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Additionally, most studies measure AMPK activity via single time-point assessments of p-AMPK Thr172, without quantifying downstream pathway dynamics (e.g., ACC phosphorylation, ULK1 activation) or tissue-specific AMPK isoform expressioncritical for understanding context-dependent regulation in NAFLD

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In contrast, the Butler group finds that the chromogranin + hormone - islet cells accounts for no more than a 2% deficit of cells in T2D[33]

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It provides endothelial surface area for substrate exchange between the plasma compartment and the muscle interstitium