Adipose Cell Number Research Articles

Relative Contributions of Acetate, Lactate and Glucose to Lipogenesis in Bovine Intramuscular and Subcutaneous Adipose Tissue

Intramuscular adipose tissue from the fifth–eighth thoracic vertebrae region of the longissimus dorsi muscle, and portions of the overlying subcutaneous adipose tissue, were obtained at 16 and 18 months of age from Angus steers fed ad libitum either a corn silage (low energy) or ground corn (high energy) diet. Carcass weight, backfat thickness, and kidney, pelvic and heart fat were significantly greater in the steers fed the high energy diet; however, there were no significant differences in marbling scores between diet groups. Additionally, feeding steers the high energy diet did not result in differences in adipocyte diameter or number of adipose cells per gram tissue in either adipose tissue depot. Intramuscular adipocytes had a peak diameter (the diameter represented by the greatest number of cells) of 104 ± 2 µm; peak diameter in subcutaneous adipose tissue was 141 ± 5 µm. The activities of ATP-citrate lyase and NADP-malate dehydrogenase increased with age in the subcutaneous adipose tissue; feeding steers the high energy diet increased enzyme activities further. Age and diet had no effect on enzyme activities in intramuscular adipose tissue. A similar pattern was observed for the incorporation of lipogenic precursors into fatty acids. Acetate provided 70–80% of the acetyl units to in vitro lipogenesis in subcutaneous adipose tissue, but only 10–25% in intramuscular adipose tissue. Conversely, glucose provided 1–10% of the acetyl units in subcutaneous adipose tissue, but 50–75% in the intramuscular depot. The contribution of lactate to lipogenesis was similar in both tissues (15–30%). The pentose cycle was estimated to contribute all of the necessary NADPH required for lipogenesis in the younger steers, and 40–85% (depending on diet and tissue site) in the 18-month-old steers. There was no effect of diet on, or difference between adipose tissue depots for, the relative contribution of the pentose cycle to lipogenesis. The data suggest that different regulatory processes control de novo fatty acid synthesis in intramuscular and subcutaneous adipose tissue.

Lipid metabolism in finishing bulls and steers implanted with oestradiol-17 β-dipropionate

ABSTRACTTwenty bull calves were assigned to one of four treatment groups: 1) intact bulls; 2) intact bulls implanted with oestradiol dipropionate; 3) steers, and 4) steers implanted with oestradiol dipropionate. Subcutaneous adipose tissue was obtained by biopsy 5 months after implantation. Experimental treatment did not alter (P> 0·05) mean adipose cell volume, diameter or cell number per g adipose tissue. Soluble protein content of adipose cells from bulls was increased by implantation, but not in steers.In vitrorates of fatty acid synthesis were higher in oestrogen-implanted cattle compared with nonimplanted cattle when expressed per g adipose tissue, but not when expressed per cell. Maximal activities of the lipogenic-related enzymes, acetyl coenzyme A carboxylase, adenosine triphosphate-citrate lyase, aconitate hydratase and NADP-isocitrate dehydrogenase were higher in implanted compared with nonimplanted cattle when the activities were expressed per g tissue and acetyl coenzyme A carboxylase and aconitase were also higher when expressed per adipose cell. Bulls and steers had the same basal and stimulated lipolytic rates and implantation of oestradiol dipropionate had no effect on either basal or stimulated lipolytic rate. In this experiment, the oestrogenic implant appeared to have a stimulatory effect onin vitroestimates of lipogenesis.

Body composition and adiposity in LH-lesioned and pair-fed obese Zucker rats.

It has been reported previously that lateral hypothalamic (LH) lesions alter body composition including reducing adipocyte cellularity in lean and obese Zucker rats. The present experiment was designed to determine whether these alterations in body composition and adipose cell number are secondary to the reduced energy consumption of LH-lesioned rats or to a direct effect of the hypothalamic lesion. Groups of lean and obese Zucker rats, sustaining lesions of the lateral hypothalamus at 10 wk of age, maintained body weight at 72% that of nonlesioned controls until killed at 32 wk. Pair-feeding nonlesioned rats to the intakes of lean and obese LH-lesioned rats produced a reduction in adipocyte number similar to that caused by lesions. However, neither the lean nor obese LH-lesioned rats displayed an increase in cell number when fed a palatable diet that markedly increased carcass lipids. This finding suggests that adipocyte number may be constrained in LH-lesioned rats. These and further observations that 1) lean control rats maintained a higher body weight than the LH-lesioned rats to which they were pair fed and 2) in obese rats, food restriction further reduced protein deposition and elevated plasma insulin relative to comparably fed LH-lesioned obese rats suggest that the LH syndrome is mimicked by simple food restriction.

Correlated Responses for Lipogenesis and Adipose Tissue Cellularity in Chickens Selected for Body Weight Gain, Food Consumption, and Food Conversion Efficiency

Cellularity of the abdominal fat pad and lipogenesis in the liver were studied in 9-week-old chickens after eight generations of selection for increased body weight gain (line W), increased food consumption (Line F), decreased food conversion ratio (line E), or at random (line C). The average volume of the adipose cells in the abdominal fat pad was greatest in the birds of line F and smallest in birds of line E. Differences in the number of adipose cells in this fat depot in birds from all the lines can be largely attributed to differences in growth rate. Lipogenesis, as measured by in vitro incorporation of 14C-glucose into lipid and the activity of NADP-malate dehydrogenase, was highest in birds from line F and lowest in birds from line E. These differences in lipogenesis among groups could not be attributed to differences in food consumption or growth rate. The biochemical basis for differences in lipogenesis among lines is not clear at this stage.

The problem of classifying obesity.

AbstractThe numerous attempts to classify obesity demonstrate the difficulty of grouping the obesity syndrome into a single schema. The criteria can be subdivided into 3 groups: the first based on etiology and pathogenesis; the second based on clinical observation, anthropomorphic measurements and adipose tissue histology; and the third based on psychological and nutritional behavior, and environmental elements. The etiological classification subdividing obesity into genetic, hypothalamic, nutritional, physical inactivity, and endocrine groups is important because it best approximates the clinical reality of obesity.Recently acquired knowledge about adipose tissue cellularity and its metabolism has become important for clinical classification of the different types of obesity. Now we can divide obesity into hypertrophic (the weight of the adipocite increases), hyperplastic (only the number of adipose cells increases), and combined (number and weight of adipocite increase). Pure hyperplastic obesity is rarely found, while combined obesity is more frequent; the hypertrophic form is associated with obesity arising in adult life.Considerable information is gained from the study of anomalous nutritional behavior. The excess of food intake has psychologically disparate motivations that are caused by emotional reaction to anxiety‐provoking events or to a developing modification of personality. The first is reactive obesity, the second developmental obesity. However, among the obese there are individuals who have no specific psychological problems and are prompted to hyperfeed by environmental factors. In this case, the term “environmental obesity” is used. As regards a proper therapeutic approach, these distinctions are very important.

Effect of early and chronic hypoinsulinism on adipose tissue cellularity in the rat.

The effect of chronic hypoinsulinism on the development of retroperitoneal adipose tissue was studied in rats injected with streptozotocin at birth. The streptozotocin injection induced an acute neonatal diabetes which regressed spontaneously after one week and led to a chronic state of chemical diabetes in the young and in the adult rat. Growth of chemically diabetic rats was normal although the retroperitoneal adipose tissue showed a relative hypoplasia which appeared at two months and evolved with age so that at 10 months the number of adipose cells in the retroperitoneal adipose tissue was largely decreased with respect to control animals (1.34 +/- 0.12 x 10(6) versus 2.23 +/- 0.11 x 10(6)). This relative hypoplasia was still present at 20 months. Whereas the hypoplasia associated with the chemical diabetes was highly reproducible, the mean adipocyte size was modified in a variable manner but was never significantly decreased in chemically diabetic rats. These findings indicate that insulin is involved in the control of retroperitoneal adipose tissue cellularity and suggest that the effect of hypoinsulinism on adipocyte number does not depend on a decrease of the mean adipocyte volume.

Cellularity of bovine adipose tissues: developmental changes from 15 to 65 percent mature weight

Changes in the cellularity of various adipose tissues in growing cattle were analyzed. Fifty male cattle were slaughtered between 15 and 65% of mature weight. The whole adipose mass, separated by dissection, was divided into three parts: subcutaneous, intermuscular, and internal adipose tissues. Lipid content, cell size and distribution, as well as cell number of these three parts were determined. Adipose cells became 15 times greater from 15 to 65% mature weight, whereas total adipose cell number increased only 1.8-fold. However, a significant hyperplasia occurred near 45% mature weight. These results suggested a cell size regulation by hyperplasia. Over the whole period studied (15-65% mature weight), hyperplasia was far higher in subcutaneous adipose tissue than in other tissues. This is discussed as related to the higher relative growth of this tissue. In each fatty tissue, two identical development periods were observed. Each of them began by an increase in small-sized cells (hyperplasia) followed by the filling of these cells (hypertrophy). These two periods were particularly clear in the case of subcutaneous tissue, in which the second hyperplasia occurred slightly later than in other fatty tissues. So, in all respects, subcutaneous fatty tissue appears to develop later than other tissues studied.

A note on the effects of heat stress on carcass composition and adipose tissue cellularity of ducklings

1. The effects of heat exposure (36 °C) from 14 or 18 to 28 d of age on ducklings were assessed by comparison with pair‐fed or ad libitum‐fed controls at 22 °C. From 28 d all groups were fed ad libitum at normal temperature until samples were killed at 41 or 54 d. 2. At 28 d performance was similar in heat‐exposed and respective pair‐fed controls, but poorer than in ad libitum‐fed controls. Food intake and gain were less for heat‐exposed than for pair‐fed birds at 41 and 54 d (data combined). 3. Proportional fat pad size, adipose cell volume and number were less for all groups than for ad libitum‐fed controls at 41 d, but these differences largely disappeared by 54 d. Carcass fat varied little between groups. 4. Carcass moisture was less in heat‐exposed than in pair‐fed birds at 54 d and carcass protein greater at 41 d.

Phosphorylase kinase deficiency and decreased fat accumulation in hybrid male mice (I X C3H).

AbstractI strain mice have a deficiency of muscle phosphorylase b kinase. Their skeletal muscle shows a three- to fivefold elevation in glycogen concentration and a decreased rate of glycogen breakdown. In addition, I strain mice accumulate less fat with age or high fat diets than control mice. The purpose of this study was to determine whether phosphorylase b kinase deficiency and decreased fat accumulation of I strain mice are related. Body weight, epididymal fat pad size, adipose cell number, and size were determined in male I, C3H, and hybrid (IxC3H) mice. Since the phosphorylase kinase deficiency is sex-linked, the male offspring of the I♂ xC3H♀ cross were used. As expected, phosphorylase b kinase activity and glycogen content in I and IxC3H skeletal muscle are similar. Body weight at 16 weeks of age in IxC3H mice resembles the body weight of I mice rather than C3H mice. Epididymal fat pad weight is not significantly different in IxC3H and I mice. Epididymal fat pad weight is significantly lower in I...

Regional adipose cellularity and reliability of adipose cell size determination

Regional adipose cell size was assessed in 18 males ranging in age from 20 to 36 years. These measures were correlated to total body fat determined by hydrostatic weighing. Adipose samples were removed from the gluteal, abdominal, and subscapular regions using a needle aspiration technique. The tissue was incubated in collagenase to release individual cells that were immediately photographed under a microscope. To establish the reliability of adipose cell size assessment over time, fat biopsies were secured on 2 separate days. No significant difference was found for any region between day 1 and 2 adipose cell measures. Gluteal cell diameter (90.3 mu) was significantly larger than the abdominal (81.0 mu) and subscapular (78.6 mu) cell diameter (90.3 mu) was significantly larger than the abdominal (81.0 mu) and subscapular (78.6 mu) cell diameters. Total body fat correlated highest with gluteal cell size (r = 0.76) compared with the abdominal (r = 0.67) or subscapular (r = 0.70) regions. This study also examined the number of adipose cells required to subscapular (r = 0.70) regions. This study also examined the number of adipose cells required to obtain a reliable and representative mean value of adipose cell size. Using a sequential estimation analysis it was found that adipose cell diameters of the abdominal, gluteal, or subscapular regions can be reliably estimated with fewer than 100 cells.

Effect of a high fat diet on body composition, cellularity, and enzyme levels during early development of the rat.

AbstractA high fat (60%) and a low fat (5%) diet were fed to female rats during gestation and lactation and to their male and female offspring for 3 weeks postweaning. The cellular effects of feeding all combinations of the two diets during the three growth periods (gestation, lactation, and rapid growth) were determined in Wistar rats. “Nutritional imprinting” of earlier dietary regimes on enzyme profiles and adipose cell number was not observed after rats were fed a control diet to maturity. The high fat diet caused reduced fat deposition during gestation. During lactation, the high fat diet caused increased fat deposition. Post-weaning rats had increased carcass fat, decreased protein, and lower carcass weight due to the high fat diet. Serum glucose was lower for fat-fed males during lactation and also for postweaning males and females. Fat feeding in lactation caused a decrease in adipose cell numbers which was not evident until rats were 6 weeks of age. The effect was only transient when rats were fe...

Cellularity of adipose tissue in fetal pig.

Adipose tissue cellularity was studied in the 85-day-old Large-White pig fetus. The aim of this work was to count the adipose cells of forming tissue in an animal species which could be a possible model for studying adipose tissue in humans. Using a morphometric method with electron microscopy, mean triglyceride volume per cell was determined independently of mean cell volume. This method is suitable for counting adipose cells in the early stage of differentiation whatever their size and lipid inclusion volume. Site-by-site dissection of adipose tissue was not feasible in the 85-day old fetus and adipose cell number was computed by dividing total carcass triglyceride volume by mean triglyceride volume per cell. The carcass triglyceride seemed to originate only from adipose cells. The mean total carcass triglyceride volume per fetus (1.84 g) was low but, owing to the low mean triglyceride volume per cell (180.28 microns3), the adipose cell number (11.15 X 10(9)) was relatively important, as it represented about 27% of the extramuscular adipose cell number in the Large-White adult pig (41 X 10(9)).

The growth of adipose tissue in children and adolescents. Cross-sectional and longitudinal studies of adipose cell number and size.

Adipocyte size and number were determined in 288 subjects ranging in age from 4 mo to 19 yr. The study was performed in 110 obese and 178 non-obese subjects. 4-yr, longitudinal, follow-up studies were also performed in 132 subjects. The results demonstrate that the contribution of cell number and size to the growth of the fat depot in nonobese children varies with age. Deviations from this normal development were observed in obese children shortly after 1 yr of age. By 11 yr of age obese children exceeded the mean cell number found in nonobese adults. Indeed, obese subjects displayed more rapid and earlier elevations in both cell number and size, which were maintained throughout the study. Thus obese children display both quantitative and qualitative differences in fat tissue development when compared to nonobese children. The data indicate that the rate and type of adipose tissue cellular development one encounters in children may play a role in the development of the enlarged fat depots found in obese subjects.

The cellularity of ovine adipose tissue

The cellular growth of adipose tissue from Dorset Horn x Merino wethers was characterized by both hypertrophy and hyperplasia of adipose cells until the sheep were c. 11 months old, after which hypertrophy of existing adipose cells was solely responsible for increases in adipose tissue mass. Omental adipose tissue contained larger adipose cells than either the perirenal or subcutaneous sites. The weight of fat which had been deposited in the boneless carcass meat and the internal adipose tissue depots were linearly and positively correlated with the volume of the adipose cells. Decreases in the mass of adipose tissue, which accompanied nutritional restriction, were due to decreased adipose cell size, since no change was observed in the number of adipose cells per carcass after loss in weight. The cellularity characteristics of rehabilitated sheep were similar to those of sheep which had undergone continuous growth.

An autoradiographic study of new fat cell formation in adipose tissue in adult mice during malnutrition and refeeding.

The renewal of adipose cells in adult mice has been autoradiographically studied. The number of adipose cells was diminished by eighty percent during malnutrition and the same number of adipose cells proliferated during the refeeding stage. The results of our study showed that adipose tissue, which had previously been believed to be stable in cell number, has the capacity for cell proliferation according to changes in nutritional status.

Adipose tissue development, growth, and food consumption in protein-malnourished rats.

Effects of protein malnutrition on adipose tissue development were studied in weanling male Sprague-Dawley rats fed isocaloric diets ad libitum containing either 22% (controls) or 8% (protein-malnourished rats) casein, and in rats pair-fed to the protein-malnourished rats with the 22% casein diet. After 32 days on the diet, protein-malnourished rats were 37% and pair-fed 67% the weight of the controls, while torso length was 37% and 73% of controls, respectively. Food consumption relative to body weight was greatest in protein-malnourished rats. Compared to control rats, the distal epididymal adipocyte number in the protein-malnourished rats was decreased in proportion to the decrease in body size and was more closely related to the protein intake than to the total calories consumed. After 32 days on diet, mean adipocyte number per 2 distal pads was 11.7 x 10(6) in controls and 4.3 x 10(6) in protein-malnourished rats. In pair-fed rats, cell number lagged behind controls at 4 and 11 days, but was normal at 32 days (11.4 x 10(6) cells). The distal epididymal pad adipocyte size and percent lipid were similar in all groups during the first 25 days of dietary treatment. Adipocyte size was increased significantly in controls at day 32 compared to the other two groups. At each time studied through day 25 on diet, epididymal pad weight was related to the adipose cell number rather than the cell size. It is concluded that severe restriction of dietary protein during the postweaning period of growth in rats results in decreased epididymal adipocyte proliferation and/or differentiation concomitant with generalized growth retardation, whereas isocaloric feeding of a diet of normal protein content is associated with only a transient delay in adipose tissue development.

Larval adipose tissue of homoeotic bithorax mutants of Drosophila

In the homoeotic bithorax mutant combination bx 3 pbx Ubx 105 of Drosophila melanogaster, the metathoracic segment is transformed to a mesothoracic segment and the adult flies have an extra pair of wings in place of the paired halteres [Lewis, E. B. (1963). Amer. Zool. 3, 33–56]. The morphology of the larval fat body, the number of cells in the fat body, and the distribution pattern of kynurenine autofluorescent materials (KAF+) in this tissue were compared in the homoeotic mutant and a wild-type strain. The mutant has an additional mass of adipose cells anterior to the posterior margin of the ventral commissure of the fat body. However, the total number of adipose cells in the two strains as well as the limits of the KAF+ cell population do not differ. Therefore, the bithorax transformation in the larval fat body involves rearrangement of the same cell population as that in the normal strain. This study suggests (1) that the bithorax mutant genes affect the pattern of cell segregation and/or migration of preblastoderm nuclei during embryogenesis and (2) that the larval fat body of Drosophila has a segmental origin.

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.

Cellularity of porcine adipose tissue: effects of growth and adiposity

Adipose tissue, from two depots in pigs of three breeding groups with different propensities to fatten, was characterized in terms of weight of the adipose tissue organ, adipose cell number, and mean cell volume as determined by electronic counting of adipose cells fixed with osmium tetroxide. Perirenal and extramuscular adipose tissue growth was accompanied by progressive adipose cell enlargement along with an increase in cell number. By approximately 18-20 weeks of life, adipose tissue growth in both lean Hampshire x Yorkshire and fat Minnesota 3 x 1 pigs occurred exclusively by cellular hypertrophy. By 24 weeks of life (37 kg), hyperplasia was complete in Hormel Miniature pigs, which contained about one-third as many extramuscular adipose cells as the conventional pigs. Adiposity in the pig was due to cellular hypertrophy rather than cellular hyperplasia, since during growth, the leaner conventional pigs (30.6% extramuscular fat) contained more adipose cells than the fatter pigs (46.6% extramuscular fat). The number of adipose cells per animal or per adipose organ was directly related to the true body size (weight of fat-free carcass) of the animal. Fat Minnesota 3 x 1 pigs had fewer adipose cells than lean Hampshire x Yorkshire pigs at an equivalent live weight due to the smaller true body size of these animals. In young animals (28 and 54 kg), growth rate was positively correlated with adipose cell number. However, growth rate was unrelated to the total number of cells in the more mature animals (83 and 109 kg). Therefore a slow, normal growth rate may delay but not alter the final cell number.

A biologic radar system for the assessment of body mass the model of a geometry sensitive endocrine system is presented

Appetite control, pubarchal timing, and catch-up growth all seem to depend, to some extent, on body mass. Information regarding this variable may be supplied to the central nervous system (“ponderostat”) by a humoral radar system employing an insulin-like molecule or dependent substrate as a signal. The intensity of this signal would vary as a function of the organism's total adipose cell surface area, which, in turn, is a product of cell size and number. The geometry of a sphere (adipose cell) is such that surface area change per unit volume change increases as the radius of the sphere is reduced. Signal shifts then are maximal when cell volume is minimal. Divergence of the adipose signal from an age-appropriate norm could influence “ponderostat” activity and, in turn, brain centers mediating appetitive and various endocrine systems. Total caloric intake and the timing of this intake with respect to somatic maturity appear to affect adipose cell volume and number respectively. If shifts in adipose surface area provide a signal source regarding organismic mass, and if this surface area reflects the quantity and chronology of antecedent nutritional events, there are obvious implications for the role of nutrition during “critical periods” in the subsequent operation of the complex systems subserving appetite, somatic growth and sexual maturation.