Trial reportDiabetes care2026
Melatonin Impairs Glucose Tolerance, First-Phase Insulin Secretion, and Insulin Feedback Inhibition; Interaction With MTNR1B Diabetes Risk Variant.
Trial report in Diabetes care, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Authors and funding
14 authors.
Funding
Abstract
objectiveMelatonin use quintupled in recent decades. The common melatonin receptor 1B gene (MTNR1B) variant increases risk of type 2 diabetes, raising concerns about melatonin's adverse metabolic effects and highlighting the need for a genotype-based personalized approach. We aimed to comprehensively characterize the actions of melatonin on glucose homeostasis, including first- and second-phase β-cell responsivity to glucose, β-cell negative feedback by exogeneous insulin, insulin sensitivity, and whether such effects are stronger in MTNR1B G-allele risk carriers compared with noncarriers. RESEARCH DESIGN AND
methodsTwenty-one healthy participants of European ancestry were studied in a randomized, double-blind, placebo-controlled, crossover trial, including 10 MTNR1B risk carriers and 11 noncarriers. Each participant underwent a highly controlled 5-day laboratory protocol, during which they received 5 mg oral melatonin or placebo in randomized order on two nonconsecutive days. Glycemic dynamics were assessed using insulin-modified intravenous glucose tolerance tests with minimal-model analysis.
resultsMelatonin worsened glucose tolerance and reduced early C-peptide responses in risk allele carriers (vs. placebo: 11.7% [95% CI 1.0-22.3] and -19.2% [-33.9 to -1.2], respectively; Padj < 0.05) but not in noncarriers. In carriers, impairments stemmed from a 40% (-52.4 to -24.3; Padj = 0.0003) suppression of glucose-stimulated first-phase β-cell responsivity, along with a slower insulin-induced decline in second-phase insulin secretion rate (64.3% [23.1-119.2]; Padj = 0.001). In carriers, melatonin also prevented exogenous insulin-induced hypoglycemia compared with placebo (zero vs. seven events, P = 0.001), but not in noncarriers.
conclusionsThese findings identify blunted β-cell responsivity to glucose and dysregulated insulin negative feedback as key mechanisms linking melatonin signaling to diabetes risk.
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