J M Wan — Page 2 | PubMed Health

PubMedDate not supplied

Invited comment: lipids and the development of immune dysfunction and infection.

Excessive W-6 PUFA metabolism due to high levels of dietary fat intake can encourage infection via prolonged inflammation, enhanced Gram negative survival, reticuloendothelial blockage, immunosuppression, and monokine depression. Lipids can influence host immunity by altering eicosanoid metabolism and membrane structure and function. Further investigations are essential to answer questions regarding the levels and properties of various essential fatty acids in TPN lipid emulsions. Combining the features of LCT in the form of W-3 PUFA (fish oil) and MCT in the form of medium-chain triglyceride in a "structured lipid" may decrease infection and may improve survival rates by producing fewer inflammatory eicosanoids of the two- and four-series, and serving as a more "efficient fuel." The introduction of W-3 polyunsaturated fatty acids into the TPN emulsions as well as into normal diets may provide an important therapeutic advance in the pathogenesis of disease. Such unique antiinflammatory properties of W-3 PUFA require intensive research.

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PubMedDate not supplied

Nutrition and tumor promotion: in vivo methods for measurement of cellular proliferation and protein metabolism.

The notion that tumors act as "nitrogen traps" has led to the belief that nutrition support of the cancer-bearing patient can enhance tumor growth. Proponents of this theory consider the provision of energy and essential nutrients as well as the influence of hormones and growth factors as responsible for this effect. On the other hand, nutrition administration in the debilitated cancer patient may improve antitumor host defense mechanisms and reduce tumor growth. This paper reviews methodologic issues related to the study of nutrition and cancer growth with emphasis on in vivo methods for measuring tumor protein turnover and cytokinetics. Using this combined approach, we previously demonstrated that dietary fat may significantly regulate tumor growth during chronic feeding as well as with short-term intravenous nutrition support in experimental models. Although the mechanism of this effect remains unclear, we have reasoned that by altering arachidonic acid metabolism and prostaglandin synthesis, omega-3 fatty acids could change tumor protein breakdown rates and inhibit the proliferation potential of these tumors. Acknowledging alternative hypotheses, we now present cytokinetic evidence that intracellular protein degradation may regulate tumor cell proliferation. Additional studies relating dietary fat, tumor protein metabolism and tumor proliferation potential are currently in progress. We propose that the effect of nutrition administration on tumor growth is complex and involves several regulatory systems. Thus, based on available evidence, an a priori tumor-enhancing effect for nutrition support is clearly not warranted. Intracellular protein breakdown and host defense mechanisms, both of which are energy dependent, are important loci at which nutrition and tumor growth regulation could interact.(ABSTRACT TRUNCATED AT 250 WORDS)

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