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This effect was alleviated with both genetic and pharmacological inhibition of adipocyte lipolysis, which decreased hepatic acetyl-CoA levels and gluconeogenesis, thereby normalizing plasma glucose in mice fed with high fat diet (HFD) (183)

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The rationale is complementary mechanisms: TB-500 drives cell migration to injury sites through actin regulation, while BPC-157 supports blood vessel formation, growth factor expression, and anti-inflammatory signalling through nitric oxide pathway modulation