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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #335258
Title: Changes in body adiposity and its associated inflammation affect metastasis of Lewis lung carcinoma in mice

Author
item Yan, Lin
item Sundaram, Sneha

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/1/2017
Publication Date: 4/1/2017
Citation: Yan, L., Sundaram, S. 2017. Changes in body adiposity and its associated inflammation affect metastasis of Lewis lung carcinoma in mice [abstract]. Journal of Federation of American Societies for Experimental Biology. 31:435.6.

Interpretive Summary:

Technical Abstract: A hallmark of obesity is the increase in body adiposity and its associated inflammation that contribute to obesity-related chronic diseases including cancer. Clinical studies show that obesity is related to poor prognosis, early recurrence and metastasis in cancer patients. Recurrence and metastasis are the most devastating aspects of cancer. We studied roles of changes in body adiposity (induced by changes in diet formulation or feeding method) in spontaneous metastasis of Lewis lung carcinoma in mice. Compared to the AIN93G control diet (16% of energy from corn oil), the high-fat diet (45% of energy from coil oil) significantly increases body fat mass and plasma concentrations of proinflammatory cytokines [e.g. monocyte chemotactic protein-1 (MCP-1) and plasminogen activator inhibitor-1 (PAI-1)] and significantly increases the extent of metastasis, evidenced by increases in number and size of metastases formed in lungs. A restriction in high-fat diet intake by 5%, which maintains the body adiposity and plasma MCP-1 and PAI-1 levels similar to mice fed the AIN93G diet, significantly reduces lung metastasis compared to unrestricted feeding of the high-fat diet. Knocking out MCP-1 or PAI-1 from mice significantly reduces high-fat diet-enhanced metastasis. The metastatic enhancement was not observed in mice fed a 45% high-sucrose diet, which did not elevate body adiposity and proinflammatory cytokines compared to a 45% high-fat diet. Furthermore, we found from a feeding study that there are no differences in proinflammatory cytokines (including MCP-1 and PAI-1) in mice fed high-fat diets containing oils with different amounts of n3 and n6 fatty acids. Our results indicate that increases in adiposity and its associated proinflammatory cytokines may contribute to the high-fat diet-enhanced metastasis and that sources of dietary energy, rather than the energy itself, may lead to differences in metastatic aggression of Lewis lung carcinoma.