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L B Salans

Publications and source records attributed to L B Salans.

34 records · Page 2Linked to original sources
PubMed1978

Glucose transport in isolated rat adipocytes with measurements of L-arabinose uptake.

Data is presented suggesting that rates of L-arabinose transport, calculated from L-[1-14C]arabinose uptake measurements, can be used as indicators of changes in the rates of glucose transport in isolated rat adipocytes. L-[1-14C]arabinose, at 37 degrees C, was found to be nonmetabolizable and taken up by adipocytes exponentially with time reaching 95% of equilibrium in 30 min. When L-arabinose is corrected for background, the corrected uptake values conform to the time-dependent monoexponential uptake relationshiop predicted for a facilitated transport system and are not significantly different from 0 in the presence of 70 micron cytochalasin B. Transport rates were calculated from corrected uptake values near the half-maximal uptake of L-arabinose and from a value of the total amount of L-arabinose in the cell at equilibrium. Competitive inhibition of L-arabinose transport by glucose and countertransport of L-arabinose in the presence of glucose suggest that L-arabinose and glucose share the same transport system. Data is presented demonstrating the effect of insulin and dexamethasone on the transport system that confirms the conclusions obtained by other investigators using other methods.

Adipose Tissue↗
PubMed1978

Determinations of adipose cell size and number in suspensions of isolated rat and human adipose cells.

The osmic acid fixation-Coulter electronic counter method described for determining adipose cell size and number in intact adipose tissue fragments has been modified for use with suspensions of isolated rat and human adipose cells. Mean cell sizes in tissue fragments and isolated cell suspensions prepared from the same tissue are virtually identical in rats of various weights. No statistically significant difference in mean adipose cell size between tissue and isolated cell suspension was observed in human adipose tissue although the variability was much greater than in rat tissue. The distribution of cell sizes among replicate samples is more uniform in the isolated cell preparations, possibly reflecting the considerably larger quantities of tissue used in preparing isolated cells than in determining cell size and number directly from tissue fragments. An example of the utility of the modified method during routine metabolic studies with isolated rat epididymal adipose cells is described; isolated cells of increasing size can be obtained from rats of increasing body weight, or from the separated distal and proximal portions of the fat pads of rats of the same weight.

Adipose Tissue↗
PubMed1974

Glucose metabolism and the response to insulin by human adipose tissue in spontaneous and experimental obesity. Effects of dietary composition and adipose cell size.

[1-(14)C]glucose oxidation to CO(2) and conversion into glyceride by adipose tissue from nonobese and obese subjects has been studied in vitro in the presence of varying medium glucose and insulin concentrations as functions of adipose cell size, the composition of the diet, and antecedent weight gain or loss. Increasing medium glucose concentrations enhance the incorporation of glucose carbons by human adipose tissue into CO(2) and glyceride-glycerol. Insulin further stimulates the conversion of glucose carbons into CO(2), but not into glyceride-glycerol. Incorporation of [1-(14)C]glucose into glyceride-fatty acids by these tissues could not be demonstrated under any of the conditions tested. Both adipose cell size and dietary composition influence the in vitro metabolism of glucose in, and the response to insulin by, human adipose tissue. During periods of ingestion of weight-maintenance isocaloric diets of similar carbohydrate, fat, and protein composition, increasing adipose cell size is associated with (a) unchanging rates of glucose oxidation and increasing rates of glucose carbon incorporation into glyceride-glycerol in the absence of insulin, but (b) decreasing stimulation of glucose oxidation by insulin. On the other hand, when cell size is kept constant, increasing dietary carbohydrate intake is associated with an increased basal rate of glucose metabolism and response to insulin by both small and large adipose cells. Thus, the rate of glucose oxidation and the magnitude of the insulin response of large adipose cells from individuals ingesting a high carbohydrate diet may be similar to or greater than that in smaller cells from individuals ingesting an isocaloric lower carbohydrate diet.The alterations in basal glucose metabolism and insulin response observed in adipose tissue from patients with spontaneous obesity are reproduced by weight gain induced experimentally in nonobese volunteers; these metabolic changes are reversible with weight loss. The relationships among adipose cell size, dietary composition, and the metabolism of adipose tissue are similar in spontaneous and in experimental obesity.

Adipose Tissue↗
PubMed1973

Studies of human adipose tissue. Adipose cell size and number in nonobese and obese patients.

The cellular character of the adipose tissue of 21 nonobese and 78 obese patients has been examined. Adipose cell size (lipid per cell) was determined in three different subcutaneous and deep fat depots in each patient and the total number of adipose cells in the body estimated by division of total body fat by various combinations of the adipose cell sizes at six different sites. Cell number has also been estimated on the basis of various assumed distribution of total fat between the subcutaneous and deep fat depots. Obese patients, as a group, have larger adipose cells than do nonobese patients; cell size, however, varies considerably among the fat depots of individuals of either group. The variation in cell size exists not only between, but also within subcutaneous and deep sites. Estimates of total adipose cell number for a given individual based upon cell size can, therefore, vary by as much as 85%. On the basis of these studies it is suggested that the total adipose number of an individual is best and most practically estimated, at this time, by division of total body fat by the mean of the adipose cell sizes of at least three subcutaneous sites. IRRESPECTIVE OF THE METHOD BY WHICH TOTAL ADIPOSE CELL NUMBER IS ESTIMATED, TWO PATTERNS OF OBESITY EMERGE WITH RESPECT TO THE CELLULAR CHARACTER OF THE ADIPOSE TISSUE MASS OF THESE PATIENTS: hyperplastic, with increased adipose cell number and normal or increased size, and hypertrophic, with increased cell size alone. These two cellular patterns of obesity are independent of a variety of assumed distributions of fat among the subcutaneous and deep depots. When these different cellular patterns are examined in terms of various aspects of body size, body composition, and the degree, duration, and age of onset of obesity, only the latter uniquely distinguishes the hyperplastic from the hypertrophic: hyperplastic obesity is characterized by an early age of onset, hypertrophic, by a late age of onset. These studies indicate that there are two distinct periods early in life during which hypercellularity of the adipose tissue are most likely to occur: very early within the first few years, and again from age 9 to 13 yr.

Adipose Tissue↗
PubMed1972

Effect of insulin upon the cellular character of rat adipose tissue.

The effect of insulin upon the lipid content, and the number and size of fat cells in the epididymal, retroperitoneal, and subcutaneous adipose tissue of a large number of rats were examined. Insulin administration began either in early life (birth, 1, or 3 wk of age) or during adulthood (age 10 wk). At different times during growth, groups of treated and control animals were killed and the size and number of fat cells in each of the three adipose depots were determined. Insulin-treated animals gained weight at an increased rate and had fatter epididymal, retroperitoneal, and subcutaneous adipose depots than untreated controls. In each site the expanded adipose tissue was accompanied by an increase in the lipid content per cell (cell size), but in no case was there an increase in the number of adipose cells. This was the case regardless of whether insulin treatment was initiated before weaning (birth, 1 wk of age), at weaning (3 wk), or post weaning (10 wk) and irrespective of the duration of the insulin treatment.

Adipose Tissue↗
PubMed1971

Experimental obesity in man: cellular character of the adipose tissue.

Studies of adipose tissue cellularity were carried out in a group of nonobese adult male volunteers who gained 15-25% of their body weight as the result of prolonged high caloric intake. Adipose cell size (lipid content per cell) was determined in tissue obtained from three subcutaneous sites (gluteal, anterior abdominal wall, and triceps) and total adipose cell number estimated from measurement of total body fat. Five experimental subjects gained an average of 16.2 kg of body weight, of which 10.4 kg was determined to be fat. Expansion of the adipose mass was accompanied by a significant and relatively uniform increase in fat cell size in each subcutaneous site tested. Total adipose cell number did not change as a result of weight gain and expansion of the adipose depot in adult life. Subsequent loss of weight and restoration of original body fat was associated with a reduction in adipose cell size at each subcutaneous site, but no change in total number. In two control subjects who neither gained nor lost weight there were no changes in total adipose cell number or cell size. These observations suggest that expansion and retraction of the adipose depot in adult life is accompanied by changes in adipose cell size only. Significant differences in both the size and total number of adipose cells were observed between subjects in both the experimental and control groups. In addition, within individuals of both groups there were significant differences in cell size when adipose cells from the three subcutaneous sites were compared. These findings indicate that wide variations in adipose cell size and number exist in nonobese individuals having similar adipose depot sizes.

Adipose Tissue↗
PubMed1971

The effect of insulin upon glucose metabolism by adipose cells of different size. Influence of cell lipid and protein content, age, and nutritional state.

Glucose metabolism and insulin sensitivity of isolated rat epididymal fat cells and of their delipidated derivatives ("ghosts") was studied as a function of cellular lipid content (fat cell size), cellular protein content, animal age, and state of nutrition in an effort to examine the relationship of adipose cell size to adipose tissue insulin sensitivity.In ad libitum-fed rats, basal rates of glucose-1-(14)C incorporation into CO(2) and triglyceride are similar over a wide range of adipose cell size. In contrast, the insulin sensitivity of intact fat cells from rats fed ad libitum is inversely related to their lipid content: the larger the cell, the less the response to insulin. This "resistance" of the enlarged adipose cell to the action of insulin was demonstrated by a reduction in the per cent rise above the basal rate as well as in the absolute rate of glucose oxidation and lipogenesis caused by insulin. The protein content of fat cells was found to be relatively constant over a wide range of fat cell size. Thus, enlarged insulin "resistant" fat cells contained the same amount of protein as smaller insulin "sensitive" cells. These relationships between insulin sensitivity and cellular lipid or protein content were true regardless of whether cells of different sizes were obtained from animals of different body weights and ages, or from different portions of the epididymal fat pads of animals of the same weight and age.Acute delipidation of intact fat cells did not appear to alter these relationships between basal glucose metabolism, insulin sensitivity, and cell size. "Ghosts" prepared from fat cells of widely different sizes metabolized glucose to CO(2) and triglyceride at similar rates. The insulin sensitivity of the fat cell "ghost" appeared to be inversely related to the size of the intact cell from which it was derived: the larger the intact cell the less insulin sensitive its "ghost."Although the insulin "resistance" of adipose tissue was reversed by weight loss and reduction of fat cell size, these studies also demonstrate that the insulin sensitivity of adipose cells of similar sizes can vary widely depending upon the state of nutrition and growth of the animal. Thus, factors other than cell size can also influence the insulin sensitivity of the adipose tissue.

Adipose Tissue↗
PubMed1968

The role of adipose cell size and adipose tissue insulin sensitivity in the carbohydrate intolerance of human obesity.

Glucose metabolism and insulin sensitivity of isolated human adipose tissue was studied as a function of adipose cell size and number. Glucose metabolism by these tissues was closely related to the number of cells in the fragment, irrespective of cell size. Adipose cells of obese individuals metabolized glucose to carbon dioxide and triglyceride at rates similar to adipose cells of nonobese subjects. In contrast, insulin responsiveness of adipose tissue was dependent upon adipose cell size. The larger its adipose cells the less insulin sensitive was the tissue. Thus, adipose tissue of obese subjects, with enlarged cells, showed a diminished response to insulin. After weight loss and reduction in adipose cell size, insulin sensitivity of the adipose tissue of obese patients was restored to normal. When adipose tissue of obese individuals showed impaired responsiveness to insulin, their plasma insulin levels, after oral glucose, were elevated. Weight loss and reduction in adipose cell size restored plasma insulin concentration to normal, concomitant with the return of normal tissue insulin sensitivity.

Journal Article↗