PubMed Health⌕ Search

Biomedical subjects

B P Yu

Publications and source records attributed to B P Yu.

At least 127 records · Page 7Linked to original sources
PubMed1981

Quantitative changes in adipocyte plasma membrane in response to nutritional manipulations.

The effects of changes in adipocyte size and the effects of nutritional manipulations on the quantity of plasma membrane per adipocyte were investigated. A method for estimating the quantity of plasma membrane was developed based on the specific labeling of adipocyte plasma membrane protein with the nonpermeable labeling agent 125I-labeled diazotized diiodosulfanilic acid. By studying rats (ranging in age from 50 to 125 days) fed a standard laboratory chow or a low fat diet or a high fat diet, a wide range of mean fat cell sizes was obtained. It was found that as the volume of the fat cell increased, the amount of plasma membrane increased in a linear fashion and that this linear relationship had the same slope whether the size of the adipocyte increased slowly with age or rapidly in response to a high fat diet. In contrast, fasting for up to 3 days caused a marked decrease in the mean volume of the adipocytes, but either no change or much less change in the amount of plasma membrane per cell than would have been predicted from the linear relationship between adipocytes, but either no change or much less change in the amount of plasma membrane per cell than would have been predicted form the linear relationship between adipocyte volume and amount of plasma membrane per cell obtained with fed rats, i.e., adipocytes from fasted rats contain more plasma membrane per cell than do fat cells of the same size from fed rats. Neither feeding a high fat diet nor fasting caused detectable changes in the protein and lipid composition of the adipocyte plasma membrane.

Adipose Tissue↗
PubMed1980

Nutrition-aging influence of catecholamine-promoted lipolysis.

Male SPF Fischer 344 rats were fed ad lib. (group A) or 60% ad lib. intake (group R) from 6 wk of age. The group R rats had a markedly increased median length of life. Starting at 6 mo of age, rats were periodically killed and free adipocytes prepared from the epididymal and perirenal depots. The free adipocytes were used for the in vitro study of the effects of age on the promotion of lipolysis by catecholamines. At 6 mo of age, the response of the adipocytes from group A and group R rats was similar when the data are expressed as mumole glycerol released/10(6) adipocytes. With increasing age, however, this lipolytic response to catecholamines of group A rats markedly declined. The catecholamine-stimulated lipolysis/10(6) adipocytes from group R rats changed little between 6 and 18 mo of age, and the decline noted after 18 mo of age was less marked than that occurring in adipocytes from group A rats. The data based on rates of lipolysis/10(6) adipocytes indicate that it is the lifelong nutritional history of a rat population that determines the age-related changes in responsiveness of adipocytes to catecholamines. However, if the data are expressed per sq mm of adipocyte surface, a somewhat different picture emerges. These data are presented and their relevance is discussed.

Adipose Tissue↗
PubMed1980

Changes in adipose mass and cellularity through the adult life of rats fed ad libitum or a life-prolonging restricted diet.

Male Fischer 344 rats were either fed ad libitum (Group A) or 60% of the ad libitum intake (Group R) starting at 6 weeks of age; the latter is a life prolonging food restriction. Total adipose mass increased with increasing age in both Group A and Group R rats until about 70% of the life span after which it declined. The results indicate that the lower adipose mass of the Group R rats is probably not related to life prolongation. Adipocyte hypertrophy is involved in growth of the epididymal and perirenal depots in adult Group R rats and is the sole basis of epididymal depot growth in adult Group A rats. Increasing adipocyte number is the sole basis of perirenal depot growth in adult Group A rats and is involved in the growth of both depots in adult Group R rats. Decreasing adipose mass during senescence involves decreasing mean adipocyte volume but not a decrease in the adipocyte number.

Adipose Tissue↗
PubMed1980

Food restriction as a modulator of age-related changes in serum lipids.

Fischer 344 male rats were either fed ad libitum or 60% of the ad libitum intake. The restriction of food intake markedly increased the median length of life. Postabsorptive serum cholesterol and phospholipid concentrations increase in the ad libitum-fed rats with increasing age. Life-prolonging food restriction does not influence the serum levels of these lipids in young rats but delays the age-related increase in concentrations. Postabsorptive serum free fatty acid (FFA) concentrations decrease with advancing age in ad libitum-fed rats. Life-prolonging food restriction, while not affecting the serum FFA levels in young rats, delays and possibly partially prevents the age-related decrease in concentration. Food restriction lowers postabsorptive serum triglyceride levels at all ages studied. The data on serum cholesterol, phospholipids, and FFA provide further evidence that food restriction delays age-related changes in the physiological systems of rats. This delay of physiological decline may well retard the occurrence of age-related disease processes, thus prolonging life.

Aging↗
PubMed1980

Maintenance of glucagon-promoted lipolysis in adipocytes by food restriction.

Life-prolonging food restriction is known to delay physiological changes that occur during senescence. The aim of the present study was to learn if this nutritional manipulation also can influence changes that occur during the developmental phase of life. Male, specific pathogen-free Fischer 344 rats were fed ad libitum (group A) or 60% of the ad libitum intake (group R) beginning at 6 weeks of age. The group R rats had a markedly increased median length of life. Starting at 6 months of age, rats were periodically killed, and free adipocytes were prepared from epididymal and perirenal depots. The free adipocytes were used for the in vitro study of the promotion of lipolysis by glucagon. At 6 months of age and all older ages, adipocytes from group A rats were not responsive to the lipolytic action of glucagon; this agrees with earlier studies showing a marked loss in responsiveness to glucagon between 4-15 weeks of age. However, adipocytes from group R rats were quite responsive to glucagon at 6 and 12 months of age. Although after 12 months of age there was a loss in responsiveness to glucagon, this response remained significant through 36 months of age in the group R rats. Thus, life-prolonging food restriction delays not only functional changes that take place late in life (senescent changes) but also those occurring during the developmental period of life. The value of these findings as a model for experimental gerontology is discussed.

Adipose Tissue↗
PubMed1980

Nutritional probe of the aging process.

It has long been known that food restriction markedly increases the length of life of rats and other laboratory rodents. It has been further shown that life-prolonging food restriction delays the occurrence or slows the progression of those diseases believed to limit the life span of the animal. However, the mechanisms responsible for this increase in longevity and for the delay in occurrence of age-associated disease are not known. Surprisingly little work hs been done on the effect of these life-prolonging dietary regimens on the many changes in physiological processes and biochemical characteristics that occur with age. Since biochemical and physiological explorations might well provide the information needed to investigate the basic mechanisms underlying these actions of food restriction, such a study was initiated in our laboratory. It was found that in most of the age-related functions studied changes were delayed or partially prevented by food restriction. Our studies provide a start in analyzing the mechanisms by which food restriction prolongs life and delays disease and it is to be anticipated that future research along this line will not only further define these mechanisms but in addition should greatly contribute to our knowledge of the aging process.

Adipose Tissue↗
PubMed1979

Analysis and exploration of age-related changes in mammalian structure and function.

Although there is a large body of data showing an age-associated decline in the physiological systems of mammals, there is a great need for more descriptive information on the morphological and functional changes that occur with age. A powerful approach for ascertaining the extent to which age-related physiological changes limit the functional capacity of mammals is to study the effects of age on the response to challenges. Food restriction that markedly increases the mean life span of rodents also provides a potentially effective experimental probe of the aging process. Results are reported from our current research on morphologic and functional changes during the total life span of rats and on the influence of food restriction on these age-related changes. The data from our study of the lean body mass, adipose tissue mass, and adipose tissue structure indicate that current dogmas need to be reexamined; moreover, they clearly show the need for and the power of life-long descriptive studies. Our research on the influence of food restriction on age-related changes in functional activity supports the hypothesis that one mechanism by which food restriction increases the life span of rats relates to the delay in time of onset and a change in chronologic course of physiologic decline.

Adipose Tissue↗
PubMed1978

Increasing adipocyte number as the basis for perirenal depot growth in adult rats.

The mass of the perirenal adipose depot in male Fischer 344 rats increases between 6 and 18 months of age. This increase is due to an increase in the number of adipocytes in this depot, in contrast with the concept that adipocyte number is constant throughout adult life. The epididymal depot increases in mass between 6 and 18 months of age by adipocyte hypertrophy alone.

Adipose Tissue↗
PubMed1978

Isolation of subunits from trypsin-cleaved sarcoplasmic reticulum Ca2+ transport adenosine triphosphatase.

Controlled tryptic digestion of purified rat skeletal muscle sarcoplasmic reticulum (Ca2+ + Mg2+)-adenosine triphosphate yields two products designated Fragments 3a and 3b with molecular weights of 65,000 and 56,000 respectively. The isolation of these products in high yield should facilitate exploration of the molecular characteristics of this adenosine triphosphatase. A simple, rapid method for accomplishing this isolation was developed which provides a high yield and utilizes mild conditions. The fragments obtained by this method were used to determine the phospholipid and sulfhydryl contents of Fragments 3a and 3b. In addition, information was obtained on the orientation of these adenosine triphosphatase components in the enzyme lipoprotein complex.

Adenosine Triphosphatases↗
PubMed1976

Analysis of the arrangement of protein components in the sarcomplasmic reticulum of rat skeletal muscle.

The nature of the protein components and their location in the sarcoplasmic reticulum membrane were studied using sarcoplasmic reticulum vesicles isolated from rat skeletal muscle and purified by a density gradient centrifugation system. On the basis of analysis by means of sodium dodecyl sulfate gel electrophoresis, the protein components appear to be similar if not identical with those reported by others for rabbit sarcoplasmic reticulum, and the relative amount of each component is also similar to that found with rabbit sarcoplasmic reticulum. Evidence is presented that radioiodine-labeled diazotized diiodosulfanilic acid is a nonpermeant labeling agent of the protein components of sarcoplasmic reticulum vesicles; this agent minimally disturbs the functional activities of these membranes. By means of this labeling agent and perturbing agents, it is concluded that the protein components with molecular weights greater than 120,000 and the (Ca2+ + Mg2+)-adenosine triphosphatase partially or totally reside on or at the external surface of the sarcoplasmic reticulum vesicles. In the case of the adenosine triphosphatase, highly controlled trypsin treatment cleaves the molecule into two products, a 65,000 molecular weight fragment and a 56,000 molecular weight fragment. The evidence indicates that the 65,000 molecular weight component of the (Ca2+ + Mg2+)-adenosine triphosphatase is located in a more exposed fashion on the external surface of the vesicles than the 56,000 molecular weight compoenet and that some adenosine triphosphatase molecules have a more exposed position on the external surface of the vesicle than others. The protein components designated by MacLennan (MacLennan, D. H. (1975) Can. J. Biochem. 53, 251-261) as "calsequestrin" and "high affinity Ca2+ binding protein" are shown not to be on the external surface of the rat sarcoplasmic reticulum vesicle but rather to reside either within the core of the membrane or on the inside surface of the vesicle. The results of this study are in agreement with the model for the organization of the protein components of the sarcoplasmic reticulum membrene recently proposed by MacLennan (MacLennan, D. H. (1975) Can. J. Biochem. 53, 251-261).

Adenosine Triphosphatases↗