Background: Hyperglycemia has been tried to explain by diﬀerent mechanisms, but glucose-sensing tongue taste buds-geniculate ganglia-facial nerve-vagal nerve-pancreas web relation has not been adequately investigated.
Objectives: We aimed to investigate if there is any relationship between the described taste buds network degeneration and blood glucose levels following subarachnoid hemorrhage (SAH).
Methods: This study was conducted on 32 rabbits. Blood glucose levels were measured at the beginning, mid-phase, and the end of the experiment. Animals were divided into the groups of control (n = 5), physiologic serum saline (SHAM; n = 5), and subarachnoid hemorrhage with 0.5 cc homolog blood injection into cisterna magna (study; n = 22) three times a week and were sacrificed under general anesthesia after two weeks. The blood glucose level of 113 ± 20 mg/dL was accepted as normal (G-I; n = 11), lower than 80 mg/dl as hypoglycemic (G-II; n = 6), and higher than 149 mg/dl as hyperglycemic (G-III; n = 5). Their neuron densities of geniculate ganglia were examined by stereological methods. The statistical analysis was done between glucose levels/ degenerated taste bud/neurons using Kruskal-Wallis and Mann-Whitney U tests. We accepted P > 0.005 as non-significance.
Results: The mean normal blood glucose level was 115 ± 9 mg/dl before surgery. The pre-sacrificed glucose level was 113 ± 8 mg/dL and the neuron density of the geniculate ganglia was 7.421 ± 530/mm3. The degenerated neuron density of geniculate ganglia was 13 ± 4/mm3 in controls 21 ± 7/mm3 in SHAM, 27 ± 7/mm3 in G-I, 21 ± 5/mm3 in G-II, and 112 ± 18/mm3 in G-III groups. The P values of glucose levels-degenerated neuron density of geniculate ganglia between control/G-III was: P < 0.00001; SHAM/G-III: P < 0.0005; GI/GII: P < 0.005.
Conclusions: Glucose sensing tongue taste buds-geniculate ganglia-facial nerve-vagal nerve-pancreas circuitry should be an unexplained web for the regulation of blood glucose level.