<p>METTL14 mediates N6-methyladenosine (m⁶A) RNA modification, while YTHDC1 and YTHDF2 specifically bind m⁶A-methylated RNA to regulate RNA fate. POMC neurons constitute the core of the central melanocortin circuit, and POMC deficiency causes obesity in both mice and humans. However, how m⁶A-based epitranscriptomics regulates melanocortin circuit function remains unclear. Here, we generated and characterized POMC neuron-specific knockout mice lacking <i>Mettl14</i> (<i>Mettl14</i>^{<i>ΔPOMC</i>}), <i>Ythdc1</i> (<i>Ythdc1</i>^{<i>ΔPOMC</i>}), or <i>Ythdf2</i> (<i>Ythdf2</i> ^{<i>ΔPOMC</i>}). <i>Mettl14</i>^{<i>ΔPOMC</i>} and <i>Ythdc1</i>^{<i>ΔPOMC</i>} mice develop hyperphagia, obesity, glucose intolerance, insulin resistance, and hepatic steatosis in both sexes under standard chow conditions, accompanied by POMC downregulation. Conversely, POMC neuron-specific overexpression of METTL14 or YTHDC1 protects against diet-induced obesity. In contrast, <i>Ythdf2</i> ^{<i>ΔPOMC</i>} mice are resistant to obesity, revealing an m⁶A-dependent balance between YTHDC1 and YTHDF2. Mechanistically, the METTL14/YTHDC1 pathway is indispensable for embryonic POMC neurogenesis, while in adults YTHDC1 maintains melanocortin circuit integrity/function. METTL14 and YTHDC1 directly target <i>POMC</i> and <i>ISL1</i> transcripts to regulate protein expression. POMC neuron-specific restoration of POMC reverses obesity and metabolic phenotypes in <i>Mettl14</i>^{<i>ΔPOMC</i>} and <i>Ythdc1</i>^{<i>ΔPOMC</i>} mice, defining an anti-obesity METTL14/m⁶A/YTHDC1/POMC axis. These findings identify METTL14 as the m⁶A writer for <i>POMC</i>/<i>ISL1</i> and YTHDC1 and YTHDF2 as their readers, uncovering a critical role of m⁶A epitranscriptomic regulation in melanocortin circuit development and maintenance.</p>