ReviewJournal of lipid research2026
Mitochondria-endoplasmic reticulum-lipid droplet crosstalk in lipid metabolic reprogramming in type 2 diabetes mellitus.
Review in Journal of lipid research, 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
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
Type 2 diabetes mellitus (T2DM) is characterized by progressive metabolic reprogramming in which lipid metabolism imbalance links nutrient excess to insulin resistance, organelle stress, and tissue dysfunction. Although mitochondria, the endoplasmic reticulum (ER), and lipid droplets (LDs) each have established roles in metabolic homeostasis, how their coordinated interactions govern lipid remodeling in T2DM remains incompletely defined, owing in part to the technical difficulty of resolving these highly dynamic contact sites in space and time. In this review, we integrate current evidence on mito-ER-LD interactions in T2DM, spanning advances in omics, imaging, and biochemical approaches, and summarize their structural organization, regulatory machinery, tissue-specific remodeling, and therapeutic modulation. Emerging data identify this tri-organelle network as a central metabolic interface that couples phospholipid synthesis and trafficking, calcium flux, mitochondrial dynamics, LD biogenesis and turnover, fatty-acid oxidation, autophagy, and stress signaling. Disruption of this network, including mitochondria-associated ER membrane (MAM) instability, altered balance between cytoplasmic and peridroplet mitochondria, and pathological LD expansion, reprograms lipid handling across liver, adipose tissue, skeletal muscle, and pancreatic β cells, thereby promoting lipotoxicity, oxidative and ER stress, mitochondrial dysfunction, β-cell failure, and systemic insulin resistance. Notably, glucose-lowering drugs and lifestyle interventions may exert part of their metabolic benefit by restoring organelle crosstalk and reestablishing lipid homeostasis. Together, this review positions mito-ER-LD contact sites not simply as structural interfaces but as core nodes that regulate lipid metabolic reprogramming in T2DM, thereby providing a mechanistic framework for targeting organelle crosstalk in metabolic disease.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.