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There are a number of reasons for this, with the most prominent being the need to treat chronic pain after developing diabetic neuropathy (pain resulting from nerve damage) as a side effect of insulin resistance

Here we have shown that the EnzChek substrate can be used to quantify LPL activity in bLPL, (Figure 5A), LPL enriched HR fractions from BV-2 microglia, but not in HF fractions from BV-2 microglia where LPL expression has been knocked out using CRISPR-Cas9 (Figure 5B), and PHP (Figure 5C)

I think something is changing in the reward pathway in the brain. GLP-1 drugs like semaglutide stimulate the production of insulin, which can cross the blood-brain barrier

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