Autonomic control and bariatric procedures

Abstract

The sudden improvement of metabolic profile and the remission of type 2 diabetes after bariatric surgery, well before weight loss, raise important new questions regarding glycemic control. Currently, various types of bariatric procedures target type 2 diabetes in obese and non-obese patients. Nevertheless, the origin of the dramatic metabolic improvements, including glucose homeostasis, is poorly understood, and the role of the gastrointestinal (GI) tract remains relatively speculative, as well as why these procedures are variably effective. One neglected explanation is that such interventions disrupt neural networks mediating GI-brain communication and could alter the autonomic output to the visceral organs, including the liver. Incretins, e.g., glucagon-like peptide 1 (GLP-1), have major influence on the central nervous system. Moreover, the level of GLP-1 is observed to significantly increase after bariatric surgery and could be a key factor in the weight-independent, anti-diabetic effect. Therefore, this review will evaluate the effect of GLP-1 on the central nervous system, with emphasis on the cellular effects of GLP-1, and will provide an overview of the autonomic control of the liver.

Keywords: Autonomic control of the liver; Brainstem; Glucagon-like peptide 1; Neuronal properties; Paraventricular nucleus of the hypothalamus.