The correlation between obesity and the occurrence and development of breast cancer

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

This study reviews the mechanisms by which obesity affects the development and progression of breast cancer (BC). The association between obesity and BC is mainly due to three aspects: disruption of glycolipid metabolism, abnormal cell function and imbalance of adipokine levels. The dysregulation of glycolipid metabolism caused by obesity, including the accumulation of cholesterol and fatty acids and the reprogramming of glucose metabolism, promotes the growth and invasion of tumour cells. Obesity triggers multiple cellular abnormalities, particularly in lipid-associated macrophages and cancer-associated adipocytes, which promote tumour progression and immunosuppression by secreting inflammatory factors and various fatty acids into the tumour microenvironment. Obesity leads to an imbalance in the expression of several adipokines. Leptin upregulation is closely associated with BC metastasis and resistance to endocrine therapy, while reduced adiponectin levels attenuate the protective effect. At the same time, chronic inflammation and insulin resistance not only further increase the risk of BC, but also exacerbate tumour resistance. In terms of treatment, weight-loss drugs and metformin can improve the efficacy of obesity-related BC treatment to some extent. Intervention strategies targeting adipose tissue remodelling, lipid metabolism and leptin regulation also show potential cl

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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