Fat Cells In Adipose Tissue Research Articles

Preferential expression of cholesteryl ester transfer protein mRNA by stromal-vascular cells of human adipose tissue

Cholesteryl ester transfer protein (CETP) mRNA is more abundantly expressed in small mature adipocytes as compared to large, lipid-rich adipocytes [Radeau et al., J. Lipid Res. 36 (1995) 2552–2561]. In the present study, the stromal vascular fraction (SVF) of human adipose tissue was isolated and the presence of very small fat cells in this fraction confirmed by electron microscopy and by demonstrating the presence of mRNA for adipsin and for CCAAT enhancer binding protein α (C/EBPα), a marker of adipocyte differentiation. sn-Glycerol 3-phosphate dehydrogenase (GPDH) activity was present in the SVF but not in the preadipocyte fraction. Northern blot analysis of human adipose tissue demonstrated that CETP mRNA expression was significantly greater (+96%, P<0.03) in stromal-vascular cells (SVC) as compared to mature fat cells. By comparison, lipoprotein lipase mRNA expression was lower (−75%, P<0.03) in SVC while apolipoprotein E mRNA expression was not significantly different in SVC as compared to isolated adipocytes. By RT-PCR analysis, we demonstrated that CETP mRNA was expressed by human pre-adipocytes at levels less than those of SVC and adipocytes. The absence of monocytes/macrophages in SVC was confirmed by the absence of FcγRIII (CD16) mRNA in these fractions. These data demonstrate that CETP mRNA is most highly expressed in the immature fat cells of human adipose tissue, consistent with other experiments from this laboratory demonstrating that CETP plays an important local role in adipocyte cholesterol accumulation.

Leptin secretion from adipose tissue in women. Relationship to plasma levels and gene expression.

The role of expression and secretion of the ob gene product, leptin, for the regulation of plasma leptin levels has been investigated in vitro using abdominal subcutaneous adipose tissue of 20 obese, otherwise healthy, and 11 nonobese women. Body mass index (BMI, mean+/-SEM; kg/m2) in the two groups was 41+/-2 and 23+/-1, respectively. Fat cell volume was 815+/-55 pl in the obese and 320+/-46 pl in the nonobese group. In the obese group, plasma leptin concentrations and adipose leptin mRNA (relative to gamma actin) were increased five and two times, respectively. Moreover, adipose tissue secretion rates per gram lipid weight or per fat cell number were also increased two and seven times, respectively, in the obese group. There were strong linear correlations (r = 0.6-0.8) between plasma leptin, leptin secretion, and leptin mRNA. All of these leptin measurements correlated strongly with BMI and fat cell volume (r = 0.7- 0.9). About 60% of the variation in plasma leptin could be attributed to variations in leptin secretion rate, BMI, or fat cell volume. We conclude that elevated circulating levels of leptin in obese women above all result from accelerated secretion rates of the peptide from adipose tissue because of increased ob gene expression. However, leptin mRNA, leptin secretion, and circulating leptin levels are all more closely related to the stored amount of lipids in the fat cells of adipose tissue than they are to an arbitrary division into obese versus nonobese.

Transgenic mice overexpressing the beta 1-adrenergic receptor in adipose tissue are resistant to obesity.

The ratio of alpha- to beta-receptors is thought to regulate the lipolytic index of adipose depots. To determine whether increasing the activity of the beta 1-adrenergic receptor (AR) in adipose tissue would affect the lipolytic rate or the development of this tissue, we used the enhancer-promoter region of the adipocyte lipid-binding protein (aP2) gene to direct expression of the human beta 1 AR cDNA to adipose tissue. Expression of the transgene was seen only in brown and white adipose tissue. Adipocytes from transgenic mice were more responsive to beta AR agonists than were adipocytes from nontransgenic mice, both in terms of cAMP production and lipolytic rates. Transgenic animals were partially resistant to diet-induced obesity. They had smaller adipose tissue depots than their nontransgenic littermates, reflecting decreased lipid accumulation in their adipocytes. In addition to increasing the lipolytic rate, overexpression of the beta 1 AR induced the abundant appearance of brown fat cells in subcutaneous white adipose tissue. These results demonstrate that the beta 1 AR is involved in both stimulation of lipolysis and the proliferation of brown fat cells in the context of the whole organism. Moreover, it appears that it is the overall beta AR activity, rather than the particular subtype, that controls these phenomena.

Patterns of Ice Formation in Normal and Malignant Breast Tissue

Normal and malignant human breast tissues were obtained from resection surgery and frozen on a directional solidification stage with controlled and uniform cooling rates. The frozen samples were freeze substituted and examined with a light microscope. It was observed that in both normal and malignant tissue, ice forms first in the connective tissue. The ice propagates along the connective tissue, which surrounds fat cells in normal adipose tissue and clumps of tightly packed malignant cells in the diseased tissue. This mode of freezing affects the osmotic response of malignant cells, causing intracellular ice crystal formation at unusually low cooling rates.

Hamster Adipocyte α2-Adrenoceptor Changes during Fat Mass Modifications Are Not Directly Dependent on Adipose Tissue Norepinephrine Content

It is questioned whether alterations of the sympathetic nervous system can explain the specific increment of the adipocyte alpha 2-adrenoceptor observed during white adipose tissue (WAT) enlargement and fat cell size increment. The impact of a 6-hydroxydopamine-induced sympathectomy, validated by determination of the WAT norepinephrine content, was tested on isolated white fat cell alpha 2-adrenoceptor function and binding [( 3H]RX 821002 and [3H]UK 14304 binding). Chemical sympathectomy of standard adult hamsters, neither alters the alpha 2-adrenergic-dependent antilipolysis nor the adipocyte alpha 2-adrenergic binding. A slight hypersensitivity of the beta 1-adrenergic lipolytic response was observed, without modification in beta-adrenergic binding [( 125I]cyanopindolol binding). Compared with controls, caloric restriction (10 days) of adult hamsters induced a large decrease in adipocyte alpha 2-adrenoceptor (P less than 0.001) with a parallel decrement in the mean fat cell size (P less than 0.001) and alpha 2-adrenergic responsiveness while there was no significant variation of the WAT norepinephrine content (on a per pad basis). 6-Hydroxydopamine treatment of the restricted animals (from day 6 to day 9) induced a higher preservation of adipocyte alpha 2-adrenoceptor density (P less than 0.001), no change in alpha 2-adrenergic responsiveness, and higher preservation of mean fat cell size (P less than 0.05) than in the restricted only animals. No significant modification in the beta-adrenergic binding was observed whatever the conditions. It was concluded that the specific increment in the adipocyte alpha 2-adrenoceptor during fat mass enlargement was not directly dependent on sympathetic nervous system alterations. Nevertheless, the sympathetic-dependent mobilization of the fat stores, after induction of caloric restriction, can indirectly modulate the alpha 2-adrenoceptor density in the adipocyte by promoting changes in white fat cell size.

Influence of Androgenic Status on the α2/β-Adrenergic Control of Lipolysis in White Fat Cells: Predominant α2-Antilipolytic Response in Testosterone-Treated-Castrated Hamsters*

The aim of this study was to evaluate the influence of castration with or without testosterone propionate (TP) administration (one daily injection of 1 mg for 10 days) on the fat cell lipolytic activity in male hamsters. Basal and maximal lipolytic responses to the pure beta-adrenergic agonist isoproterenol, the mixed alpha 2-and beta-adrenergic agonist epinephrine, and the nonadrenergic compounds ACTH and 3-isobutyl-1-methylxanthine were all reduced by half in castrated animals. TP treatment restored these defective responses to control values, except the response to epinephrine which remained paradoxically unchanged. Sensitivity of lipolysis to epinephrine was unimpaired by castration but markedly reduced (10-fold) in TP-treated castrated hamsters. The antilipolytic potencies of the alpha 2-component of epinephrine and of the two alpha 2-agonists, UK 14304 and clonidine, were reduced by half in castrated animals, and returned to a value slightly higher than control after TP treatment. These changes in lipolysis were accompanied by parallel alterations in the stimulated cAMP responses to isoproterenol and forskolin but not to epinephrine. The latter was either unimpaired by castration or was clearly inhibited after TP treatment. Castration also induced a 2-fold decrease in the inhibitory potency of clonidine toward forskolin-stimulated cAMP production. Finally, these changes in the potency of clonidine were accompanied by parallel variations of the number of fat cell alpha 2-adrenoreceptors. These results indicate that testosterone in vivo, while increasing the beta-adrenergic lipolytic action of catecholamines (possibly through enhancement of the adenylate cyclase activity), promotes, to a greater extent, their alpha 2-adrenoreceptor-mediated antilipolytic potency. By providing the first demonstration that the androgenic status controls the functional alpha 2/beta-adrenergic balance in fat cells, this study also emphasizes the potential importance of such a control in the mechanisms underlying the sex-related differences in adipose tissue regional distribution and fat cell size.

Adipose tissue development in the fetal pig after decapitation.

The effect of fetal decapitation on adipose tissue development in utero was studied in the pig. Pig fetuses were decapitated at 45 days of gestation, and dorsal subcutaneous adipose tissue was analyzed at 110 days of gestation. The histology, histochemistry, ultrastructure, size and lipoprotein lipase activity of adipocytes from decapitated and sham-decapitated control fetuses were determined. Decapitation resulted in a poorly developed dermis and epidermis, a poorly developed outer layer of adipose tissue and larger fat cells that were metabolically and structurally more mature. Fewer fat cell clusters in decapitated fetuses were associated with fewer blood vessels in the subcutaneous layers. The results of this study demonstrate that fat cell development in subcutaneous tissues may be an integral aspect of the development of skin and associated structures.

Morphological studies on isolated rat adipocytes. I. Effect of starvation.

Morphological changes of fat cells in epididymal adipose tissue of rats during starvation were examined by scanning electron microscopy (SEM) and transmission electron microscopy (TEM). By SEM, fat cells from fed rats appeared spherical with a smooth surface, but with many craters or pits of 4μm mean diameter. These corresponded to small circular electron-lucent areas seen at the periphery surrounded by a thin cytoplasmic layer by TEM. During starvation SEM showed that the fat cells developed an indented, uneven surface without pits. TEM of these cells showed an increase in number and size of vesicles in the cytoplasmic matrix with a wrinkled plasmic membrane. It is suggested that the increase in the cytoplasmic vesicles in fat cells during starvation is related to, or involved in an increase in lipolytic activity.

Diet, pregnancy, and lactation: Effects on adipose tissue, lipoprotein lipase, and fat cell size

Adipose tissue fat cell size and lipoprotein lipase (LPL) activity were determined in the retroperitoneal and subscapular depots of nonpregnant, pregnant, and postpartum rats fed either a standard laboratory diet or a high-fat diet containing 55% fat by wieght. High-fat feeding for 20 days increased, in nonpregnant rats, fat cell size and LPL activity two-to threefold in both depots. In pregnant rats at term, fat cell size was increased and LPL activity was depressed in both dietary groups. Twenty days postpartum, both retroperitoneal fat cell size and LPL activity were decreased in proportion to the size of the litter. Rats not allowed to lactate had fat cell sizes and LPL activity that were not significantly different than in nonpregnant controls. Fat cell size and LPL activity in rats nursing four pups were reduced to 77% and 36% of control, respectively. Those nursing a normal-sized litter of eight pups demonstrated a further reduction of fat cell size to 38% and of LPL activity to 2% of nonpregnant control values. High-fat feeding and obesity did not prevent the fat loss and decreased LPL activity associated with lactation; fat cell size was decreased to 61% and LPL activity to 3% of control values. Values for the subscapular depot followed essentially the same pattern as that observed for the retroperitoneal depot. Mammary LPL activity was increased more than tenfold in animals nursing four or eight pups compared with values at term, whereas no activity was detected in rats not allowed to lactate.

Preparation of anti-lipolytic substance from Panax ginseng.

It was found that water extract of Panax ginseng strongly inhibited adrenaline-induced lipolysis in isolated fat cells of rat epididymal adipose tissue. Anti-lipolytic action of the water extract was easily inactivated by treatment with pronase, suggesting that the active principle might be a protein or a peptide. The water extract was dialyzed against distilled water. The outer dialysate was treated with DEAE-cellulose and the eluate was subjected to gel filtration on Sephadex G-50 column, Avicel cellulose column chromatography and phosphocellulose column chromatography, successively. With these procedures, a peptide (P II), which had anti-lipolytic activity, was isolated in a purified form.

Effect of maturation and senescence on carbohydrate utilization and insulin responsiveness of rat adipose tissue

The aim of the present investigation was to study the effect of aging upon the metabolism and the responsiveness to insulin of epididymal adipose tissue from rats (6 weeks, 6 and 24 months). Basal glucose metabolism by these tissues and adipocytes was positively related to cell size, for each age group. But age per se plays an important role: for the same diameter, the U-14C-glucose oxidation to CO2 and its incorporation into triglycerides described markedly between 6 weeks and 6 months, as reported peviously, and decreased still further between 6 months and 24 months, for any diameter. In contrast, insulin responsiveness of adipose tissue fragments and fat cells was negatively correlated to adipose cell size, when we analyzed the role of cell diameter for a group of given age. When comparing the sensitivity to hormone for a given cell volume but at different ages, it appeared that insulin resistance increased considerably between 6 weeks and 6 months and was still more marked in old age. The mechanisms underlying these facts have been discussed.

Effects of long-term physical training on body fat, metabolism, and blood pressure in obesity

Twenty-seven women with varying degrees of obesity were physically trained for 6 mo on an ad lib. diet. Body fat changes were positively correlated with the number of fat cells in adipose tissue. Obese women with fewer fat cells decreased in weight during training whereas women with severe obesity and an increased number of fat cells even gained weight. Blood pressure decreased consistently after training. Blood pressure elevation was not associated with body fat mass, nor was a decrease in blood pressure associated with a decrease in body fat or with pretraining blood pressure level. There were, instead, correlations between decreases in blood pressure on the one hand and initial concentrations and decreases in plasma insulin and triglycerides and blood glucose on the other. These results suggest an association between elevated blood pressure and metabolic variables. The possibility of treating and preventing early essential hypertension with methods that also correct the metabolic derangement, such as diet and exercise, should be given high priority in further research.

Formation and disintegration of lipid droplets associated with cell organelles, especially smooth-surfaced endoplasmic reticulum in the white adipose cell

Although a number of ultrastructural studies on the white adipose cell have been reported, not a few unsolved problems still remain on the morphological and functional relationships between formation or disintegration of lipid droplets and cell organelles in those cells. In order to re-examine such the points, we have made electron microscopical studies on the epididymal adipose cells from normal and starved Wistar adult rats, and on these cells from rats refed ordinary animal food or given only lipid without carbohydrate after a period of starvation. Additionally, for the same purpose we have observed the ultrastructure of developing and differentiating fat cells in the epididymal adipose tissue of rats ranging from newborn to 5 weeks old.The adipose cell from normal adult rats shows that the peripheral cytoplasm which envelopes a central large lipid mass contains well-developed cell organelles and occasionally small lipid droplets. These lipid droplets have no limiting membrane, but are often observed to be closely encircled by fenestrated profiles of smooth-surfaced endoplasmic reticulum (SER) which connects with a part of rough-surfaced endoplasmic reticulum (RER) in places (Fig. 1).

Regulation of cholesterol synthesis and storage in fat cells

The fat cells of rat epididymal adipose tissue contain an average of 0.5 mg of cholesterol per gram of triglyceride. Of this cholesterol, 90% is nonesterified and 80% is located in the lipid storage compartment. The fat cell cholesterol content correlated positively with cell size. During fasting the free cholesterol of the adipocyte decreased in parallel with triglyceride, whereas the amount of esterified cholesterol did not change. The fat cell cholesterol content is independent of the amount of dietary cholesterol. On in vitro incubation of rat fat cells with radiolabeled acetate, mevalonate, glucose, leucine, or water, labeled cholesterol was synthesized. The rate of cholesterol synthesis increased with fat cell size. Fasting suppressed cholesterol synthesis by 90%, whereas refeeding stimulated the synthesis above values found in normally fed rats. Stimulation of lipolysis with theophylline or with dibutyryl cyclic AMP markedly inhibited cholesterol synthesis in fat cells. Insulin increased the incorporation of glucose and leucine into fat cell cholesterol. The cholesterol synthesis in fat cells was not suppressed by a high cholesterol diet. Addition of very low or low density lipoprotein into the incubation medium suppressed fat cell cholesterol synthesis whereas high density lipoprotein did not. The lipoprotein-free serum stimulated cholesterol synthesis compared with serum-free medium. The rate of cholesterol synthesis in total adipose tissue of rat was estimated to be 4% of that in the liver. It seems unlikely that the increased body cholesterol turnover present in obesity is accounted for by the enhanced cholesterol formation in the enlarged adipose tissue.

A colorimetric method for the determination of deoxyribonucleic acid in adipose tissue

A method is described for measuring the deoxyribonucleic acid (DNA) content of small samples of adipose tissue or free fat cells. Lipids and acid-soluble nucleotides are first removed by extraction with a cold diethyl ether-ethanol mixture containing 10 per cent. m/V of trichloroacetic acid. DNA is then measured by hydrolysing the nucleoprotein residue in a 5 per cent. solution of trichloroacetic acid at 90 °C for 20 min, followed by treatment with p-nitro-phenylhydrazine and measurement of the hydrazone at 560 nm.

Physical development at 7 years of age in relation to velocity of weight gain in infancy with special reference to incidence of overweight.

As a result of a carefully controlled study on obese children, Borjeson (1962) concluded that obesity in childhood is not a problem of physical health, and that although it may be a major psychological problem for some children, in most cases there is no evidence of emotional conflict caused by obesity itself. Nevertheless, most physicians consider obesity in children to be a major health problem calling for preventive and therapeutic action. Besides a wide spread moral attitude towards overconsumption of food as the suspected cause of overweight, this concern gains support from the claim that obesity in adults implies a considerably increased risk of secondary disease and premature death (Kannel et al, 1967) and the fact that very often adult obesity starts in childhood (Mullins, 1958). In the view of physicians responsible for adult care, treatment of obesity should therefore start in childhood. Paedia tricians, however, have all experienced extreme difficulties in endeavours to achieve long-term weight reduction in obese children (Lloyd, Wolff, and Whelen, 1961; Spranger and Dorken, 1967; Lodi, 1970). Therefore the possibility of early preventive action, preferably in infancy, has to be considered seriously. This preventive attitude has been supported by the findings of Knittle and Hirsch (1968) that the number of fat cells in adipose tissue is significantly increased in rats overfed during the first 10 weeks of life. It is not yet known whether human infants behave in the same way as rats in this respect. It has been found in the human species as well as in the rat, however, that the total number of fat cells in adult life cannot be reduced (Bjorntorp and Sjostrom, 1971). In a study on obese children and adults published recently, Brook, Lloyd, and Wolff (1972) showed that the early onset of obesity is associated with an increased number of fat cells. In a longitudinal study in Sheffield, England, Eid (1970) found a significantly increased incidence of overweight and obesity in those children who had gained weight rapidly during the first six months of life, as compared with normally growing infants. However, these results may not be representative for a 'normal' population, since it was shown later by Taitz (1971) that no less than 60% of artificially fed infants from the same region gained weight above the 90th centile of generally accepted British standards. In Sweden the physical life conditions have for a long time been fairly similar for the great majority of infants; the frequency of breast-feeding is generally low, and artificial nutrition has been highly standardized during the last decades. The market for baby food is completely dominated by two manu facturers, whose products are similar and in accord ance with the recommendations of leading paedia tricians. The information about infant nutrition provided by child welfare centres and private paediatricians is uniform throughout the country, and the attendance rate at the well baby clinics approaches 100%. In case of deviations from normal weight development, substantial efforts are made to correct errors in nutrition which may have occurred. The present investigation was started with the aim of finding out how many of the obese children in a representative population of school children started as 'rapidly weight gaining' infants, and how many of such infants in a representative infant population will eventually be obese, if infant nutrition is fairly well controlled by a uniform programme.

Stimulation of release of lipoprotein lipase activity from isolated fat cells by rat serum.

IT is generally accepted that lipoprotein lipase (LPL) is responsible for removal of triglyceride fatty acids from the plasma by the extra-hepatic tissues1. Recently our studies have been focused on the energy dependent release of LPL activity from isolated fat cells2,3. We have proposed that release of this enzyme from the fat cells in adipose tissue regulates removal of triglycerides from the circulation.

Carbohydrate and lipid metabolism in relation to body composition in myotonic dystrophy.

Body composition and carbohydrate and lipid metabolism were examined in seventeen patients with myotonic dystrophy (MD). Body cell mass and body fat were determined with isotope dilution methods. Adipose tissue fat cell weight was measured and total fat cell number of the body could be estimated. Fasting concentrations of blood glucose, plasma triglyceride, cholesterol, and insulin as well as of glucose and insulin after ingestion of 100 gm. of glucose were also determined. In comparison with pertinent controls, MD patients showed no difference in body weight, although body composition was markedly altered with decreased body cell mass and increased body fat mass. Patients without physical impairment showed no derangements, of metabolism. However, disabled MD patients with pronounced decrease of body cell mass had decreased glucose tolerance and increased levels of fasting plasma insulin and lipids. It was concluded that deranged lipid or carbohydrate metabolism is not a primary characteristic of MD but a phenomenon secondary to muscular impairment and atrophy. Intact muscle function is probably important in regulation of lipid and carbohydrate metabolism.

Mechanisms of Enzyme and Substrate Activation by Lipoprotein Lipase Cofactors: I. A SPECIFIC REQUIREMENT OF PHYSIOLOGICAL CONCENTRATIONS OF CALCIUM FOR ENZYME ACTIVITY

Abstract Lipoprotein lipase can hydrolyze triglyceride emulsions formed by incubation of triolein coated on solid supports in the presence of serum albumin, but only after substrate activation by a serum cofactor. The effect of Ca2+ on the rate of fatty acid release in this system has been studied. Experiments in which the rate of triglyceride hydrolysis by post-heparin plasma or partially purified lipase preparations was determined in the presence of varying concentrations of Ca2+ have shown that the Km value for the metal is 0.02 to 0.06 mm and that as little as 0.20 mm is required for attaining maximal reaction rates. During the incubation of post-heparin plasma in the absence of serum, the addition of Ca2+ is sufficient for maximal activation of the substrate by the plasma cofactor. Preactivation of the substrate by the cofactor is not necessary, since activation occurs rapidly. The rate of release of fatty acids by the enzyme in partially purified preparations, heart homogenates, or extracts of acetone powder of adipose tissue can be increased by increasing serum concentrations in the incubation medium. However, higher Vmax values and lower Km values for serum are observed in the presence of 0.5 mm Ca2+. A protein cofactor, partially purified from rat serum by a lipid adsorption technique, has been found to activate the substrate, but only in the presence of Ca2+. Examining the rate of hydrolysis of varying substrate concentrations under different experimental conditions has shown that Ca2+ itself has no effect on enzyme activity; fatty acid release being observed only in the presence of both the protein and metal cofactors. Binding studies with 45Ca2+ lead to the conclusion that the cofactor role of Ca2+ is that of enzyme activator. From 8 to 25% of the metal in the incubation system can be bound by the enzyme-substrate complex, whereas only a fraction is bound by the substrate alone. The complex-bound calcium can be sequestered by EDTA, suggesting that metal binding by the enzyme-substrate complex is reversible. Thus, for maximal enzymatic activity the system requires substrate activation by the protein cofactor and enzyme activation by Ca2+. The hydrolysis of serum chylomicrons and very low density lipoproteins by the enzyme can be enhanced by serum, but much faster reaction rates are observed in the presence of Ca2+. Because of this fact and in view of the low range of Ca2+ concentrations required for enzyme activation, a physiological role for the metal in the in vivo hydrolysis of these natural substrates of the enzyme outside the fat cells of adipose tissue is proposed. Experimental results further show that EDTA can inhibit the activity of the lipase and that this inhibition can be reversed by excess Ca2+. The inhibition by 1 m NaCl, heparin, and protamine sulfate cannot be prevented by Ca2+. Citrate and pyrophosphate are not found to be inhibitory in the present system.

The composition and metabolism in vitro of adipose tissue fat cells of different sizes.

Abstract. Fat cells of different sizes were isolated from the same sample of adipose tissue by collagenase treatment and fractionation by flotation in an isoosmolar medium. Protein, phospholipid and cholesterol increased with increasing fat cell size. Cholesterol correlated most closely with fat cell volume but phospholipid apparently with surface. Most of fat cell cholesterol was found in the triglyceride droplet, and only a smaller part in a particulate fraction from fat cells. Incorporation of labelled glucose into triglyceride increased with fat cell size, apparently in proportion to fat cell surface rather than diameter or volume. This was the case also with incorporation into fatty acids. The association between fat cell size and metabolism was present also in alloxan diabetic rats. Short term insulin deficiency thus does not abolish the increase of metabolic activity with fat cell size. Analyses of activities of selected glycolytic enzymes and of fatty acid synthesis from acetate in cell‐free systems showed a similar dependence on fat cell size, demonstrating that isotope dilution phenomena in large and small fat cells are probably not responsible. — Lipolytic activity in the basal state and after epinephrine stimulation was increased in large fat cells, which also reesterified more fatty acids than small fat cells when calculated according to the balance method. — It was concluded that larger fat cells are metabolically more active than smaller fat cells. The increase of glyceride‐glycerol labelling and of glycerol release from larger fat cells suggests an increased triglyceride turn‐over in these fat cells. Large fat cells might thus be considered as an active metabolic sub‐compartment of adipose tissue.