Clinical Trial Details
— Status: Completed
Administrative data
| NCT number |
NCT02921906 |
| Other study ID # |
R&D no 1701366 |
| Secondary ID |
|
| Status |
Completed |
| Phase |
N/A
|
| First received |
|
| Last updated |
|
| Start date |
June 2016 |
| Est. completion date |
June 20, 2022 |
Study information
| Verified date |
October 2022 |
| Source |
Royal Devon and Exeter NHS Foundation Trust |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Interventional
|
Clinical Trial Summary
Neonatal diabetes is diagnosed before 6 months of age and causes high blood glucose levels
due to the pancreas not secreting insulin. Neonatal diabetes can be caused by a change in a
DNA region called the KCNJ11 gene. KCNJ11 encodes a channel in the pancreas that acts as a
switch to turn 'on' and 'off' insulin secretion. A change in KCNJ11 results in a faulty
channel, which keeps insulin secretion 'switched off'. The diabetes can be treated with
tablets called sulphonylureas that switch the pancreatic channel 'on', allowing it to secrete
insulin in response to gut hormones called incretins. Previous research has shown that
patients who switch from insulin to sulphonylureas have better blood glucose control,
including fewer episodes of hypoglycaemia (glucose dropping too low), and also avoid the need
for injections. It is thought that serious side effects from sulphonylureas are uncommon in
KCNJ11 neonatal diabetes. Some patients report low glucose after meals and we think this may
be because they make too much insulin if they eat a meal with protein but low amounts of
carbohydrate. The investigators will test this by giving study participants different meals
and measuring the amount of insulin, glucose and incretin hormone in the blood afterwards.
Description:
Anecdotal evidence from routine clinical care suggests that patients with
sulphonylurea-treated KCNJ11 neonatal diabetes, when they eat, may experience mild
hypoglycaemia if the food consumed lacks carbohydrate. It has been suggested that this may be
due to regulation of insulin secretion via the incretin pathway as opposed to the classical
ATP pathway. Therefore the investigators hypothesise that foods with a relatively high
protein content compared to those with a relatively high carbohydrate content will result in
excessive insulin secretion and relatively lower glucose values in KCNJ11 patients. This
would be in contrast to healthy control subjects or subjects with SU-treated T2D where the
insulin secretion will be moderated by the ambient glucose via the classical ATP pathway. The
investigators will formally study this hypothesis by comparing the insulin, glucose and
incretin hormone responses to a high protein meal with a high carbohydrate meal in people
with KCNJ11 neonatal diabetes, people without diabetes and people with sulphonylurea-treated
Type 2 Diabetes. To assess whether any effect seen is due to direct stimulation of the beta
cell by the sulphonylurea itself, people with KCNJ11 neonatal diabetes will also undergo the
same tests in the fasting state, having taken the sulphonylurea in the absence of any food.
