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1,4 Hyperglycemia, dyslipidemia, and insulin resistance activate various metabolic pathways, resulting in oxidative stress, mitochondrial dysfunction, inflammation, and microvascular damage, culminating in neuronal injury, Schwann cell damage, and myelin sheath degeneration

Readouts most often include glycerol release and free fatty acid quantification in the supernatant, alongside cellular ATP or viability measures to confirm that observed lipolysis reflects genuine metabolic signaling rather than cytotoxic membrane disruption

Figure 7.2 Chain of events occurring after sclerotherapy