Mitotic activity in the liver of the mouse during inanition followed by refeeding with different levels of protein

Leduc, Elizabeth H.

doi:10.1002/aja.1000840304

Cited by 65 publications

(16 citation statements)

References 25 publications

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“…increased to 365 g within a week. The elevated food intake provided a significant growth stimulus also for the liver as has been known for many years (28 time ( Fig. 3) but had recovered a few weeks later (data not shown).…”

Section: Resultsmentioning

confidence: 56%

Food restriction eliminates preneoplastic cells through apoptosis and antagonizes carcinogenesis in rat liver.

Grasl‐Kraupp

Bursch

Ruttkay-Nedecký

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

252

138

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Restriction of dietary calories reduces cancer formation in experimental animals and probably also in humans. This effect is generally attributed to the inhibitory effect of fasting on cell proliferation. Here we studied the effect of fasting on physiological cell death through apoptosis by using rat liver as a model. (i) In normal liver, involution of hyperplasia by apoptosis was reinforced by food withdrawal and suppressed by feeding. Complete food withdrawal for 8 days or food reduction by 40% for 3 months eliminated 20-30% of normal liver cells through apoptosis. (ii) Putative preneoplastic liver foci exhibited severalfold higher rates of DNA replication and apoptosis than unaltered liver. Food restriction lowered DNA replication but increased apoptosis, which reduced the number and volume of putative preneoplastic liver foci by 85% within 3 months. Subsequent return to ad libitum feeding normalized cell replication and apoptosis but clear differences in the volume and number of putative preneoplastic liver foci persisted throughout the following 17 months. Treatment of animals after food restriction with nafenopin, a peroxisome proliferator and potent tumor promoter, produced only half as many hepatocellular adenomas and rcinomas as in animals fed unr c throughout their lifetime. This indicates that food restriction had actually eliminated a part of the initiated cells. This study demonstrates that food restriction preferentiday enhances apoptosis of preneoplastic cells. This effect in combination with lowered cell replication provides protection from carcinogenesis.

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Section: Resultsmentioning

confidence: 56%

Food restriction eliminates preneoplastic cells through apoptosis and antagonizes carcinogenesis in rat liver.

Grasl‐Kraupp

Bursch

Ruttkay-Nedecký

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

252

138

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“…Therefore, the expression of the growth-related genes in the liver was specifically affected by protein nutrition. It has been reported that mitotic activity (29) and DNA synthesis (5-7) could be induced by feeding a casein diet if animals had been maintained on low-protein or protein-free diets prior to the feeding of protein. Then, we examined whether quality of protein affected the induction of DNA synthesis and expression of growth related genes in liver and kidney of growing rats that had been adapted to 2h feeding schedule and then fed protein-free diet for 3 days in the same manner.…”

Section: Resultsmentioning

confidence: 99%

Effects of Dietary Protein on the Induction of DNA Synthesis and Expression of Growth-Related Genes in Liver and Kidney of Growing Rats.

Yokota

Kanamoto

Hayashi

1995

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryTo investigate molecular mechanisms of growth control by protein nutrition, we examined whether nutritive quality of protein affects the induction of DNA synthesis in liver and kidney of growing rats in relation to expression of growth-related genes such as c-myc, c-fos, c-Ha-ras, and ornithine decarboxylase (ODC). Rats were adapted to 2-h meal feeding schedule at first with laboratory chow for 10 days and then with a protein-free diet for 3 days prior to experiments. When protein free diet was fed to the rats, the levels of c-myc, ODC and c-Ha-ras mRNAs increased in the liver within 2 days. However, substantial changes in the levels of those mRNAs were not observed in the kidney. The level of c-fos mRNA in these tissues was too low to detect by our method. Feeding of casein diet to rats that had been maintained on protein-free diet for 3 days caused a rapid decrease in the level of c-myc mRNA and induced DNA synthesis in the liver. On the other hand, zein diet, which lacks tryptophan and lysine, did not lower the c-myc mRNA level nor induced DNA synthesis in the liver. However, if zein diet was supplemented with tryptophan and lysine, a decrease in c-myc mRNA level and an induction of DNA synthesis were observed. The levels of ODC and c-Ha-ras mRNAs were not changed by feeding of casein or zein diet. Neither casein nor zein induced DNA synthesis and changed the levels of the mRNA in the kidney. The amount of food intake during the 2-h feeding period was not different among the diets. These results suggest that the liver cells are arrested in G 1 phase during the feeding of protein-free diet and good quality of protein is required to progress the cell cycle to enter S phase.

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“…Maturation of fat cells occurred rapidly, the interval between completion of DNA synthesis and significant lipid accumulation being between 2 and 5 days, and it is clear that the processes of differentiation and maturation of primordial fat cells were not hastened by refeeding after a period of fasting. As in other tissues (17,18) fasting depressed DNA synthesis in fat cells and stromal elements, and it is of some interest that this effect was more profound in the fat cell fraction.…”

Section: Discussionmentioning

confidence: 95%

Regulation of DNA synthesis in fat cells and stromal elements from rat adipose tissue

Hollenberg¹,

Vost²

1968

J. Clin. Invest.

137

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A B S T R A C T The incorporation of tritiated thymidine into the deoxyribonucleic acid (DNA) of adipose fat and stromal cells was followed under a variety of conditions. After in vitro incubation of adipose slices or up to 2 days after in vivo injection of the isotope, all DNA radioactivity was in the stromal cell fraction. From 2 to 15 days after thymidine injection total tissue DNA radioactivity was constant, while between 2 and 5 days after injection label in fat cell DNA increased markedly. Thus new labeled fat cells, initially collected in the stromal pool, required 2-5 days after completion of DNA synthesis to accumulate sufficient lipid to be harvested in the fat cell fraction. Fasting before thymidine injection practically abolished DNA synthesis in primordial fat cells and reduced less drastically formation of stromal elements. However fasting sufficient to deplete lipid stores by 50% neither destroyed mature fat cells nor impaired their capacity to reaccumulate fat with refeeding. Other studies evaluated the role of new fat cell formation in the process of lipid accretion accompanying refeeding. These experiments indicated that at least during the early phase of rapid weight gain, accumulation of fat was due to deposition of triglyceride in existing cells rather than to accelerated formation of new fat cells. Studies with hypophysectomized rats demonstrated that pituitary ablation variably affected stromal DNA synthesis and nearly abolished the formation and (or) maturation of primordial fat cells. In these animals growth hormone markedly enhanced thymidine incorporation into stromal DNA but had no effect on fat cell preReceived for publication 10 April 1968 and in revised form 7 June 1968. cursors. In intact animals the predominant effect of growth hormone was also on the stromal fraction, although an action of the hormone of lesser magnitude on fat cell precursors was also evident. INTRODUCTIONWhile information concerning the accretion and mobilization of adipose lipid has accumulated rapidly over the past decade, there is still surprisingly little known about the regulation of fat cell formation, another mechanism that can influence adipose mass. Hindering work in this area is the difficulty in the histological recognition of primitive fat cells and the fact that only a part of total adipose tissue deoxyribonucleic acid (DNA) is contained in fat cells (1). The information that is available has been derived from the use of radioautography, chemical DNA analysis, and counting of adipose cells. These data indicate that the new fat cells are continually formed in the growing animal (2), that expansion of adipose mass by fat feeding is associated with an increase in total adipose tissue DNA (3), and that in human and in some experimental forms of obesity an increase in adipose cell number accompanies an increase in adipose cell size (4, 5). Although these data suggest an influence of diet on fat cell synthesis, the precise nutritional and hormonal factors that control the formation and maturation of ...

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Mitotic activity in the liver of the mouse during inanition followed by refeeding with different levels of protein

Cited by 65 publications

References 25 publications

Food restriction eliminates preneoplastic cells through apoptosis and antagonizes carcinogenesis in rat liver.

Food restriction eliminates preneoplastic cells through apoptosis and antagonizes carcinogenesis in rat liver.

Effects of Dietary Protein on the Induction of DNA Synthesis and Expression of Growth-Related Genes in Liver and Kidney of Growing Rats.

Regulation of DNA synthesis in fat cells and stromal elements from rat adipose tissue

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