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Assessment of Gastric Emptying in Non-obese Diabetic Mice Using a [13C]-octanoic Acid Breath Test
Published on: March 23, 2013
Hyperglycaemia stimulates pyloric motility in normal subjects
1Gastroenterology Unit, Royal Adelaide Hospital, South Australia.
Gut
|May 1, 1991
Summary
Hyperglycemia, or high blood sugar, alters stomach motility by increasing pyloric contractions and decreasing antral contractions, leading to delayed gastric emptying. This suggests high blood sugar itself may cause abnormal stomach function in diabetes.
Area of Science:
- Gastroenterology
- Endocrinology
- Physiology
Background:
- Hyperglycemia is known to delay gastric emptying.
- The specific motor correlates responsible for this delay are not fully understood.
- This study investigates the direct impact of hyperglycemia on gastroduodenal motility.
Purpose of the Study:
- To investigate the motor correlates of delayed gastric emptying caused by hyperglycemia.
- To differentiate the effects of hyperglycemia from potential autonomic neuropathy in diabetes.
- To elucidate the mechanisms by which elevated blood glucose impacts stomach function.
Main Methods:
- Recruited 11 healthy volunteers for the study.
- Measured gastroduodenal motility during euglycemia and induced hyperglycemia using intravenous dextrose.
- Utilized sleeve/sidehole manometry across the pylorus and transmucosal potential difference measurements.
Main Results:
- Hyperglycemia stimulated isolated pyloric pressure waves (p<0.05).
- Hyperglycemia inhibited antral pressure waves (p<0.05).
- Duodenal 'phase III like' activity occurred in 9/11 subjects during hyperglycemia.
Conclusions:
- Stimulation of pyloric contractions and inhibition of antral contractions contribute to hyperglycemia-induced delayed gastric emptying.
- Abnormal gastric motility in diabetes may result from hyperglycemia itself.
- This challenges the notion that such motility issues are solely due to irreversible autonomic neuropathy.
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