Skip to main content

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 422))

  • 174 Accesses

Abstract

Consumption of dietary lipids varying in fatty acid composition has been implicated in the etiology and prevention of a variety of chronic illnesses including colon cancer. It is well established that fatty acid composition of a high fat diet is an important determining factor in exerting a tumor enhancing or an inhibitory effect. A variety of mechanism(s) has been proposed to explain how different lipids may modulate tumor growth. It is proposed that a tumor promoting diet would increase and a tumor inhibitory diet would decrease colonic cell proliferation. In the present study we assessed the number of cycling cells by quantifying the cells exhibiting PCNA among the colons of rats fed 5% or 23.4% corn oil, canola oil, olive oil and beef tallow diets. A group of rats were fed high fat diets along with 2% calcium (4X the normal level). All diets were based on AIN-76A diet modified to contain high fat diets. Male Sprague Dawley rats (90–100g) were fed the test diets for four weeks. The PCNA labelling index (PCNA-LI) were assessed in the distal and mid colon.The PCNA-LI were lower in the distal colon than their counterparts in the mid colon. All groups fed 5% fat had lower PCNA-LI than those fed high fat diets (p‹ 0.05). The PCNA-LI among the low fat groups ranged from, distal colon 5–9 and mid colon 6–11. The PCNA-LI among the high fat groups ranged from distal colon 14–33 and mid colon 10–30 Among the high fat groups the lowest PCNA-LI were noted for the corn oil (distal 14, mid 10) and highest in the beef tallow group (distal 33, mid 30). Additional calcium in the diet further increased the PCNA-LI among the corn oil, canola oil and olive oil groups and decreased it in the beef tallow group. The highest increment in the PCNA-LI was noted for the high calcium-corn oil group when compared to its normal calcium counterpart (37,35 vs 14,10). This study demonstrated that A) a high corn oil and a high beef tallow tumor promotary diets did not alter the proliferative responses in the colon in a similar manner;B) all high fat diets increased the proliferative status of the colonic epithelium; C) distal colon responded differently to dietary lipids than mid colon and D) fatty acid composition of dietary lipids was an important variable in modulating the PCNA-LI in the colon, however, only in the high fat environment and was influenced by a high calcium diet. Particulate and soluble protein kinase-C activity did not correlate with the PCNA- LI in all groups. (Supported by the American Inst. Cancer Research and the Canadian Cancer Research Society Inc.)

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 84.99
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 109.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 109.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

Author information

Authors and Affiliations

Consortia

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 1997 Springer Science+Business Media New York

About this chapter

Cite this chapter

American Institute for Cancer Research. (1997). Abstracts. In: Dietary Fat and Cancer. Advances in Experimental Medicine and Biology, vol 422. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-2670-1_16

Download citation

  • DOI: https://doi.org/10.1007/978-1-4757-2670-1_16

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4419-3282-2

  • Online ISBN: 978-1-4757-2670-1

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics