• Does Controlling Glycemia Increase Gastric Emptying in Patients with Diabetes?

Does Controlling Glycemia Increase Gastric Emptying in Patients with Diabetes?

Two-thirds of patients with poorly controlled type 2 diabetes have mostly asymptomatic yet abnormal gastric emptying, researchers report in the March issue of Clinical Gastroenterology and Hepatology. However, sustained improvements in glycemic control do not affect gastric emptying, the researchers found in a prospective study.

Diabetes is associated with delayed (gastroparesis) or more rapid gastric emptying, possibly caused by neuropathy, enteropathy, or hyperglycemia. It is not clear whether improved control of glycemia affects gastric emptying in patients with diabetes.

The link between hyperglycemia and gastric emptying is complex. Some studies have suggested that the rate of gastric emptying in patients with diabetic gastroparesis is determined by circulating levels of glucose. Clinicians have therefore been advised to check and control glucose levels in diabetics, because improving glycemic control will improve gastric function. However, there is not strong evidence to support this concept.

Adil E. Bharucha et al investigated whether gastric emptying changes with either overnight or short-term (6 months) improvements in glycemic control in 30 patients with poorly controlled type 2 diabetes without overt gastrointestinal symptoms.

They used the [13C]-Spirulina platensis breath test to measure gastric emptying after overnight administration of insulin or saline, 1 week later, and 6 months after intensive therapy for type 2 diabetes.

Relationship between fasting plasma glucose concentrations and half-time of gastric emptying. Fourteen patients had delayed  and 6 patients had rapid gastric emptying at baseline. Half time of gastric emptying correlated inversely with fasting plasma glucose concentrations during baseline and after insulin or saline administration.

Relationship between fasting plasma glucose concentrations and half-time of gastric emptying. Fourteen patients had delayed and 6 patients had rapid gastric emptying at baseline. Half-time of gastric emptying correlated inversely with fasting plasma glucose concentrations at baseline (left) and after administration of insulin or saline (right).

At the first visit, gastric emptying was normal in 10 patients, delayed in 14, and accelerated in 6. Six patients had gastrointestinal symptoms; vagal dysfunction was associated with delayed gastric emptying. Higher fasting blood levels of glucose were associated with shorter half-times of gastric emptying at the first 2 visits.

However, although administration of insulin reduced blood levels of glucose compared with saline, it did not increase the speed of gastric emptying.

After 6 months of intensive therapy, levels of glycosylated hemoglobin decreased, but the speed of gastric emptying did not change (92 ± 8 min before vs 92 ± 7 min after treatment). Gastric emptying did not correlate with plasma levels of glucagon-like peptide 1 or amylin in these patients.

Bharucha et al conclude that most patients with poorly controlled type 2 diabetes have abnormal gastric emptying, and that higher fasting blood levels of glucose are associated with faster gastric emptying. However, improved glycemic control does not affect gastric emptying.

In an editorial that accompanies the article, Pankaj Jay Pasricha explains that acute hyperglycemia affects gastric emptying in healthy subjects and in some, but not all, diabetics by multiple neuro-hormonal control mechanisms that affect different regions of the stomach. Hyperglycemia produces lower tone of the proximal stomach (leading to greater retention of the bolus), inhibition of antral activity, and increased pyloric contractility. Together, these slow gastric emptying.

Pasricha says that these effects may be mediated by hyperglycemic inhibition of vagal to cholinergic signaling, via direct effects of glucose on vagal afferents or by glucose-sensing nuclei in the central nervous system.

Pasricha adds that in addition to production of incretins, such as glucagon-like peptide-1 and gastric inhibitory polypeptide, increased blood glucose induces the release of other hormones such as amylin (islet associated pancreatic polypeptide), which is secreted with insulin in response to increasing levels of glucose.

Diabetes could disrupt these signaling pathways to dissociate glucose levels from rates of gastric emptying. Pasricha explains that neuropathy of the gastric vagus would therefore not only cause a persistent delay in gastric emptying but also make it unlikely to respond to any further modulatory factors.

 

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