KATP channel closure ameliorates the impaired insulinotropic effect of glucose-dependent insulinotropic polypeptide in patients with type 2 diabetes

What Was Tested

Researchers studied GIP (Gastric Inhibitory Polypeptide) in this randomized controlled trial publication.

The K(ATP) channels of the beta-cell appear to be essential for the function of GIP in mice, and mutations in the gene encoding these channels have been linked to the development of type 2 diabetes.

With this study the researchers therefore aimed at clarifying the role of K(ATP) channel malfunction in the impaired function of GIP.

Who Took Part

The study group was 12 subjects.

By PubMed's age tags, the people studied were middle-aged adults and older adults, both men and women.

How the Study Was Run

In design terms this was a randomized study.

The subjects were allocated by chance, so the GIP (Gastric Inhibitory Polypeptide) group and the comparison group should start out alike.

Blood was sampled to measure plasma concentrations of glucose, intact GIP, insulin, C-peptide, and glucagon.

What Was Measured

Topics PubMed links to this paper include Blood Glucose, Diabetes Mellitus, Type 2, Gastric Inhibitory Polypeptide, Glucagon, Glucose Clamp Technique, Hypoglycemic Agents and Infusion Pumps.

What This Means in Plain Language

The paper is a randomized study of GIP (Gastric Inhibitory Polypeptide) in 12 subjects.

With fewer than 40 people, it is a small study, so it is better read as an early signal for further research than as a settled answer.

Its findings take up roughly 2 sentences of the abstract and are left out here on purpose; the source paper is the place to read them.

The publication is from 2009 (The Journal of clinical endocrinology and metabolism), a journal based in United States.

More context: the GIP (Gastric Inhibitory Polypeptide) compound page, all human trials.