ReviewLife (Basel, Switzerland)2026
Adipose Tissue Circadian Dysregulation Beyond BMI: Implications for Cardiometabolic Risk and Cardiovascular Disease.
Review in Life (Basel, Switzerland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Adipokine profiles and genetic variants of leptin receptor, adiponectin, and ghrelin pathways in obesity: prospective 12-month outcomes after bariatric interventions.Frontiers in endocrinology · 2026Observational
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
No grant is acknowledged in the PubMed record.
Abstract
Cardiometabolic and cardiovascular risks are commonly assessed using body mass index (BMI) and static measures of adiposity; however, individuals with similar BMI frequently exhibit markedly different metabolic and cardiovascular outcomes. This heterogeneity reflects not only differences in fat distribution but also variation in adipose tissue function and its temporal regulation. Adipose tissue contains intrinsic circadian clocks that coordinate daily rhythms in lipid storage and mobilization, insulin sensitivity, adipokine secretion, and immune activity in alignment with sleep-wake and feeding-fasting cycles. Circadian misalignment, as occurs with shift work, irregular sleep, or mistimed food intake, disrupts this coordination and promotes adipose tissue dysfunction characterized by impaired rhythmic lipid handling, altered endocrine signaling, inflammation, fibrosis, and oxidative stress. Emerging evidence suggests that circadian dysregulation may differentially affect adipose depots, including visceral, epicardial, and perivascular fat, thereby linking chronodisruption to insulin resistance, endothelial dysfunction, atherosclerosis, heart failure phenotypes, and arrhythmia susceptibility. This narrative review synthesizes human, experimental, and translational studies examining adipose tissue circadian regulation as a functional determinant of cardiometabolic and cardiovascular risk beyond BMI. We also discuss the clinical implications of circadian-informed strategies, including chrononutrition and time-restricted eating, as potential tools to improve risk stratification and cardiometabolic health.
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.