Type 2 Diabetes Mellitus (T2DM) isn't just high blood sugar—it’s a systemic failure of communication between key organs!
Here’s how multi-organ crosstalk goes awry, and the mediators behind the dysfunction:
🔑 Key Players & Mediators:
➡️ Adipose Tissue (Fat):
Releases non-esterified fatty acids (NEFA), leading to lipid accumulation in the liver, muscle, and pancreas.
Produces pro-inflammatory cytokines (e.g., TNF, IL-6), which promote insulin resistance.
Dysfunctional fat releases lipokines like ceramides and diacylglycerols that disrupt insulin signaling.
➡️ Skeletal Muscle:
Impaired glucose uptake due to elevated branched-chain amino acids (BCAA) and metabolic stress.
Excess lipid metabolites activate novel protein kinase C (nPKC), inhibiting insulin pathways.
Reduced mitochondrial function limits glucose and lipid metabolism.
➡️ Liver:
Overproduces glucose while accumulating fat, driven by signals from adipose tissue and circulating lipids.
Releases ceramide-loaded exosomes and inflammatory markers that exacerbate insulin resistance.
➡️ Gut Microbiota:
Imbalanced microbiota reduces short-chain fatty acids (SCFA), which normally enhance insulin sensitivity.
Releases harmful metabolites that drive inflammation and dysregulated glucose metabolism.
➡️ Brain:
Hypothalamic inflammation affects appetite control and insulin regulation.
🔬 Why This Matters:These mediators—lipids, cytokines, metabolites, and exosomes—turn organs into "dysfunction amplifiers," creating a vicious cycle that drives T2DM progression.
Xourafa, G., Korbmacher, M., & Roden, M. (2024). Inter-organ crosstalk during development and progression of type 2 diabetes mellitus. Nature Reviews Endocrinology, 20(1), 27-49. https://doi.org/10.1038/s41574-023-00898-1
#DiabetesAwareness #T2DM #MultiOrganCrosstalk #InsulinResistance #ResearchBreakthroughs #PrecisionMedicine
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