feedback was tested by measuring food intake after an isocaloric lipid or sucrose pre‐load. Results Vagal deafferentation of the gut increases meal number in lean chow‐fed rats. Switching to a HFHS diet exacerbates overeating and body weight gain. The breakpoint for sugar or fat solution did not differ between groups, suggesting that increased palatability may not drive HFHS‐induced hyperphagia. Instead, decreased satiation in response to intra‐gastric infusion of fat, but not sugar, promotes hyperphagia in CCK‐Saporin‐treated rats fed with HFHS diet. Conclusions We conclude that intact sensory vagal neurones prevent hyperphagia and exacerbation of weight gain in response to a HFHS diet by promoting lipid‐mediated satiation. |
| Databáze: | OpenAIRE |
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