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Dysfunctional adipose tissue promotes increased cardiovascular and diabetes disease risk via multiple pathways including increased free fatty acids (FFA) in the liver, infiltration of visceral fat deposits by proinflammatory macrophages resulting in chronic low-grade inflammation, and reduced buffering capacity for protective lipid storage [7]
GLP-1-Induced AMPK Activation Inhibits PARP-1 and Promotes LXR-Mediated ABCA1 Expression to Protect Pancreatic -Cells Against Cholesterol-Induced Toxicity Through Cholesterol Efflux
From in vitro studies using human SH-SY5Y neuronal cells, it was demonstrated that cell proliferation is increased with GLP-1 treatment (Li et al., 2010
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