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(2022). https://pubmed.ncbi.nlm.nih.gov/35015083/ DOI: 10.2337/dc21-1314","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Endogenous melatonin and evening glucose handling","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"b1c66dd3-b698-5b14-a076-47968f0c1c36","evidence_kind":"source_excerpt","locator":"Lines 1163-1174","start_line":1163,"end_line":1174,"excerpt":"### melatonin-late-challenge-glucose\nGlucose AUC was about 8.3% higher in the late condition, with greater impairment in MTNR1B risk carriers.\nCondition category: normal\nnutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: A meal-timing comparison can reveal susceptibility without proving melatonin is the only mediator.\norganism: 845 Spanish adults\ntissue_or_cell_type: Endogenous melatonin and evening glucose handling\nexperimental_model: Randomized crossover early versus late glucose-challenge study\nlimitations: Glucose drinks simulated meal timing. Timing, endogenous melatonin and other circadian factors co-varied; the intervention did not selectively manipulate melatonin alone.\nexposure: 75 g OGTT four versus one hour before habitual bedtime after eight-hour fast\nevidence_span: {\"source_cache\": \"artifacts/melatonin-research/35015083.abstract.txt\", \"locator\": \"Primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"14878cd566ac009dde6fd0a6cc78adf1a4b48cfb2bc09e262568c909f84f236e\", \"start_char\": 0, \"end_char\": 1688, \"text_sha256\": \"14878cd566ac009dde6fd0a6cc78adf1a4b48cfb2bc09e262568c909f84f236e\"}\n[melatonin-p35015083] Interplay of Dinner Timing and MTNR1B Type 2 Diabetes Risk Variant on Glucose Tolerance and Insulin Secretion: A Randomized Crossover Trial. 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