Overnutrition, uncontrolled organ growth and apoptosis

W. S. Lynn, J. C. Wallwork, D. H. Coppenhaver

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Recently, we demonstrated, in vitro, that the products of excess energy intake, i.e., excess saturated fatty acids, activate both cell growth and cell death (apoptosis, DNA fragmentation). We have extended these findings to in vivo systems. We show that increased growth and accumulation of DNA fragments occur in most organs of ad libitum-fed animals obtained from three mouse models of degenerative diseases in adult animals: glomerulonephritis in NZB/NZW F1 and MRL/n strains, the induction of lymphadenopathy by retrovirus LP-BM5 in C57BL/6J mice and induction of obesity in C57BL/6J mice fed a high fat diet. With the virus, changes are most marked in lymphoid organs in the C57BL/6J strain. With the obesity model, essentially all organs, including aorta, are affected, both in the C57BL/6J strain and also in the glomerulonephritic NZB/NZW F1 and MRL/n strains. In addition, we showed that these lesions, as well as the DNA fragmentation, can be reversed in 2 to 4 weeks by restricting energy intake to 65% of ad libitum feeding or by exercise sufficient to remove storage fat. These observations suggest that excessive organ growth in mature animals, as activated by either excessive energy input or by retrovirus, leads eventually to excessive nucleosome endonuclease activity with resultant cell death.

Original languageEnglish (US)
Pages (from-to)3-15
Number of pages13
JournalJournal of Applied Nutrition
Volume44
Issue number1
StatePublished - 1992

Fingerprint

Overnutrition
Retroviridae
apoptosis
DNA Fragmentation
Apoptosis
Energy Intake
Inbred C57BL Mouse
DNA fragmentation
Cell Death
Growth
Obesity
cell death
energy intake
obesity
Nucleosomes
Endonucleases
High Fat Diet
Glomerulonephritis
glomerulonephritis
lymphatic diseases

ASJC Scopus subject areas

  • Food Science
  • Medicine (miscellaneous)

Cite this

Lynn, W. S., Wallwork, J. C., & Coppenhaver, D. H. (1992). Overnutrition, uncontrolled organ growth and apoptosis. Journal of Applied Nutrition, 44(1), 3-15.

Overnutrition, uncontrolled organ growth and apoptosis. / Lynn, W. S.; Wallwork, J. C.; Coppenhaver, D. H.

In: Journal of Applied Nutrition, Vol. 44, No. 1, 1992, p. 3-15.

Research output: Contribution to journalArticle

Lynn, WS, Wallwork, JC & Coppenhaver, DH 1992, 'Overnutrition, uncontrolled organ growth and apoptosis', Journal of Applied Nutrition, vol. 44, no. 1, pp. 3-15.
Lynn WS, Wallwork JC, Coppenhaver DH. Overnutrition, uncontrolled organ growth and apoptosis. Journal of Applied Nutrition. 1992;44(1):3-15.
Lynn, W. S. ; Wallwork, J. C. ; Coppenhaver, D. H. / Overnutrition, uncontrolled organ growth and apoptosis. In: Journal of Applied Nutrition. 1992 ; Vol. 44, No. 1. pp. 3-15.
@article{98c1993cb4c24b5889a629066ac489de,
title = "Overnutrition, uncontrolled organ growth and apoptosis",
abstract = "Recently, we demonstrated, in vitro, that the products of excess energy intake, i.e., excess saturated fatty acids, activate both cell growth and cell death (apoptosis, DNA fragmentation). We have extended these findings to in vivo systems. We show that increased growth and accumulation of DNA fragments occur in most organs of ad libitum-fed animals obtained from three mouse models of degenerative diseases in adult animals: glomerulonephritis in NZB/NZW F1 and MRL/n strains, the induction of lymphadenopathy by retrovirus LP-BM5 in C57BL/6J mice and induction of obesity in C57BL/6J mice fed a high fat diet. With the virus, changes are most marked in lymphoid organs in the C57BL/6J strain. With the obesity model, essentially all organs, including aorta, are affected, both in the C57BL/6J strain and also in the glomerulonephritic NZB/NZW F1 and MRL/n strains. In addition, we showed that these lesions, as well as the DNA fragmentation, can be reversed in 2 to 4 weeks by restricting energy intake to 65{\%} of ad libitum feeding or by exercise sufficient to remove storage fat. These observations suggest that excessive organ growth in mature animals, as activated by either excessive energy input or by retrovirus, leads eventually to excessive nucleosome endonuclease activity with resultant cell death.",
author = "Lynn, {W. S.} and Wallwork, {J. C.} and Coppenhaver, {D. H.}",
year = "1992",
language = "English (US)",
volume = "44",
pages = "3--15",
journal = "Journal of Applied Nutrition",
issn = "0021-8960",
publisher = "International & American Associations of Clinical Nutritionists",
number = "1",

}

TY - JOUR

T1 - Overnutrition, uncontrolled organ growth and apoptosis

AU - Lynn, W. S.

AU - Wallwork, J. C.

AU - Coppenhaver, D. H.

PY - 1992

Y1 - 1992

N2 - Recently, we demonstrated, in vitro, that the products of excess energy intake, i.e., excess saturated fatty acids, activate both cell growth and cell death (apoptosis, DNA fragmentation). We have extended these findings to in vivo systems. We show that increased growth and accumulation of DNA fragments occur in most organs of ad libitum-fed animals obtained from three mouse models of degenerative diseases in adult animals: glomerulonephritis in NZB/NZW F1 and MRL/n strains, the induction of lymphadenopathy by retrovirus LP-BM5 in C57BL/6J mice and induction of obesity in C57BL/6J mice fed a high fat diet. With the virus, changes are most marked in lymphoid organs in the C57BL/6J strain. With the obesity model, essentially all organs, including aorta, are affected, both in the C57BL/6J strain and also in the glomerulonephritic NZB/NZW F1 and MRL/n strains. In addition, we showed that these lesions, as well as the DNA fragmentation, can be reversed in 2 to 4 weeks by restricting energy intake to 65% of ad libitum feeding or by exercise sufficient to remove storage fat. These observations suggest that excessive organ growth in mature animals, as activated by either excessive energy input or by retrovirus, leads eventually to excessive nucleosome endonuclease activity with resultant cell death.

AB - Recently, we demonstrated, in vitro, that the products of excess energy intake, i.e., excess saturated fatty acids, activate both cell growth and cell death (apoptosis, DNA fragmentation). We have extended these findings to in vivo systems. We show that increased growth and accumulation of DNA fragments occur in most organs of ad libitum-fed animals obtained from three mouse models of degenerative diseases in adult animals: glomerulonephritis in NZB/NZW F1 and MRL/n strains, the induction of lymphadenopathy by retrovirus LP-BM5 in C57BL/6J mice and induction of obesity in C57BL/6J mice fed a high fat diet. With the virus, changes are most marked in lymphoid organs in the C57BL/6J strain. With the obesity model, essentially all organs, including aorta, are affected, both in the C57BL/6J strain and also in the glomerulonephritic NZB/NZW F1 and MRL/n strains. In addition, we showed that these lesions, as well as the DNA fragmentation, can be reversed in 2 to 4 weeks by restricting energy intake to 65% of ad libitum feeding or by exercise sufficient to remove storage fat. These observations suggest that excessive organ growth in mature animals, as activated by either excessive energy input or by retrovirus, leads eventually to excessive nucleosome endonuclease activity with resultant cell death.

UR - http://www.scopus.com/inward/record.url?scp=0026590144&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026590144&partnerID=8YFLogxK

M3 - Article

VL - 44

SP - 3

EP - 15

JO - Journal of Applied Nutrition

JF - Journal of Applied Nutrition

SN - 0021-8960

IS - 1

ER -