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Activated following a depletion of cellular energy stores, <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> will restore the energy homoeostasis by increasing energy production and limiting energy waste. At a central level, the <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> pathway will integrate peripheral signals (mostly hormones and metabolites) through neuronal networks. Hypothalamic <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> is directly implicated in feeding behaviour, brown adipose tissue (<jats:styled-content style=\"fixed-case\">BAT<\/jats:styled-content>) thermogenesis and browning of white adipose tissue (<jats:styled-content style=\"fixed-case\">WAT<\/jats:styled-content>). It also participates in other metabolic functions: glucose and muscle metabolisms, as well as hepatic function. Numerous anti\u2010obesity and\/or antidiabetic agents, such as nicotine, metformin and liraglutide, are known to induce their effects through a modulation of <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> pathway, either at central or at peripheral levels. Moreover, the weight\u2010gaining side effects of antipsychotic drugs, such as olanzapine, are also mediated by hypothalamic <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>. 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