Abnormal glucagon concentrations contribute to hyperglycemia but the mechanism(s) of α-cell dysfunction in prediabetes are unclear.
We sought to determine the relative contributions of insulin secretion and action to α-cell dysfunction in non-diabetic subjects across the spectrum of glucose tolerance.
This was a cross-sectional study. A subset of subjects (n = 120) was studied in the presence and absence of free fatty acid (FFA) elevation, achieved by infusion of intralipid + heparin, to cause insulin resistance.
An Inpatient Clinical Research Unit at an academic medical center.
A total of 310 non-diabetic subjects participated in this study.
Subjects underwent a 7-sample oral glucose tolerance test. Subsequently, 120 subjects were studied on two occasions. On one day infusion of intralipid + heparin raised FFA. On the other day subjects received glycerol (GLY) as a control.
We examined the relationship of glucagon concentration with indices of insulin action after adjusting for the effects of age, sex and weight. Subsequently, we sought to determine whether an acute decrease in insulin action, produced by FFA elevation, altered glucagon concentrations in non-diabetic subjects.
Fasting glucagon concentrations correlated positively with fasting insulin and C-peptide concentrations and inversely with insulin action (Si ). Fasting glucagon was not associated with any index of β-cell function in response to an oral challenge. As expected, FFA elevation decreased insulin action and also raised glucagon concentrations.
In non-diabetic subjects glucagon secretion is altered by changes in insulin action.
This research output has an Altmetric Attention Score of 3. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 12 March 2021.
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