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Adipose tissue (AT) inflammation may increase obesity-related cardiometabolic complications. Altered AT oxygen partial pressure (pO₂) may impact the adipocyte inflammatory phenotype. Here, we investigated the effects of <i>physiological</i> pO₂ levels on the inflammatory phenotype of abdominal (ABD) and femoral (FEM) adipocytes derived from postmenopausal women with normal weight (NW) or obesity (OB). Biopsies were collected from ABD and FEM subcutaneous AT in eighteen postmenopausal women (aged 50–65 years) with NW (BMI 18–25 kg/m², <i>n</i> = 9) or OB (BMI 30–40 kg/m², <i>n</i> = 9). We compared the effects of prolonged exposure to different <i>physiological</i> pO₂ levels on adipokine expression and secretion in differentiated human multipotent adipose-derived stem cells. Low <i>physiological</i> pO₂ (5% O₂) significantly increased leptin gene expression/secretion in ABD and FEM adipocytes derived from individuals with NW and OB compared with high <i>physiological</i> pO₂ (10% O₂) and standard laboratory conditions (21% O₂). Gene expression/secretion of IL-6, DPP-4, and MCP-1 was reduced in differentiated ABD and FEM adipocytes from individuals with OB but not NW following exposure to low compared with high <i>physiological</i> pO₂ levels. Low <i>physiological</i> pO₂ decreases gene expression and secretion of several proinflammatory factors in ABD and FEM adipocytes derived from individuals with OB but not NW.