BACKGROUND & AIMS: The roles of hyperglycemia in diabetic gastroparesis and gastric delivery in postprandial hyperglycemia of diabetic patients are unclear. The aims of this study were to assess gastric emptying and its relation to postprandial glucose metabolism in patients with asymptomatic non-insulin-dependent diabetes mellitus (NIDDM) and no autonomic neuropathy and to identify motor mechanisms responsible for any accelerated gastric emptying. METHODS: Autonomic function, gastric emptying, postprandial glucose metabolism, and hormone levels (glucagon, insulin, cholecystokinin, glucose-dependent insulinotropic polypeptide, neurotensin, and peptide YY) were assessed in healthy volunteers and patients with NIDDM. In a second study, gastric tone and motility were measured in patients with accelerated gastric emptying and in controls. 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.
BACKGROUND & AIMS: The roles of hyperglycemia in diabetic gastroparesis and gastric delivery in postprandial hyperglycemia of diabeticpatients are unclear. The aims of this study were to assess gastric emptying and its relation to postprandial glucose metabolism in patients with asymptomatic non-insulin-dependent diabetes mellitus (NIDDM) and no autonomic neuropathy and to identify motor mechanisms responsible for any accelerated gastric emptying. METHODS: Autonomic function, gastric emptying, postprandial glucose metabolism, and hormone levels (glucagon, insulin, cholecystokinin, glucose-dependent insulinotropic polypeptide, neurotensin, and peptide YY) were assessed in healthy volunteers and patients with NIDDM. In a second study, gastric tone and motility were measured in patients with accelerated gastric emptying and in controls. 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.
Authors: Nam Q Nguyen; Marianne Chapman; Robert J Fraser; Marc Ritz; Laura K Bryant; Ross Butler; Geoffrey Davidson; Betty Zacharakis; Richard H Holloway Journal: Intensive Care Med Date: 2006-06-29 Impact factor: 17.440
Authors: Bradley Anderson; Paula Carlson; Marcello Laurenti; Adrian Vella; Michael Camilleri; Anshuman Desai; Kelly Feuerhak; Adil E Bharucha Journal: Neurogastroenterol Motil Date: 2019-11-05 Impact factor: 3.598