Abstract | BACKGROUND & AIMS: METHODS: RESULTS: Gastric emptying of solids did not differ in the two groups, but liquids emptied faster in patients with NIDDM (P < 0.02). The rate of entry of ingested glucose into the systemic circulation was similar, but higher postprandial glucagon and lower insulin concentrations led to greater (P < 0.01) postprandial hepatic glucose release. Levels of other enteropeptides, gastric accommodation, and antral motility were similar, but patients with NIDDM had greater proximal gastric phasic contractions than controls (P < 0.05). CONCLUSIONS: Excessive hepatic glucose release, not rapid entry of ingested glucose, is the primary cause of postprandial hyperglycemia in patients with NIDDM. Accelerated gastric emptying in patients with nonneuropathic NIDDM is associated with increased proximal stomach phasic contractions.
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Authors | J W Frank, S B Saslow, M Camilleri, G M Thomforde, S Dinneen, R A Rizza |
Journal | Gastroenterology
(Gastroenterology)
Vol. 109
Issue 3
Pg. 755-65
(Sep 1995)
ISSN: 0016-5085 [Print] United States |
PMID | 7657103
(Publication Type: Clinical Trial, Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
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Topics |
- Autonomic Nervous System
(physiopathology)
- Diabetes Mellitus, Type 2
(complications, metabolism, physiopathology)
- Eating
- Female
- Gastric Emptying
- Gastrointestinal Motility
- Glucagon
(blood)
- Glucose
(metabolism)
- Humans
- Hyperglycemia
(etiology, metabolism, physiopathology)
- Insulin
(blood)
- Liver
(metabolism)
- Male
- Middle Aged
- Muscle Contraction
- Stomach
(physiopathology)
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