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Biomedical subjects

E J Masoro

Publications and source records attributed to E J Masoro.

At least 19 recordsLinked to original sources
PubMed1992

Skin fibroblasts from aged Fischer 344 rats undergo similar changes in replicative life span but not immortalization with caloric restriction of donors.

We have compared the in vitro replicative life span and characteristics of immortalization of skin fibroblast cultures derived from ad libitum-fed and caloric-restricted Fischer 344 rats of 6, 24, and 29 months of age. Cells from all 6-, 24-, and 29-month-old animals showed a gradual decline in proliferative potential as evidenced by decreases in harvest density, in the fraction of cells initiating DNA synthesis, and in the number of population doublings per passage. These declines were accompanied by morphological changes including cell enlargement. The replicative life span prior to immortalization decreased significantly with donor age (P less than 0.0001), while caloric restriction had no effect on the cumulative population doubling level. Prior to immortalization mitotic cells from all cultures showed a normal rat karyotype. Postcrisis cultures tended to have more polyploid cells but there were no characteristic or specific chromosomal changes found in the cells with an immortalized phenotype. Interestingly, fibroblasts derived from caloric-restricted animals had a significantly slower growth rate through the tenth week after immortalization (P less than 0.005). When these cultures were seeded at one-quarter the normal seeding density, to favor the outgrowth of the fastest growing cells, a population with a more "transformed" phenotype emerged.

Age Factors↗
PubMed1992

Retardation of aging processes by food restriction: an experimental tool.

The importance of food restriction in rats, mice, and hamsters as a tool for the study of aging is discussed. The evidence that food restriction retards the aging processes is summarized and includes its ability to extend the maximum life span, to decrease the rate of increase in age-specific mortality, to retard age changes in physiological processes, and to delay or prevent most age-associated diseases. Food restriction has its anti-aging action by reducing the intake of energy rather than a specific nutrient. Research findings on the possible mechanisms by which food restriction retards the aging processes are discussed. The use of food restriction to test theories of aging is described and the controversial issue of its possible use as an intervention of human aging is addressed.

Aging↗
PubMed1992

Dietary restriction alters characteristics of glucose fuel use.

A longitudinal study of plasma glucose and insulin concentrations in ad libitum fed and dietary restricted male F344 rats was carried out. The life span diurnal pattern of plasma glucose concentration was such that through most of the day dietary restricted rats have significantly lower plasma glucose levels than ad libitum fed rats. Throughout the life span, dietary restricted rats maintain mean 24-hour plasma glucose concentrations about 15% below those of ad libitum fed rats. Plasma insulin levels are maintained in dietary restricted rats at about 50% of the levels in ad libitum fed rats. Although plasma glucose and insulin levels are lower, dietary restricted rats use glucose fuel at the same rate per unit of metabolic mass per day as rats fed ad libitum. While these findings are consistent with the glycation hypothesis of aging and with our hypothesis that dietary restriction retards the aging processes by altering the characteristics of fuel use, they do not establish the validity of either. It is possible that this effect of dietary restriction on carbohydrate metabolism plays no role in its antiaging action. Further studies are required to define the role of these altered characteristics of carbohydrate metabolism in the aging processes.

Animals↗
PubMed1992

The role of animal models in meeting the gerontologic challenge of the 21st century.

Animal models play an important role in our quest to understand aging and develop interventions needed for the gerontologic challenge of the 21st century. Results from studies using the dietary restriction rodent model are presented as an example. Dietary restriction slows aging by inhibiting primary aging processes, by enhancing broadly protective mechanisms, or by both. Further study should identify the mechanisms and yield a data base for development of interventions. A threat to attaining these yields is the growing opposition of some to this use of animals.

Aging↗
PubMed1992

Aging and proliferative homeostasis: modulation by food restriction in rodents.

In rats fed ad libitum, the fat cell number increases with advancing age; the temporal pattern of this increase differs in the perirenal depot compared with the epididymal depot. Restriction of energy intake reduces the number of fat cells in fat depots whether the restriction is started soon after weaning or in adult life. The capacity for diet to modulate fat cell number is maintained through most, if not all, of the life span. Restriction of energy intake delayed death due to neoplasms; restriction of dietary fat or protein without restriction of energy did not have this action. In the case of leukemia/lymphoma, the data indicated that it was the age of occurrence that was delayed by the restriction of energy intake. Because restriction of dietary energy maintains most physiologic systems in a youthful state and retards a broad spectrum of disease processes, the importance of its effects on cellularity and cell proliferation in its anti-aging action remains to be established.

Adipose Tissue↗
PubMed1991

Assessment of the role of the glucocorticoid system in aging processes and in the action of food restriction.

The Glucocorticoid Cascade Hypothesis of Aging and the hypothesis that food restriction retards the aging processes by preventing the development with age of hyperadrenocorticism were investigated. A longitudinal life span study of the daily concentration pattern of plasma corticosterone was conducted in male Fischer 344 rats fed ad libitum or restricted to 60% of the mean food intake of ad libitum fed rats. In another group of ad libitum fed and food-restricted rats, the influence of age on the response of plasma corticosterone levels to restraint stress was measured as was the time course of the return of plasma corticosterone to basal levels following the stress. The findings do not support the hypothesis that food restriction retards the aging processes by preventing the development of hyperadrenocorticism with advancing age. They also indicate that the Glucocorticoid Cascade Hypothesis does not describe a major aspect of the aging processes. Rather, the results suggest the possibility that a lifetime of daily periods of mild hyperadrenocorticism may, if anything, retard the aging processes.

Age Factors↗
PubMed1991

Influence of diet on fatal neoplastic disease in male Fischer 344 rats.

The influence of dietary manipulations on fatal neoplasms in male Fischer 344 rats was assessed. Particular attention was paid to leukemia and pituitary adenoma because they are the most common potentially fatal neoplasms that occur in this rat strain. The only dietary manipulation which depressed the mortality rates due to neoplastic disease was that involving a reduction in energy intake. Reduction of mineral or protein or fat intake without a reduction of energy had, at most, marginal effects on fatal neoplastic disease.

Adenoma↗
PubMed1990

Assessment of nutritional components in prolongation of life and health by diet.

Restricting the food intake of rodents extends the median length of life and the maximum life-span. It also retards most age-associated physiologic change and age-associated diseases. Our research indicates that the ability to retard disease processes is not the major reason for the extension of life-span or for the retardation of age change in most physiologic systems. Rather, it appears that most of the actions of food restriction are due to its ability to slow the primary aging processes. We found this action to relate to the restriction of calories rather than specific nutrients (e.g., protein or fat or minerals). Our findings point to the reduction in caloric intake per rat rather than per gram lean body mass as the basis of the retardation of aging processes by food restriction. The challenge is to learn how caloric intake per rat is coupled to the aging processes. We are currently focusing on the possibility that neural and endocrine mechanisms are involved. Our preliminary findings point to the likelihood of an involvement of the insulin-glucose system.

Animals↗