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Biomedical subjects

B P Yu

Publications and source records attributed to B P Yu.

At least 109 records · Page 6Linked to original sources
PubMed1987

Diet restriction retards the age-related loss of beta-adrenergic receptors and adenylate cyclase activity in rat lung.

In the rat, dietary restriction prolongs life span and retards a variety of physiological processes that change with age. Beta-adrenergic responsiveness declines with age. We assessed beta-adrenergic receptor density and adenylate cyclase activity in lungs of 6-, 18-, 24-, and 27-month-old rats fed ad libitum or restricted to 60% of the ad libitum food after 6 weeks of age. Beta-adrenergic receptor density declined in the ad libitum group (M +/- SE, 417 +/- 30, 349 +/- 23, 297 +/- 19, 260 +/- 30 fmol/mg protein, p less than .01). In the diet-restricted group, beta-adrenergic receptor density declined between 6 and 18 months (493 +/- 35, 370 +/- 28, p less than .05) but remained unchanged from 18 to 27 months (370 +/- 28, 333 +/- 19, 360 +/- 16). Isoproterenol-stimulated adenylate cyclase activity declined with age in the ad libitum group (53.4 +/- 7.5, 46.8 +/- 8.8, 38 +/- 3.9, 27.8 +/- 3.3 p mol cAMP/mg protein, p less than .05) but not in diet-restricted group (45.1 +/- 8.9, 44 +/- 7.9, 41.8 +/- 2.4, 47.3 +/- 5.1). Changes in forskolin-stimulated adenylate cyclase activity with age were not affected by diet restriction. These data suggest that diet restriction retards some of the age-related changes in the beta-adrenergic pathway.

Adenylyl Cyclases↗
PubMed1987

Action of food restriction on age-related changes in adipocyte lipolysis.

The effects of aging and of food restriction at different times during life on rat adipocyte responses to glucagon and epinephrine were explored by studying hormone-stimulated lipolysis, hormone binding, and phosphodiesterase activity. The times of food restriction were: (a) from 6 weeks of age, (b) limited to early life, and (c) beginning in young adult life. Hormone-sensitive lipolysis is lost with age. Food restriction from 6 weeks of age prevents this loss, and food restriction started in adult life causes the recovery of this lipolysis. Hormone binding studies reveal that: (a) changes in glucagon-stimulated lipolysis parallel changes in glucagon binding; (b) glucagon binding and glucagon-stimulated lipolysis correlate inversely with cell size; (c) changes in epinephrine-stimulated lipolysis are not due to changes in beta-adrenergic binding; and (d) neither beta-adrenergic binding nor epinephrine-promoted lipolysis correlate with fat cell size. Phosphodiesterase activity is not influenced by diet, making it unlikely to be a postreceptor component lost with age.

Adipose Tissue↗
PubMed1986

An electron microscopic examination of age-related changes in the rat kidney: the influence of diet.

The changes with age in the ultrastructure of the kidneys were explored in ad libitum fed rats with restricted food intake started soon after weaning or started in young adult life or limited to early life and in rats restricted in protein but not caloric intake. Many ultrastructural changes occurred with age both in the glomeruli and the tubules. Food restriction started soon after weaning or in adult life modulated most of these age changes. By providing detailed information on basement membrane and tubular cell structure, these findings complement previous light microscopic and functional studies in regard to the effects of food restriction on progressive kidney disease in the rat. Food restriction limited to early life and protein restriction without caloric restriction were less effective in modulating these age changes in kidney ultrastructure than food restriction initiated at 6 weeks or 6 months of age and continued for the rest of the life span.

Aging↗
PubMed1985

Nutritional influences on aging of Fischer 344 rats: I. Physical, metabolic, and longevity characteristics.

The aims of this research were (a) to compare food restriction initiated in adult life of male Fischer 344 rats with that limited to early life or involving most of the life span on physical, metabolic, and longevity characteristics and (b) to study a similar level of protein restriction without caloric restriction on these characteristics. Food restriction (60% of the ad libitum intake) initiated at 6 months of age markedly increased life span as did a similar restriction started at 6 weeks of age, but food restriction limited to early life (6 weeks to 6 months of age) and protein restriction caused only a small increase in longevity. Food restriction does not act by reducing the intake of calories or other nutrient per gram of body mass, a finding not in accord with classic views. A progressive decrease in spontaneous locomotive activity with age occurred in ad libitum fed but not restricted rats.

Age Factors↗
PubMed1985

Nutritional influences on aging of Fischer 344 rats: II. Pathology.

The aim of this study was to explore the effects of nutritional manipulations on the occurrence and progression of age-related pathologic lesions in male Fischer 344 rats. The following nutritional regimens were studied: (a) ad libitum feeding, (b) food restriction initiated at 6 weeks of age, (c) food restriction initiated at 6 months of age, (d) food restriction limited to a period of early life (6 weeks to 6 months of age), (e) protein restriction without caloric restriction. The major age-related lesions observed were chronic nephropathy, cardiomyopathy, and neoplasia. Food restriction initiated at 6 months of age was as effective as food restriction initiated at 6 weeks of age in slowing the progression of chronic nephropathy and cardiomyopathy and in delaying the occurrence of neoplasia. Food restriction limited to early life was much less effective. Protein restriction in the absence of caloric restriction did not delay the occurrence of neoplasia, but it did retard chronic nephropathy and cardiomyopathy, although much less effectively than caloric restriction involving a similar level of protein restriction.

Aging↗
PubMed1985

Does food restriction retard aging by reducing the metabolic rate?

Metabolic rate was determined by measuring O2 consumption in two groups of 6-mo-old male rats fed ad libitum (group 1) or maintained on a life-prolonging food-restriction regimen for 4.5 mo (group 2). These measurements were made continuously for 23.75 h under conditions nearly identical to those of the daily life of the rats. The metabolic rate per kilogram lean body mass was the same for both groups, a finding contrary to the hypothesis that food restriction retards the aging process and prolongs life by slowing the metabolic rate per unit of metabolic mass. This and our previous work strongly suggest that the classic views of the action of food restriction on aging must be re-evaluated because retardation of the aging process can occur without the restriction of calories or any other nutrient per unit of lean body mass. The long held belief that reducing food intake lowers the metabolic rate per unit of metabolic mass may be true in short-term dietary programs but appears not to be true when a significant portion of the life span is involved.

Aging↗
PubMed1984

Lifelong food restriction prevents senile osteopenia and hyperparathyroidism in F344 rats.

Studies were carried out on male F344 rats to examine the influence of aging and life-prolonging food restriction on bone and circulating parathyroid hormone levels. In ad libitum fed animals, the weight, density and calcium content of the femur increased with age and achieved their peak levels by 12 months of age. These levels remained stable until about 24 months and by 27 months of age the ad libitum fed animals had lost appreciable amounts of bone. The maturation of the femurs of the animals maintained on 60% of the ad libitum food intake was delayed and their bones were lighter, less dense and contained less calcium than bones from ad libitum fed rats of corresponding ages. But at 6, 12 and 24 months of age, the femur strength to body weight ratios were very highly significantly greater (P less than 0.0001) for the restricted animals compared to the ad libitum fed controls. Circulating immunoreactive parathyroid hormone increased progressively with aging in the animals fed ad libitum and the animals that experienced bone loss at advanced age also had the highest level of the hormone. In contrast, in the food restricted animals aging was not associated with a marked increase in serum parathyroid hormone or with senile bone loss. The data are discussed in relation to the mechanism of the observed changes.

Aging↗
PubMed1984

Age changes in hepatic metabolic characteristics and their modulation by dietary manipulation.

Starting at 6 weeks of age, male Fischer 344 rats were provided five different dietary regimens: group 1, fed ad libitum; group 2, restricted to 60% of the food intake of group 1; group 3, restricted to 60% of the food intake of group 1 until 6 months of age and then fed ad libitum; group 4, fed ad libitum until 6 months of age and then restricted to 60% of the food intake of group 1; group 5, given the same caloric intake as group 1 but 60% of the protein intake. The weight of the liver was maintained at about 2.5% of body weight over the wide range of body weight, age (6 through 30 months of age) and diets of this study. Liver cholesterol concentration increased with age in the rats of group 1 but not in the other groups; the hepatic cholesterol concentration was lower in the rats of groups 2 and 4 than in the others. The liver microsomal 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase activity was higher in 4-month-old rats than in rats 12 months of age and older; also, the microsomal activity from group 2 and group 4 rats was higher than that from rats of the other groups. Liver triglyceride levels increased with age in groups 1, 2, 3 and 5 but not in group 4. At all ages, postabsorptive (15 h without food) hepatic glycogen concentrations were much higher in groups 2 and 4 than in the other groups. Liver phospholipid concentration was not affected by age or diet. Basal adenylate cyclase activity in liver homogenates increased with age in all but group 4, but hormone-stimulated adenylate cyclase activity was little affected by age or diet. The age-related hepatic changes in lipids and in hormone responsiveness noted in the present study were much less marked than those previously found in blood and adipose tissue.

Adenylyl Cyclases↗
PubMed1984

Plasticity of fat cell number.

Rats fed ad libitum (group 1) had little change in fat cell number in epididymal depots from 6 to 27 months of age, but a marked increase in fat cell number in perirenal depots between 6 and 18 months. Food restriction of rats to 60% of group 1 from 6 weeks of age on (group 2) reduced fat cell number in both depots throughout life and prevented an increase between 6 and 18 months in perirenal depots. Food restriction of rats to 60% of group 1 from 6 weeks to 6 months of age and then feeding ad libitum (group 3) markedly reduced fat cell number in both depots at 12 months compared to group 1. However, by 18 months of age, group 3 rats had the same fat cell number as group 1 rats in both depots. Food restriction of rats to 60% of the intake of group 1 started at 6 months of age (group 4) had no effect on fat cell number in epididymal depots but prevented an increase between 6 and 18 months in perirenal fat cell number. Group 5 rats fed ad libitum but restricted in protein (same caloric intake as group 1 rats) had epididymal and perirenal depots with the same characteristics as those of group 1. These findings and others in the literature show that modifying fat cell number is a widely used means of modifying fat mass during both early and adult life.

Adipose Tissue↗
PubMed1984

Aging and dietary modulation of rat skeleton and parathyroid hormone.

Studies were carried out on SPF F344 male rats to evaluate the effects of aging and life-prolonging food restriction, without malnutrition, on rat skeleton and circulating PTH. Six-week-old F344 rats were divided into five groups. Group 1 rats were fed ad libitum a diet that contained 21% protein. Group 2 rats were fed 60% of the mean food intake of group 1 rats from 6 weeks of age for the rest of their lives. Group 3 rats were fed 60% of the ad libitum food intake until 6 months of age and then switched to ad libitum feeding. Group 4 rats were fed ad libitum until 6 months of age, and then switched to 60% of the ad libitum food intake. Group 5 rats were fed ad libitum a diet that contained only 12.6% protein so that these animals ingested the same amount of protein per day as the group 2 rats. In group 1 animals, bone length, weight, density, and calcium content increased rapidly with age and plateaued at about 12 months of age. There was no evidence of bone loss in these animals until about 24 months of age, but by 27 months, the animals had lost appreciable amounts of bone. The circulating immunoreactive PTH levels of the animals increased with advancing age, with a marked rise at 27 months. The age-related changes in bone and serum PTH levels of rats in groups 3 and 5 were similar to those of group 1 animals, except that a terminal increase in serum PTH did not occur in group 5 rats. In the groups 2 and 4 animals which were food restricted for the longest period, bone growth and maturation were slowed down, but the animals did not experience senile bone loss or marked terminal increase in circulating PTH. The salutary effects of food restriction were, therefore, not due specifically to the restriction of protein intake or to restricting food intake only during the period of rapid growth.

Aging↗
PubMed1983

Temporal and compositional dietary restrictions modulate age-related changes in serum lipids.

Life-lon restriction of food, which markedly increases the length of life of rats, also delays the occurrence of age-related physiological deteriorations including the age-related changes in serum lipids. The aim of this study was to explore the effects of 1) food restriction limited to early life, 2) food restriction initiated in adult life and 3) restriction of protein without restriction of calories on the age-related changes in serum lipids. Food restriction started at 6 months of age was as effective as food restriction started at 6 weeks of age in modulating the age-related changes in serum lipids, whereas food restriction from 6 weeks to 6 months of age and restriction of protein but not calories were much less effective. Changes in the rate of very low density lipoprotein-triglyceride removal from the blood were not responsible for the age-related increase in triglyceride concentration or for the modulation of this increase by the dietary regimens. Age-related changes in serum or plasma levels of glucose, ketone bodies, insulin and glucagon were also measured and the modulating effects of the dietary regimens studied; possible relationships between the concentrations of these substances and the concentrations of the serum lipids are discussed.

Aging↗
PubMed1983

Lifelong dietary modulation of calcitonin levels in rats.

Studies were carried out on specific pathogen-free rats to evaluate the effects of aging and dietary manipulation on serum and thyroid calcitonin (CT) levels. Male Fischer 344 rats were randomized at 6 weeks of age to six dietary groups and subsequently maintained on the following dietary regimens. Group 1 rats were fed ad libitum throughout life; group 2 rats were fed 60% of the ad libitum food uptake, but received the same amounts of calcium, phosphorus, and vitamin D; group 3 rats were fed as the group 2 animals until 6 months of age and from then on were fed ad libitum; group 4 rats were fed ad libitum until 6 months of age and then switched to 60% food restriction; group 5 rats were fed ad libitum on food isocaloric with that of group 1 rats, but containing only 60% of the protein. Group 6 rats were killed at 6 weeks of age to serve as baseline controls. Ten rats were killed in each of the remaining five groups 15 h postprandial at 6-month intervals. The following observations were made. Serum CT increased with age similarly in the ad libitum fed group 1 and 5 rats. Food restriction markedly inhibited the increase in serum CT, and the effect was more profound in animals whose food intake was restricted after 6 months of age (group 4) than in animals on lifelong food restriction (group 2). In rats switched from food restriction to ad libitum feeding (group 3) at 6 months of age, serum CT increased with age to levels identical with those of lifelong ad libitum fed group 1 animals. Thyroid CT showed a similar pattern of age-dependent and dietary modulated changes. In contrast, aging and dietary modulation had no appreciable effect on serum calcium levels, except at 27 months of age when the serum calcium level of group 1 animals increased dramatically from the level for 24-month-old animals. There was a weak positive correlation between serum calcium and serum CT (r = 0.627; P = 0.02) and a highly significant positive correlation between serum CT and thyroid CT (r = 0.917; P = 0.001). These findings indicate that elective and therapeutic restriction of food intake might also attenulate CT levels in humans, with potentially adverse implications for skeletal homeostasis.

Aging↗
PubMed1982

Action of food restriction in delaying the aging process.

Food restriction has long been known to prolong life in rodents, and recent studies have shown it to have antiaging effects in regard to a variety of physiologic and pathologic processes. It has been suggested that these actions of food restriction relate to the reduction of metabolic rate per unit of body mass brought about by this dietary regimen. Data are presented in this report showing that food restriction can have a marked life-prolonging action in rats without reducing caloric intake per gram of body weight. Moreover, the food-restricted rats consumed a greater number of calories per gram of body weight during their lifetimes than did the rats fed ad lib, yet they lived longer. Thus, the data in this report do not support the concept that food restriction slows the rate of aging by decreasing the metabolic rate.

Aging↗
PubMed1982

Life span study of SPF Fischer 344 male rats fed ad libitum or restricted diets: longevity, growth, lean body mass and disease.

A life-span study was carried out on longevity, pathologic lesions, growth, lean body mass and selected aspects of muscle of barrier-maintained SPF Fischer 344 rats fed either ad libitum (Group A) or 60% of the ad libitum intake (Group R). Food restriction was as effective in prolonging the life of already long-lived SPF rats as previously shown for rats maintained in conventional facilities. Food restriction not only increased the mean length of life but also acted to extend life span since more than 60% of the Group R rats lived longer than the longest lived Group A rat. Renal lesions occurred at an earlier age in Group A rats than in Group R rats and progressed more rapidly. Death of most Group A rats was associated with severe renal lesions while few Group R rats showed such lesions at death. Food restriction was also found to delay or prevent interstitial cell tumors of the testes, bile duct hyperplasia, myocardial fibrosis and myocardial degeneration. Gastrocnemius muscle mass declined in advanced age and food restriction delayed this decline. Interestingly, however, lean body mass did not progressively decline with increasing age but rather decline occurred only after the onset of the terminal disease process.

Aging↗
PubMed1982

Rat muscle structure and metabolism in relation to age and food intake.

Age changes in oxygen consumption and the structural composition of the lateral omohyoideus muscle were studied in adult male rats. The rate were either fed ad libitum (group A) or 60% of the ad libitum intake (group R). An age-related loss in muscle mass did not occur even at advanced ages in group A or group R rats. Muscle fiber diameter decreased with age in both groups but a concomitant increase in the number of fibers prevented a change in muscle mass. The muscles of group R rats contained the same number of fibers as those of group A rats at all ages. The muscles of group A rats showed a progressive loss in rate of resting oxygen consumption until 18 mo of age. A similar but less marked loss in oxygen consumption occurred in the muscles of group R rats. These results provide further evidence that life-prolonging food restriction modulates physiological changes associated with the aging process.

Aging↗
PubMed1982

Effect of aging on urinary concentrating mechanism and vasopressin-dependent cAMP in rats.

The effect of aging on urinary concentrating ability and the pathogenic mechanism involved were investigated in Fischer 344 rats. While the rats had free access to drinking water, 24-mo-old rats were polydipsic and polyuric compared with 6- and 12-mo-old rats. The maximum urinary concentrating ability after 40-58 h of water deprivation was not different between 6- and 12-mo-old rats (Uosmol 2,941 +/- 173 vs. 2,706 +/- 96 (SE) mosmol/kg), but it was significantly decreased in 24-mo-old rats (1,885 +/- 172 mosmol/kg, P less than 0.01). Similarly, although 5 mU/ml vasopressin increased the concentration of cAMP and papillary slices in 12-mo-old rats (delta +2.81 +/- 0.62 pmol/mg tissue, P less than 0.01), the same concentration of vasopressin failed to increase the cAMP concentration in 24-mo-old rats (delta +0.25 +/- 0.21 pmol/mg tissue, P greater than 0.05). In the adenylate cyclase preparation of renal papilla, the response to low concentrations of vasopressin was diminished in 24-mo-old rats. The dose-response curve was shifted to the right and the ED50 concentration of vasopressin was increased in 24-mo-old rats compared with 12-mo-old rats: 1.40 +/- 0.12 mU/ml vasopressin vs. 3.04 +/- 0.22. These results suggest that the decrease in vasopressin-dependent cAMP generation may in part be responsible for the impairment of urinary concentrating ability in 24-mo-old rats.

Adenylyl Cyclases↗