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Key successes include the validation of BDNF deficits, hippocampal atrophy, and monoaminergic dysfunction as central mechanisms in human populations

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The peptide appears to act on fat metabolism without influencing appetite

FGF21 also increases energy expenditure in mice via UCP1-dependent (232) and UCP1-independent (233) mechanisms, which include browning of white adipose tissue by upregulating PGC1 (234)