The autonomic nervous system regulates postprandial hepatic lipid metabolism

2013 ◽  
Vol 304 (10) ◽  
pp. E1089-E1096 ◽  
Author(s):  
Eveline Bruinstroop ◽  
Susanne E. la Fleur ◽  
Mariette T. Ackermans ◽  
Ewout Foppen ◽  
Joke Wortel ◽  
...  

The liver is a key organ in controlling glucose and lipid metabolism during feeding and fasting. In addition to hormones and nutrients, inputs from the autonomic nervous system are also involved in fine-tuning hepatic metabolic regulation. Previously, we have shown in rats that during fasting an intact sympathetic innervation of the liver is essential to maintain the secretion of triglycerides by the liver. In the current study, we hypothesized that in the postprandial condition the parasympathetic input to the liver inhibits hepatic VLDL-TG secretion. To test our hypothesis, we determined the effect of selective surgical hepatic denervations on triglyceride metabolism after a meal in male Wistar rats. We report that postprandial plasma triglyceride concentrations were significantly elevated in parasympathetically denervated rats compared with control rats ( P = 0.008), and VLDL-TG production tended to be increased ( P = 0.066). Sympathetically denervated rats also showed a small rise in postprandial triglyceride concentrations ( P = 0.045). On the other hand, in rats fed on a six-meals-a-day schedule for several weeks, a parasympathetic denervation resulted in >70% higher plasma triglycerides during the day ( P = 0.001), whereas a sympathetic denervation had no effect. Our results show that abolishing the parasympathetic input to the liver results in increased plasma triglyceride levels during postprandial conditions.

2005 ◽  
Vol 93 (S1) ◽  
pp. S147-S156 ◽  
Author(s):  
Rémy Burcelin

The glucoincretins, glucagon-like peptide-1 (GLP-1) and gastric inhibitory peptide (GIP), are intestinal peptides secreted in response to glucose or lipid intake. Data on isolated intestinal tissues, dietary treatments and knockout mice strongly suggest that GIP and GLP-1 secretion requires glucose and lipid metabolism by intestinal cells. However, incretin secretion can also be induced by non-digestible carbohydrates and involves the autonomic nervous system and endocrine factors such as GIP itself and cholecystokinin. The classical pharmacological approach and the recent use of knockout mice for the incretin receptors have shown that a remarkable feature of incretins is the ability to stimulate insulin secretion in the presence of hyperglycaemia only, hence avoiding any hypoglycaemic episode. This important role is the basis of ongoing clinical trials using GLP-1 analogues. Since most of the data concern GLP-1, we will focus on this incretin. In addition, GLP-1 is involved in glucose sensing by the autonomic nervous system of the hepato-portal vein controlling muscle glucose utilization and indirectly insulin secretion. GLP-1 has been shown to decrease glucagon secretion, food intake and gastric emptying, preventing excessive hyperglycaemia and overfeeding. Another remarkable feature of GLP-1 is its secretion by the brain. Recently, elegant data showed that cerebral GLP-1 is involved in cognition and memory. Experiments using knockout mice suggest that the lack of the GIP receptor prevents diet-induced obesity. Consequently, macronutrients controlling intestinal glucose and lipid metabolism would control incretin secretion and would consequently be beneficial for health. The control of incretin secretion represents a major goal for new therapeutic as well as nutrition strategies for treating and/or reducing the risk of hyperglycaemic syndromes, excessive body weight and thus improvement of well-being.


2022 ◽  
Vol 2 ◽  
Author(s):  
Dylan T. Wolff ◽  
Stephen J. Walker

Interstitial cystitis/bladder pain syndrome (IC/BPS) is a highly heterogeneous chronic and debilitating condition which effects millions of women and men in the United States. While primarily defined by urinary symptoms and pain perceived to be emanating from the bladder, IC/BPS patients frequently have co-occurring conditions and symptoms, many of which affect diverse body systems related to autonomic nervous system function. The impact on the autonomic system appears to stem from increased sympathetic innervation of the urinary tract, along with increased systemic sympathetic tone and decreased parasympathetic tone. Concurrent with these findings is evidence for destruction of peripheral sympathetic innervation to the sweat glands which may relate to small fiber polyneuropathy. It is unknown to what degree the wider alterations in autonomic function are also related to destruction/alterations in the small fibers carrying autonomic innervation. This potential nexus is an important point of investigation to better understand the unclarified pathophysiology of interstitial cystitis/bladder pain syndrome, the numerous co-occurring symptoms and syndromes, and for the identification of novel targeted therapeutic strategies.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Satoshi Hirako ◽  
Nobuhiro Wada ◽  
Haruaki Kageyama ◽  
Fumiko Takenoya ◽  
Yoshihiko Izumida ◽  
...  

2011 ◽  
Vol 10 (1) ◽  
pp. 192 ◽  
Author(s):  
Elisabetta Pistorio ◽  
Maria Luca ◽  
Antonina Luca ◽  
Vincenzo Messina ◽  
Carmela Calandra

Author(s):  
Daniela Carnevale ◽  
Giuseppe Lembo

Abstract Our body is continuously in contact with external stimuli that need a fine integration with the internal milieu in order to maintain the homoeostasis. Similarly, perturbations of the internal environment are responsible for the alterations of the physiological mechanisms regulating our main functions. The nervous system and the immune system represent the main interfaces between the internal and the external environment. In carrying out these functions, they share many similarities, being able to recognize, integrate, and organize responses to a wide variety of stimuli, with the final aim to re-establish the homoeostasis. The autonomic nervous system, which collectively refers to the ensemble of afferent and efferent neurons that wire the central nervous system with visceral effectors throughout the body, is the prototype system controlling the homoeostasis through reflex arches. On the other hand, immune cells continuously patrol our body against external enemies and internal perturbations, organizing acute responses and forming memory for future encounters. Interesting to notice, the integration of the two systems provides a further unique opportunity for fine tuning of our body’s homoeostasis. In fact, the autonomic nervous system guides the development of lymphoid and myeloid organs, as well as the deployment of immune cells towards peripheral tissues where they can affect and control several physiological functions. In turn, every specific immune cell type can contribute to regulate neural circuits involved in cardiovascular function, metabolism, and inflammation. Here, we review current understanding of the cross-regulation between these systems in cardiovascular diseases.


2011 ◽  
Vol 9 (3) ◽  
pp. 145-145
Author(s):  
Eveline Bruinstroop ◽  
Joke Wortel ◽  
Eric Fliers ◽  
Andries Kalsbeek ◽  
Susanne la Fleur

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