Oesophageal dysmotility, delayed gastric emptying and autonomic neuropathy correlate to disturbed glucose homeostasis.

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Aims/hypothesis Among diabetic patients, glucose homeostasis may be affected by abnormal gastrointestinal motility and autonomic neuropathy. This study analysed whether oesophageal dysmotility, delayed gastric emptying or autonomic neuropathy affect glucose homeostasis. Materials and methods Oesophageal manometry and gastric emptying scintigraphy were performed in 20 diabetic patients. Heart-rate variation during deep breathing (expiration/inspiration [E/I] ratio) and continuous subcutaneous glucose concentrations for a period of 72 h were also monitored in the same patients. Results Oesophageal dysmotility was found in eight of 14 patients. Eleven of 20 patients had delayed gastric emptying (abnormal gastric emptying half-time [T (50)]) and nine of 18 had an abnormal E/I ratio. Complaints of abdominal fullness were predictive of delayed gastric emptying. A low peristaltic speed of the oesophagus was associated with impaired T (50) (r (s) =-0.67; p=0.02). One hour after breakfast, subcutaneous glucose levels decreased in patients with delayed gastric emptying but continued to rise in those with normal emptying. Consequently, the median glucose level 2.5 h after breakfast was lower in the former (9.1 [4.2-12.5] vs 14.3 [11.2-17.7] mmol/l; p < 0.05). Glucose fluctuations during the 72 h were significantly higher in patients with an abnormal E/I ratio than in those with a normal E/I ratio (coefficient of variation: 41 [46-49] vs 28 [27-34]%; p=0.008). Conclusions/interpretation Abdominal fullness predicted delayed gastric emptying that was associated with diminished glucose uptake after breakfast. Low oesophageal peristaltic speed was associated with slow gastric emptying whereas parasympathetic neuropathy was associated with increased glucose variations.
Sidor (från-till)2010-2014
Nummer2006 Jul 11
StatusPublished - 2006

Bibliografisk information

The information about affiliations in this record was updated in December 2015.
The record was previously connected to the following departments: Chronic Inflammatory and Degenerative Diseases Research Unit (013242530), Hypertension and Cardiovascular Disease (013242540), Clinical Physiology and Nuclear Medicine Unit (013242320), Medical Radiology Unit (013241410), Diabetes Epidemiology and Neuropathy (013241560), Department of Clinical Sciences, Malmö (013240000)

Ämnesklassifikation (UKÄ)

  • Endokrinologi och diabetes


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