ArticleHormones (Athens, Greece)2025
Effect of melatonin on adipokines, biochemical parameters, clock genes, and lipid metabolism in a rat obesity model.
Article in Hormones (Athens, Greece), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- The effects of melatonin supplementation on obesity and glycemic indices in women with overweight and obesity: a systematic review and meta-analysis of randomized controlled trials.Diabetology & metabolic syndrome · 2026Article
- Loss of melatonin signaling increases the risk of T2DM caused by metabolic disorders.Cell communication and signaling : CCS · 2025Article
- Parathyroid disease, gut microbiome, biologic age, and more.Hormones (Athens, Greece) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Obesity, characterized by excessive fat accumulation, disrupts metabolism, leading to insulin resistance, hyperglycemia, and dyslipidemia. Circadian rhythm genes such as BMAL1 and CRY1 regulate energy balance, lipid metabolism, and glucose homeostasis, with enzymes, for example, DGAT1 and DGAT2, playing critical roles in triglyceride synthesis. Melatonin, a circadian regulator, influences metabolic processes, including glucose and insulin regulation. This study examined melatonin's therapeutic effects in obese Wistar rats. A total of 48 male rats were fed either a standard diet (C group) or a high-fat diet for 11 weeks to induce obesity. Once the obese group was established, the latter animals were subdivided into two experimental groups, namely, OB (obesity-induced) and OB-M (obesity-induced + melatonin), each under two circadian shifts (9 h and 21 h). During the subsequent 6 weeks, all animals received standard diets plus/minus melatonin supplementation (25 µg/mL in drinking water). The 9 h and 21 h time points were selected to evaluate the effects of circadian rhythm alignment or disruption on metabolic outcomes and melatonin efficacy. Body weight, food intake, and water consumption were recorded every third day. Melatonin supplementation significantly reduced body weight in OB-M group, with no effect observed in the control animals. It also improved glucose, cholesterol, and triglyceride levels compared to diet change alone. Leptin and IL-1β levels decreased with melatonin, suggesting anti-inflammatory and metabolic regulatory effects. Additionally, melatonin influenced circadian gene expression, including BMAL1 and CRY1, and showed correlations with metabolic and inflammatory markers. These findings indicate that melatonin supplementation, when combined with dietary modifications, improves metabolic outcomes and contributes to the restoration of circadian and inflammatory balance in obesity. However, further research is required to elucidate the underlying mechanisms.
Indexed as
Identifiers
40957975What 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.