Neuroinflammatory and autonomic mechanisms in diabetes and hypertension

Am J Physiol Endocrinol Metab. 2016 Jul 1;311(1):E32-41. doi: 10.1152/ajpendo.00012.2016. Epub 2016 May 10.

Abstract

Interdisciplinary studies in the research fields of endocrinology and immunology show that obesity-associated overnutrition leads to neuroinflammatory molecular changes, in particular in the hypothalamus, chronically causing various disorders known as elements of metabolic syndrome. In this process, neural or hypothalamic inflammation impairs the neuroendocrine and autonomic regulation of the brain over blood pressure and glucose homeostasis as well as insulin secretion, and elevated sympathetic activation has been appreciated as a critical mediator. This review describes the involved physiology and mechanisms, with a focus on glucose and blood pressure balance, and suggests that neuroinflammation employs the autonomic nervous system to mediate the development of diabetes and hypertension.

Keywords: autonomic nervous system; hypothalamus; inflammation.

Publication types

  • Review

MeSH terms

  • Animals
  • Autonomic Nervous System / immunology
  • Autonomic Nervous System / metabolism
  • Autonomic Nervous System / physiopathology
  • Blood Glucose / metabolism
  • Blood Pressure / physiology
  • Brain / immunology
  • Brain / metabolism
  • Brain / physiopathology
  • Diabetes Mellitus / immunology
  • Diabetes Mellitus / metabolism*
  • Glucose / metabolism
  • Homeostasis
  • Humans
  • Hypertension / immunology
  • Hypertension / metabolism*
  • Hypertension / physiopathology
  • Hypothalamus / immunology
  • Hypothalamus / metabolism*
  • Hypothalamus / physiopathology
  • Inflammation
  • Insulin / metabolism
  • Insulin Secretion
  • Metabolic Syndrome / immunology
  • Metabolic Syndrome / metabolism*
  • Obesity / immunology
  • Obesity / metabolism*
  • Overnutrition / immunology
  • Overnutrition / metabolism*
  • Sympathetic Nervous System / immunology
  • Sympathetic Nervous System / metabolism*
  • Sympathetic Nervous System / physiopathology

Substances

  • Blood Glucose
  • Insulin
  • Glucose