Does the route of insulin delivery affect glycogen storage in type I diabetes?

This study evaluated the influence of systemic insulin delivery on liver glycogen levels in patients with type 1 diabetes mellitus. 

Type I diabetes is an autoimmune disease where the body no longer produces insulin. In the liver, insulin promotes glucose uptake by stimulating its storage as glycogen while inhibiting glycogen breakdown. Previous studies have shown that the liver's capacity to store glycogen is reduced in patients with type 1 diabetes mellitus, but it remains unclear whether this is due to hyperglycemia (a high blood glucose level), or whether the route of insulin supply could contribute to this occurrence.

Systemic insulin delivery prevents removal or loss (metabolism) of insulin by the body before it becomes available for use. This study investigated the effects of systemic insulin delivery (via an insulin pump under the skin) on glycogen storage in type I diabetes patients by comparing their liver glycogen levels to patients with type I diabetes who had undergone pancreas–kidney transplants (performed for patients who have kidney failure as a complication of type 1 diabetes mellitus). These transplant patients have normal glucose levels, are not usually on any form of insulin regime and so represent a suitable human model against which to compare the effects of systemic insulin delivery in type I diabetes. 

This study involved 25 participants. Nine were type I diabetes patients who had undergone successful pancreas-kidney transplantation, seven were patients with type 1 diabetes mellitus who had not undergone such a transplantation and were receiving insuling via an insulin pump, while the remaining subjects were healthy participants used as controls (a group used as a basis to compare the results of the experiment).

Results showed that patients with type 1 diabetes mellitus and those with pancreas-kidney transplants had a lower liver glycogen measurement than controls. Compared to the control group, participants with pancreas-kidney transplantation had 14% less and type 1 diabetes patients had 21% less liver glycogen after eating.

The three groups showed a general increase in postprandial liver glycogen content compared to fasting state (before eating). Compared to the fasting state, those with pancreas-kidney transplants had 25% more postprandial liver glycogen content, type 1 diabetes patients had a 12% increase and the control group had a 30% increase. 

In summary, this study concluded that the route of insulin supply does not affect postprandial liver glycogen storage capacity in patients with type 1 diabetes mellitus.

This study included a very small number of participants. Larger studies are necessary to confirm these findings.

In addition, participants with pancreas-kidney transplants used immunosuppressive drugs. The influence of these drugs on liver glycogen metabolism was not determined.