Key result
Obesity-related alterations in adipokines, such as adiponectin, leptin, resistin, and ghrelin, along with insulin resistance, are closely related to the pathogenesis of colorectal cancer.
Why the study?
What is the role of adipokines and insulin in colorectal cancer pathogenesis?
What is the role of adipokines and insulin in colorectal cancer pathogenesis?
This review highlights the pathogenic link between obesity-related adipokines, insulin resistance, and colorectal cancer.
Adipokine alterations may represent modifiable CRC risk factors; leaves open whether targeted interventions improve outcomes.
Obesity-related diseases are an important part of public health; and obesity is related with colorectal cancer. Adipocyte hypertrophy and visceral adipose tissue accumulation can cause adipocitis-related diseases and pathogenic adipocyte formation. Adipose tissue has a very important and active role in immune response formation. Cytokines/adipokines, which are secreted from adipose tissue, have an active role in communication between adipocytes and macrophages. Thus, visceral adipocyte is related with low-grade chronic systemic inflammation. Adipocytes have an important role in colorectal cancer pathogenesis because of proinflammatory cytokines, growth factors, and hormones secretion. Most highlighted cytokines are adiponectin, resistin, and ghrelin. Also, insulin resistance, glucose intolerance, increased plasma insulin levels, body mass index, insulin-like growth factor (IGF-1), glucose, and serum free fatty acids levels are considered to be related with colorectal cancer pathogenesis. Thus, in this review, we focus on the role of adipokines and insulin in colorectal cancer.
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Uyar et al. (2018) conducted a review in Colorectal cancer. Adipokines and insulin was evaluated. Obesity-related alterations in adipokines, such as adiponectin, leptin, resistin, and ghrelin, along with insulin resistance, are closely related to the pathogenesis of colorectal cancer.
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