ArticleDiabetes, obesity & metabolism2026
Postprandial Glucagon Action in the Human Brain.
Article in Diabetes, obesity & metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
aimsElevated fasting glucagon is linked to hyperglycemia, but postprandial glucagon effects are less understood. Recent evidence suggests metabolic benefits of rising glucagon after oral glucose intake, potentially impacting brain-mediated whole-body metabolism. To elucidate the translational relevance of these findings, we studied postprandial effects of glucagon on the human brain. MATERIALS AND
methodsWe performed oral glucose tolerance tests (OGTT) combined with functional magnetic resonance imaging to quantify brain activity and connectivity at fasting, 30 and 120 min post glucose load in 30 volunteers. In 14 participants with suppressed glucagon, low-dose glucagon infusion mimicked non-suppressed glucagon after OGTT. This was compared to 7 participants with endogenous rising glucagon during OGTT.
resultsLow-dose glucagon infusion did not elevate plasma glucose levels during OGTT. Also, no changes in insulin sensitivity and insulin secretion were observed. However, experimentally elevating glucagon during OGTT in individuals with physiological suppression of glucagon significantly increased postprandial brain responsivity in the hippocampal gyrus and in brain regions important for the homeostatic and hedonic regulation of food intake as well as systemic metabolism (i.e., hypothalamus and ventral striatum). Most postprandial brain responsiveness during glucagon infusion was directionally consistent with the findings in persons with endogenously rising glucagon. Moreover, the postprandial brain response correlated with the rise in glucagon, regardless of exogenous or endogenous source of glucagon. Although the overall glucagon trajectory during OGTT was not significantly different over the full 0-150 min period, the groups differed at key post-challenge timepoints and in integrated glucagon exposure. Together with the infusion and correlation analyses, this supports a relationship between postprandial glucagon and brain responsivity, while more subtle differences in glucagon kinetics will require larger studies.
conclusionsOur findings demonstrate postprandial effects of glucagon in metabolically relevant human brain areas. This may underlie the promising effects on body weight achieved with pharmacological multi-agonists that activate the glucagon receptor.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.