ReviewMetabolites2026
Adipose Tissue-Central Nervous System Axis in Obesity: Molecular Mechanisms, Inflammation, and Nutritional and Technological Implications.
Review in Metabolites, 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
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Authors and funding
8 authors.
Funding
Abstract
Obesity is a multifactorial condition characterized by profound metabolic and inflammatory dysregulation that alters the adipose tissue-central nervous system (CNS) relationship. This paper critically summarizes the biochemical and cellular mechanisms governing this bidirectional crosstalk, moving beyond a descriptive perspective to propose an integrated model of peripheral-central interaction. White adipose tissue (WAT) and brown adipose tissue (BAT), modulated by the sympathetic nervous system (SNS), communicate with hypothalamic circuits (POMC and AgRP neurons) both through traditional endocrine signals (leptin, adiponectin, resistin, apelin) and through lipid mediators and extracellular vesicles (EVs) capable of crossing the blood-brain barrier (BBB). Under conditions of nutritional excess, the accumulation of lipotoxic lipid species (such as palmitate and ceramides) and the inflammatory polarization of brain macrophages (M1/BAMs) induce mitochondrial stress and central resistance to leptin and insulin, altering the adiposity set point. In parallel, we review emerging nutritional strategies based on polyunsaturated fatty acids (PUFAs), polyphenols, and short-chain fatty acids (SCFAs), and critically evaluate innovative technological platforms (nanoencapsulation, precision fermentation, and 3D food printing) designed to optimize nutrient bioaccessibility and restore adipose-CNS axis homeostasis, discussing current challenges for clinical translation.
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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 OpenQuestion graph.