Effect of altering gastric emptying on glucose tolerance following a physiologic meal in type II diabetic patients

Diabetes mellitus and gastric emptying: questions and issues in clinical practice

“…It has been hypothesized that prokinetic drugs may actually improve glycaemic control by facilitating a more predictable absorption of nutrients [105]. However, the rapid acceleration of gastric emptying associated with erythromycin therapy has been shown to actually worsen postprandial glucose control [103,106]. In addition, a number of other side effects may occur with erythromycin, including nausea, vomiting, and abdominal pain [76].…”

Give the Receptor a Brake: Slowing Gastric Emptying by GLP-1

“…Yet it is important to note that much of the variance in oral glucose tolerance is accounted for by differences in GE rate, an observation made over two decades ago (1). Even a minor perturbation in GE carries a substantial impact on postprandial glycemia in healthy individuals (1) and those with diabetes (3), such that more rapid GE results in a greater initial glycemic response and slower gastric delivery of meal contents to the intestine leads to smaller glucose excursion (4).…”

Mechanisms and Clinical Efficacy of Lixisenatide for the Management of Type 2 Diabetes

“…However, because the human stomach empties at an overall rate of 1−4 kcal/min in health [20,21], most humans are predominantly in the postprandial or postabsorptive state, with the duration of fasting limited, in most cases, to perhaps about 4 h before breakfast. Moreover, gastric empting is often abnormally delayed (and occasionally, more rapid) in patients with T2DM and is a major determinant of postprandial glycemia [22][23][24]. In T2DM patients with delayed emptying, the magnitude of this delay is often modest [22][23][24], hence the fact that both endogenous and exogenous GLP-1 slow gastric emptying is of fundamental significance.…”

“…Moreover, gastric empting is often abnormally delayed (and occasionally, more rapid) in patients with T2DM and is a major determinant of postprandial glycemia [22][23][24]. In T2DM patients with delayed emptying, the magnitude of this delay is often modest [22][23][24], hence the fact that both endogenous and exogenous GLP-1 slow gastric emptying is of fundamental significance. Moreover, the secretion of GLP-1 is dependent on the small intestinal glucose load being released in much greater amounts when the rate of carbohydrate exposure is at the upper end of the normal physiological range [25].…”