Designing a Bioelectronic Treatment for Type 1 Diabetes: Targeted Parasympathetic Modulation of Insulin Secretion

Abstract

The pancreas is a visceral organ with exocrine functions for digestion and endocrine functions for maintenance of blood glucose homeostasis. In pancreatic diseases such as Type 1 diabetes, islets of the endocrine pancreas become dysfunctional and normal regulation of blood glucose concentration ceases. In healthy individuals, parasympathetic signaling to islets via the vagus nerve, triggers release of insulin from pancreatic β-cells and glucagon from α-cells. Using electrical stimulation to augment parasympathetic signaling may provide a way to control pancreatic endocrine functions and ultimately control blood glucose. Historical data suggest that cervical vagus nerve stimulation recruits many visceral organ systems. Simultaneous modulation of liver and digestive function along with pancreatic function provides differential signals that work to both raise and lower blood glucose. Targeted pancreatic vagus nerve stimulation may provide a solution to minimizing off-target effects through careful electrode placement just prior to pancreatic insertion.

Keywords::

• autoimmune disease
• bioengineering
• diabetes
• electroceuticals
• neuroanatomy
• neurofunction
• neuromodulation
• vagus nerve

Financial & competing interests disclosure

This work was sponsored by the Defense Advanced Research Projects Agency (DARPA) BTO under the auspices of D Weber and EV Gieson through the DARPA Contracts Management Office (Grant No. HR0011-17-2-0019) and by a National Institute of Diabetes and Digestive and Kidney Diseases T32 training grant (5T32DK108736-03). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

This work was sponsored by the Defense Advanced Research Projects Agency (DARPA) BTO under the auspices of D Weber and EV Gieson through the DARPA Contracts Management Office (Grant No. HR0011-17-2-0019) and by a National Institute of Diabetes and Digestive and Kidney Diseases T32 training grant (5T32DK108736-03). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.