Investigating the effect of olfactory bulbectomy on vagal circuits and the pancreas: A new hypothesis

It is well known how the olfactory nerves regulate the pancreas via the vagal nerves. However, there is no clear information explaining the actual neuropathological mechanism of how olfactory pathway damage destroys pancreatic beta cells. The aim of this study was to investigate whether the dorsal vagal nucleus and pancreas are histologically affected in olfactory bulb lesions.

This study was conducted on twenty-six male rats. Group-I was the control group (n: 5), group-II was the SHAM group (n: 5) and group-III was the olfactory bulbectomy group (n: 16). All animals were observed for ten weeks and then decapitated. Olfactory bulb volume and degenerated neuron densities of the dorsal vagal motor nucleus and degenerated pancreatic beta cells per cubic millimeter were determined stereologically.

The mean olfactory bulb volume, degenerated dorsal vagal motor nucleus and degenerated pancreatic beta cells were measured as 4.31 ± 0.25 mm³, 4 ± 1/mm³, 2 ± 1/mm³ in the control group (Group-I); 3.92 ± 0.38 mm³, 9 ± 3/mm³, 7 ± 3/mm³ in the SHAM group (Group-II) and 2.97 ± 0.41 mm³, 29 ± 5/ mm³, 43 ± 9/ mm³ in the olfactory bulbectomy group (Group-III). Main p value for all data: p < 0.005 between Group-I and Group-II, p < 0.0005 between Group-II and Group-III; p < 0.0001 between Group-I and Group-III CONCLUSIONS: It can be suggested that olfactory bulb lesion causes denervation injury in intrapancreatic ganglia and beta cells due to decreased effect of vagal efferents, which stimulate intrapancreatic neuro-beta cell communication by decreasing olfactory signals stimulating vagal nerve nuclei. This study may help clinicians to investigate etiological factors in cases of impaired insulin and glucose metabolism.