Obesity-driven inflammation and colorectal cancer

Area of Science:

• Oncology
• Metabolic Syndrome
• Inflammation Biology

Background:

• Visceral obesity is linked to increased cardiovascular disease and cancer risk, particularly colorectal cancer (CRC).
• The mechanisms connecting excess visceral adipose tissue (VAT) to cancer are not fully understood but involve chronic inflammation.
• Obesity-related inflammatory pathways and specific adipokines secreted by VAT play a role in CRC initiation and progression.

Purpose of the Study:

• To review the molecular and clinical evidence linking VAT-related inflammation to CRC.
• To summarize the role of adipokines (adiponectin, leptin, resistin) in CRC pathogenesis.
• To discuss the impact of lifestyle interventions on CRC prevention and prognosis.

Main Methods:

• Literature review of molecular and clinical studies.
• Analysis of evidence on adipokine secretion patterns in obesity and CRC.
• Synthesis of data on dietary and physical activity interventions for weight management and CRC.

Main Results:

• Visceral obesity promotes a pro-inflammatory and insulin-resistant state, fostering CRC tumorigenesis.
• Adiponectin, leptin, and resistin from VAT contribute to a positive feedback loop that enhances inflammation and promotes cancer.
• These adipokines are emerging as potential prognostic factors and therapeutic targets for CRC.

Conclusions:

• VAT-related inflammation is a key factor in colorectal cancer development and progression.
• Targeting obesity-related inflammation and specific adipokines presents opportunities for CRC prevention and treatment.
• Lifestyle interventions promoting weight control and physical activity are crucial for managing CRC risk and prognosis.