A model of oxytocin in the regulation of metabolic status has described one of oxytocin synthesis and release from the neurohypophysis in response to leptin, to suppress further leptin release. In addition, a lipogenic role for oxytocin has been suggested, consistent with an insulinergic action. This model, however, may be incorrect. Oxytocin reduces fat mass in the absence of either leptin or leptin receptor signalling, thereby challenging the interdependence between leptin and oxytocin. An oxytocin induced production of the anti-lipolytic prostaglandin E₂ (PGE₂) might account for this. Media from 3T3-L1 differentiated adipocytes treated with oxytocin (0–50 nmol.L⁻¹) for 24 hrs were assayed for PGE₂, leptin, adiponectin, and glycerol. Harvested cells were analysed for lipid droplet triglyceride and cytosolic free fatty acid (FFA) by flow cytometry, and for altered expression of lipolytic and lipogenic associated gene ontology transcripts by cDNA array. Both PGE₂ and leptin secretion were significantly increased by oxytocin treatment whilst adiponectin secretion was not. A significant increase in cytosolic FFA was detected following oxytocin treatment, similar to that determined following treatment with isoproterenol (positive control). A significant increase in glycerol release to the culture media confirmed a lipolytic effect. No enrichment of lipolytic and lipogenic associated gene ontology transcripts was determined, but significant overrepresentation of chemosensory olfactory transcripts was. In conclusion, oxytocin stimulates lipolysis in 3T3-L1 adipocytes, mediated by autocrine/paracrine actions of PGE₂ and leptin. To confirm that this response is mediated solely by the oxytocin receptor, further experiments would require those effects being blocked by a specific oxytocin antagonist.

一种调节代谢状态的催产素模型描述了一种催产素的合成和神经垂体响应瘦素的释放，以抑制瘦素的进一步释放。此外，已经提出催产素的脂肪生成作用，这与胰岛素能作用一致。然而，这个模型可能是不正确的。催产素在没有瘦素或瘦素受体信号传导的情况下减少脂肪量，从而挑战瘦素和催产素之间的相互依赖性。催产素诱导的抗脂解前列腺素 E ₂ (PGE ₂ ) 的产生可能解释了这一点。测定来自用催产素 (0–50 nmol.L ^-1 ) 处理 24 小时的3T3-L1 分化脂肪细胞的培养基中的 PGE ₂、瘦素、脂联素和甘油。通过流式细胞术分析收获的细胞的脂滴甘油三酯和胞质游离脂肪酸 (FFA)，并通过 cDNA 阵列分析脂解和脂肪生成相关基因本体转录本的改变表达。PGE ₂催产素处理显着增加了瘦素和瘦素的分泌，而脂联素的分泌则没有。催产素处理后检测到细胞溶质 FFA 的显着增加，与用异丙肾上腺素处理后确定的相似（阳性对照）。甘油释放到培养基中的显着增加证实了脂解作用。没有确定脂肪分解和脂肪生成相关基因本体转录本的富集，但化学感应嗅觉转录本的显着过度表现是。总之，催产素刺激 3T3-L1 脂肪细胞中的脂肪分解，由 PGE _{2 的}自分泌/旁分泌作用介导和瘦素。为了证实这种反应仅由催产素受体介导，进一步的实验需要用特定的催产素拮抗剂阻断这些作用。