The reversal of NET function results in efflux of cytoplasmic norepinephrine, normally contained in the , readily releasable pool 12) into the synaptic cleft, independent of calcium influx and the normal process of vesicular release (Raiteri and Levi, 1986
with lesser fat storage being the primary reason for such
Assoc.J.,2010, 4, 310-316 16
These multifaceted metabolic effects position dual GLP-1/GIP receptor agonists as superior therapeutic candidates for MASLD, especially in patients with coexisting obesity and T2DM, where dysregulated glucose and lipid metabolism drive the progression of the disease
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