Cancer insuline

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The Relationship Between Insulin and Cancer: Insights from Recent Research

Insulin as a Growth Factor in Cancer Cells

Insulin, beyond its role as a metabolic hormone, acts as a growth factor with significant mitogenic effects, particularly in malignant cells that often overexpress the insulin receptor. This overexpression can lead to increased cancer cell proliferation and survival, contributing to cancer progression . The insulin/insulin-like growth factor (IGF) system is crucial in enhancing tumor cell proliferation through the tyrosine kinase growth factor cascade, which is particularly evident in cancers such as colon, prostate, pancreatic, and breast cancer.

Hyperinsulinemia and Cancer Risk

Patients with metabolic diseases characterized by hyperinsulinemia, such as obesity, type 2 diabetes, and metabolic syndrome, have a higher incidence of several types of cancer and increased cancer-related mortality . Hyperinsulinemia can influence cancer occurrence and prognosis, although the exact degree of this influence remains unclear and requires further scientific investigation.

Insulin Therapy and Cancer Risk

The use of exogenous insulin therapies in diabetic patients has been associated with varying cancer risks. A systematic review and meta-analysis found that new users of insulin had an increased risk of pancreatic cancer and prostate cancer but a decreased risk of colorectal cancer. However, these results should be interpreted with caution due to the limitations of the included studies. Another meta-analysis focusing on breast cancer risk found no significant increase in risk associated with insulin therapy compared to non-insulin therapies.

Insulin Resistance in Cancer Patients

Insulin resistance, a critical cause of metabolic dysfunction, is common in cancer patients and is associated with higher cancer recurrence rates and reduced overall survival. A meta-analysis revealed that cancer patients are markedly insulin-resistant, suggesting that addressing insulin resistance could potentially improve cancer outcomes. Insulin resistance is also a significant risk factor for endometrial cancer, with high insulin levels promoting cell proliferation and survival through the PI3K/Akt and Ras/MAPK pathways.

Insulin and Cancer Cachexia

In weight-losing cancer patients, insulin treatment has shown potential benefits in attenuating the progression of cancer cachexia, improving metabolism, and enhancing physical functioning. Insulin treatment stimulated carbohydrate intake, decreased serum-free fatty acids, and increased whole body fat without affecting fat-free lean tissue mass. Importantly, insulin treatment did not stimulate tumor growth and was associated with improved survival.

Modulating the Insulin/IGF-1 System in Cancer Treatment

Dietary and pharmacological modifications of the insulin/IGF-1 system have shown promise in reducing cancer incidence and growth. Dietary restriction and insulin-lowering drugs like metformin and diazoxide can target multiple molecular pathways involved in cancer growth. However, the metabolic response to these interventions can differ between animal models and humans, highlighting the need for more human data.

Insulin-PI3K Signaling and Oncogenesis

The insulin-PI3K signaling pathway plays a significant role in oncogenesis by regulating cellular metabolism, growth, and survival. Chronic activation of this pathway can drive malignant transformation. Targeting the PI3K signaling cascade, while managing systemic insulin levels, could enhance the efficacy of cancer treatments.

Conclusion

The relationship between insulin and cancer is complex and multifaceted, involving hyperinsulinemia, insulin resistance, and the insulin/IGF-1 signaling pathways. While insulin therapy in diabetic patients presents varying cancer risks, addressing insulin resistance and modulating the insulin/IGF-1 system offer promising avenues for improving cancer outcomes. Further research is essential to fully understand these mechanisms and develop effective strategies for cancer prevention and treatment.