Abstract

Hypothalamus and brain stem play important roles in Glucose Homeostasis. There are two types of cells in the hypothalamus: Glucose excited (GE) and Glucose inhibited (GI). GE increases glucose concentration and GI decreases glucose concentration. They are located in ventromedial (VMH), arcuate, lateral, dorsomedial and paraventricular areas of hypothalamus. Nucleus of solitary tract, area postrema, dorsomedial nucleus of vagus and basolateral medulla are also related to glucose homeostasis. VMH contains sympathetic nucleus and upregulates plasma glucose and decreases hepatic glycogen, while lateral hypothalamus contains parasympathetic and down regulates plasma glucose. Through Glut-1, dependent transport glucose enters neurons and astrocytes. Glucose is metabolized and provides energy for GE and GI neurons. Their activity is guided by blood sugar level. Blood sugar level sends numerous signals through vagal pathway from periphery. Neuron astrocyte establishes via autonomic system connections with liver, pancreas, adrenal gland and maintains glucose homeostasis. Post prandial glucose levels are regulated by CNS.

Highlights

  • Homeostasis can be defined as a property of an organism or system that helps it maintain its parameters within a normal range of values

  • Glucose is metabolized and provides energy for Glucose excited (GE) and Glucose inhibited (GI) neurons. Their activity is guided by blood sugar level

  • Post prandial glucose levels are regulated by CNS

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Summary

Historical Background

1849: Claud Bernard showed puncturing floor of the fourth ventricle in brain, produced hyperglycemia in a few days time. 1953: Jean Mayer described two types of cells GE/GI neurons existence in brain. 1994: Borg showed that lesions of VMH produced hypoglycemia due to decrease of hormonal counter regulation Raman lates plasma glucose. 1994: Borg showed that lesions of VMH produced hypoglycemia due to decrease of hormonal counter regulation

Introduction
Effect of High Fat Diet on Neuro-Gluco Regulation
Central GLP-1 Actions
Neuronal Biochemical Sensors
10. Conclusion
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