[The effect of overfeeding of children on the structure and function of adipose tissue. 2. Adipose tissue].
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Adipose Tissue↗
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The hydrolysis of cholesterol esters in plasma lipoproteins by hormone-sensitive cholesterol esterase from adipose tissue.
Adipose tissue contains a high level of neutral esterase active against emulsions of cholesteryl oleate. The present studies show that this enzyme can also effectively hydrolyze the cholesterol esters in native rat plasma high density lipoproteins (HDL) and low density lipoproteins (LDL). The hydrolysis of lipoprotein cholesterol esters by a pH 5.2 isoelectric precipitate fraction from the freshly prepared 100,000 X g supernatant of chicken adipose tissue was low, but increased more than 50-fold on activation with cyclic AMP-dependent protein kinase. Rat adipose tissue homogenates were also very active against lipoprotein cholesterol esters, hydrolyzing as much as 60% of the total labeled cholesterol ester in HDL or LDL in 1 h. Activity was optimal at pH 7 and very low at pH 4. No protease activity was detected at pH 7 and, since assays were done in 2 mM EDTA, phospholipase A activity was presumably negligible. The results show that hormone-sensitive cholesterol esterase of adipose tissue has ready access to the neutral lipid core of plasma lipoproteins, either because the enzyme penetrates the polar shell or because the cholesterol ester in the core is exposed, at least intermittently, to allow enzyme-substrate complex formation. Whether or not this enzyme activity plays a role in lipoprotein degradation by adipose tissue remains to be determined.
Adipose Tissue↗
Fish oil-induced yellow fat disease in rats. II. Enzyme histochemistry of adipose tissue.
Adipose tissue in various stages of fish oil-induced yellow fat disease in the rat had the same acid phosphatase and 5-nucleotidase activity pattern as similar stages of the disorder in mink and pig. A weak acid phosphatase and 5-nucleotidase activity was seen in interstitial lipofuscin-laden macrophages in "stage M" yellow fat disease without fat cell degeneration. Activity of these macrophagic enzymes increased when there was fat cell degeneration ("stage S" and "stage E" yellow fat disease). This different phosphatase activity in the same cell type may result from phagocytosis of substrates with variable digestibility. Macrophages directly surrounding affected fat cells in steatitis areas ("stage S" and "stage E") had strong acid phosphatase and 5-nucleotidase activity. As in the pig, increased 5-nucleotidase activity was found in affected fat cells, which probably indicates plasma membrane damage. Increased nonspecific esterase activity occurred around affected fat cells. Only a small part of this esterase activity originated from inflammatory cells. This indicates that an increase of esterase activity in degenerating adipose tissue may be an endogeneous process in this tissue.
Acid Phosphatase↗
Serum triglycerides and fatty acid incorporation into human adipose tissue (TIAT). Their relations with adipose tissue characteristics and glucose tolerance.
Fatty acid incorporation into adipose tissue (FIAT), the metabolic process assimilating plasma triglyceride fatty acids liberated by lipoprotein lipase, was recently found to be lower in hyper- than in normotriglyceridaemia. In the present report, the relation of FIAT to glucose tolerance and adipose tissue morphology and fatty acid composition has been studied in a popoulation of men with normo- and hypertriglyceridaemia, using needle biopsy specimens. In addition, the associations between plasma triglyceride concentration and these factors as well as FIAT were examined by statistical methods. FIAT and GLIAT (glucose incorporation into adipose tissue) activities per cell were positively correlated with fat cell diameter but not with fat cell number. FIAT activities per cell and per unit surface area were lower in hyper- than in normo-triglyceridaemic subjects. The k-value of the i.v.glucose tolerance test and glycerol release from adipose tissue did not correlate with FIAT or GLIAT activities. The proportion of stearic acid in adipose tissue was negatively correlated with the serum triglyceride level and with fat cell diameter, but positively correlated with FIAT. Linolenic acid in adipose tissue correlated positively with the k-value. The negative correlation between serum triglycerides and FIAT remained when the other variables which were significantly correlated with FIAT or the serum triglycerides were entered in partial correlat-on analysis. These results suggest that although low FIAT activity is related in part to other characteristics, it occurs in hypertriglyceridaemia independent of glucose tolerance or various characteristics in fat. With serum triglyceride concentration as dependent variable, stepwise regression analysis was performed, entering all other variables as independent ones. The highest multiple --value was 0.76 (p less than 0.001) and it was obtained with three adipose tissue parameters: FIAT (or GLIAT), content of linolenic acid and of stearic acid. The other parameters did not give rise to any further improvement in the prediction of the serum triglyceride concentration which is better than 50% (R2 = 0.57).
Adipose Tissue↗
Effects of vitamin B6 deficiency on liver, kidney, and adipose tissue enzymes associated with carbohydrate and lipid metabolism, and on glucose uptake by rat epididymal adipose tissue.
Adipose tissue and liver from vitamin B6-deficient rats have an increased lipogenic capacity. Whether this phenomenon is accompanied by changes in the activities of certain enzymes involved in the metabolism of carbohydrate and lipid, or by altered transport of glucose into adipocytes, has been studied. Five glycolytic enzymes (hexokinase, phosphoglucose isomerase, phosphofructokinase, aldolase, and pyruvate kinase), two pentose phosphate pathway enzymes (glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase), malic enzyme, and ATP citrate lyase were measured in the epididymal adipose tissue, livers and kidneys of vitamin B6-deficient and control rats. Vitamin B6 deficiency did not significantly affect the glycolytic enzyme levels in the tissues studied, or the dehydrogenases measured in adipose tissue and kidneys. Liver glucose-6-phosphate dehydrogenase, and adipose tissue and liver malic enzyme were significantly lowered in deficient rats compared to ad libitum and pair-fed controls. Adipose tissue and liver ATP citrate lyase activities were also significantly decreased by vitamin B6 deficiency. In the presence of insulin, the uptake of glucose and 3-O-methyl glucose, a non-metabolizable sugar, by fat pads from deficient rats was greater than uptake by fat pads from control rats. These observations suggest that the increased glucose utilization by adipose tissue and liver of vitamin B6-deficient rats is not directly related to changes in the enzymes studied, but in the case of adipose tissue, may be explained, at least in part, by enhanced glucose uptake.
ATP Citrate (pro-S)-Lyase↗
[Obesity and adipose tissue. 2. Hormonal regulation of adipose tissue metabolism].
The effects of hormones on human adipose tissue are reviewed with respect to the pathogenesis, prevention and therapy of obesity. Insulin. The insulin-resistance in the obese is associated with a decrease of the number of insulin receptor sites, which is likely to be secondary to increased insulin levels. Catecholamines. Human adipose tissue contains alpha- and beta-adrenergic receptors. Alterations in the relation of alpha- and beta-adrenergic responsiveness may be important in the pathogenesis of regional forms of obesity. Gastrointestinal hormones. As opposed to adipose tissue of other species lipolytic effects of gastrointestinal hormones were as yet not clearly demonstrated in human fat cells. Prostaglandins were implicated in the pathogenesis of metabolic obesity. However, the effects of these C-20 fatty acids on human adipose tissue remain to be elucidated. Parathyroid hormone has been shown to possess lipolytic activity in vitro. This property may be important under physiological conditions too. Triglyceride storage diseases and lipomatoses are discussed as models for studying impaired hormonal responsiveness in human adipose tissue.
Adipose Tissue↗
Fatty acid synthesis in vivo in brown adipose tissue, liver and white adipose tissue of the cold-acclimated rat.
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Acclimatization↗
Glycerolipid biosynthesis in rat adipose tissue. Influence of adipose-cell size and site of adipose tissue on triacylglycerol formation in lean and obese rats.
The rates of lipid formation were compared in different fat-depots from lean and obese rats by using [14C]glycerol 3-phosphate, [14C]glucose or [14C]acetate as substrates. In lean animals, subcutaneous adipose tissue showed significantly lower rates of lipid synthesis than did perirenal and gonadal fat-tissue. In obese animals, the rates of lipid synthesis were significantly higher and did not vary from one fat-depot to another. Differences in the rates of lipid formation between lean and obese rats disappeared during dietary restriction of obese animals. The isolated adipocyte preparation did not reflect the true metabolic activity of the adipose organ, since this preparation was mainly derived from smaller adipocytes that were metabolically less active than larger adipocytes. The present study suggests that it is better to use whole tissue preparations to measure lipogenesis and esterification reactions, because these measurements represent the contribution of both larger and smaller adipocytes towards lipid formation.
Acetates↗
Glucocorticoid receptors in adipose tissue.
Although adipose tissue appears to be a target organ for glucocorticoid hormones, previous studies have failed to detect glucocorticoid receptors in this tissue. In the present study, the addition of thioglycerol and trasylol to the homogenization medium provided an enuironment in which receptors were successfully demonstrated. [3H]Dexamethasone binding studies were carried out at 0 C in cytosol from various adipose tissues of adrenalectomized rats and bound hormone was separated from free by Sephadex chromtography. Despite the presence of protein protective agents, receptor binding decayed significantly over 24 h but appeared stable from 1 to 5 h. Epididymal fat pad cytosol had an apparent Kdiss at 0 C for dexamethasone of approximately 6 nM and a binding capacity of approximately 200 fmol per mg protein. To prove that the receptors were located in fat cells and not in surrounding connective tissue, isolated adipocytes were prepared by collagenase digestion and receptors were demonstrable in the cytosol from these cells as well. The affinity of series of steroids for the receptor was in the sequence: dexamethasone greater than corticosterone greater than progesterone greater than aldosterone greater than cortexolone greater than testosterone greater than estradiol. Receptors of roughly the same affinity but somewhat fewer binding sites on the basis of cytosol protein were also found on other fat depots including peri-renal, peri-scrotal and popliteal. Of interest is the fact that interscapular brown fat and human subcutaneous fat also possessed similar these receptors, the higher competitive capacity of dexamethasone indicated that the binding was to glucorticoid rather than mineralocorticoid receptors. The data suggest that fat cells contain glucocorticoid receptors which are similar to those seen in other glucocorticoid targets. Presumably these receptors mediate the effects of glucorticoids on adipose tissue.
Adipose Tissue↗
Morphological studies on the adrenergic innervation of white adipose tissue.
White adipose tissue was obtained from the mesentery, epididymis, omentum and subcutis of rats which were fed, fasted or fasted and then refed. Tissue samples were prepared using the glyoxylic acid method to detect adrenergic nerves by fluorescence histochemistry. Other tissue samples were fixed with an aldehyde solution containing sodium molybdate which is specific for catecholamine granules in nerve terminals. Thin and serial thick sections (0.25-0.5 micron) were viewed with a conventional electron microscope and with the high voltage electron microscope. With fluorescence microscopy it was found that most of the blood vessels except veins and venules were richly innervated. The most extensive branching of nerves down to the capillary level was found in the mesentery and epididymal fat of fasted-refed rats. Relatively few adipocytes appeared to be innervated. With electron microscopy, nerve terminals were found distributed with most blood vessels including capillaries, and with some adipocytes. Only 2-3% of all dipocytes were innervated by adrenergic nerves. It is suggested that in the adipose tissue sites studied the major adrenergic innervation is mainly for the supply of blood vessels.
Adipose Tissue↗
Morphology and biochemical properties of perirenal adipose tissue from lamb (Ovis aries). A comparison with brown adipose tissue.
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Adipose Tissue↗
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.
Adipose Tissue↗
Validity of the ultrasonic technique as a method of measuring subcutaneous adipose tissue.
Subcutaneous adipose tissue measurements, at abdomen, suprailiac, subscapular, and mid-triceps sites, made with the ultrasonic and skinfold caliper techniques were compared using data from 20 women and 17 men from a pool of subjects of 22 women and 20 men. In addition, comparisons were made between ultrasonic, soft-tissue roentgenographic and skinfold caliper techniques at the suprailiac and mid-triceps sites on 6 women and 12 men. Repeat measurements with the ultrasonic technique produced correlation coefficients of 0-87 and above. Correlations between skinfold caliper and ultrasonic measurements were generally higher among women than men over each of the four sites. A highly significant relationship, r = 0-88, was observed between the ultrasonic measurements and soft-tissue roentgenograms over the mid-triceps site. The correlation between the fat-muscle interface measured on the roentgenogram and ultrasonic measurements at the suprailiac site was 0-78. Multiple echoes and interfaces were observed at the suprailiac site on some subjects.
Abdomen↗
Relationship between intracellular cyclic AMP and lipolysis in human adipose tissue.
Human subcutaneous adipose tissue has been incubated in vitro in the presence and absence of isoprenaline (ISNA). The tissue concentration of cyclic AMP (cAMP) and the release of glycerol into the incubation medium were measured after various incubation periods. In the presence of ISNA (6 X 10(-5) mol/l), the tissue concentration of cAMP reached a peak after around 10 min and then declined to a level significantly lower than that at the start of the incubation. In contrast, the ISNA-induced rate of lipolysis was a linear function of the incubation time. The addition of propranolol (13 mumol/l) at different times after ISNA did not influence the rate of lipolysis, although it resulted in a decrease in the tissue level of cAMP. There was a positive correlation between the maximal increase in tissue cAMP and the rate of lipolysis in adipose tissue exposed to ISNA, both in individual experiments and in a group of 23 persons. No correlation was found between the rate of lipolysis and the tissue level of cAMP in adipose tissue incubated under basal conditions. The findings are compatible with the theory that the beta-adrenergic-induced lipolysis by human adipose tissue is a function of the maximal rise in the concentration of tissue cAMP. It is concluded that this peak level of cAMP represents single compartment of the nucleotide.
Adipose Tissue↗
Hormonal control of adipose-tissue lipolysis.
Adipose-tissue triacylglycerol is the major energy store in man. The physiological importance and biochemical mechanism of the hormonal control of lipolysis in white adipose tissue is reviewed. Rates of lipolysis and fatty acid release observed when adipose tissue is incubated in vitro are compared with rates of triacylglycerol turnover in man. It appears that enhanced rates of lipolysis in vivo, for example during fasting and exercise, may be a substantial fraction of the maximum obtainable by hormone stimulation in vitro. There is considerable species variation in the hormonal sensitivity of adipose tissue. Some hormones that stimulate lipolysis in vitro may not be significant lipolytic agents at physiological concentrations in vivo. In man and rat, the most important acutely acting lipolytic and anti-lipolytic hormones are catecholamines and insulin respectively. The sympathetic nervous system may play a role at least as important as circulating catecholamines in the mobilization of stored triacylglycerol. The effects of acute lipolytic hormones are modulated in the long term by corticosteroids and thyroid hormone. Stimulation of lipolysis is believed to be mediated by the increased intracellular cyclic AMP concentration that occurs after interaction of hormones with specific receptors in the plasma membrane. The properties of membrane receptors, adenylate cyclase, cyclic AMP phosphodiesterase, cyclic AMP-dependent protein kinase and triacylglycerol lipase, as studied in rat and human adipose tissue, are discussed. Several features of the action of lipolytic hormones in vitro are difficult to account for by the hypothesis that cyclic AMP is the only "second messenger" regulating lipase activity. These include anomalous effects of hormones at high concentrations and the possible existence of feedback inhibition limiting the accumulation of cyclic AMP and the stimulation of lipolysis. The mechanism of the anti-lipolytic action of insulin is at present unknown.
2',3'-Cyclic-Nucleotide Phosphodiesterases↗
Identification of small cells in fetal and infant adipose tissue.
In developing adipose tissue, cells of size less than 25 micron may make a major contribution to adipose tissue cell populations. This study reports the separation, identification, and sizing of infant and foetal adipose tissue small cells. Subcutaneous adipose tissue was taken from the anterior abdominal wall of children aged 2 months and 22 months. Subcutaneous tissue was also obtained from a paraumbilical site in 4 fetuses of gestational age 16 weeks. Tissue samples were fixed in buffered osmium tetroxide solution containing collidine. Aliquots of cell preparations suspended in saline on microscope slides were viewed and separated using a dissecting microscope. A diameter distribution of particle size was obtained using at least 200 cells for each preparation. There was a substantial number of cells that were smaller than 20 micron. Their modal cell size was remarkably constant in fetuses and in 2-month-old and 22-month-old infants. Ultrastructural studies show that the tissue is composed of a relatively uniform population of cells within sparsely collagenous connective tissue. Although some of the cells show no intracytoplasmic aggregates of lipid material, others show variable amounts of lipid material which can occupy a very large part of the cell volume.
Adipose Tissue↗
[Studies on the excitation-metabolism coupling mechanism in brown adipose tissues, 2; Effects of K+ and norepinephrine on the lipolysis in brown adipose tissues (author's transl)].
This investigation was undertaken to clarify the lipolytic response caused by K+ and norepinephrine in brown adipose tissues. 1. Lipolytic response was obviously observed at the concentration of 50 mM in the K+-induced stimulation, and at 1.0 microgram/ml in the norepinephrine-induced stimulation, respectively. 2. K+- and norepinephrine-stimulated lipolysis were inhibited in the Ca2+-deficient tissues, and were inhibited by the addition of Mg2+, Mn2+ and La3+. 3. In the K+-stimulated lipolysis Ca2+ could be substituted only by Sr2+, while in the norepinephrine-stimulated lipolysis the substitution was possible with both Sr2+ and Ba2+. 4. K+- and norepinephrine-stimulated lipolysis were inhibited by the addition of propranolol and procaine. Accordingly, these positive results suggest that K+- and norepinephrine-stimulated lipolysis are dependent on the presence of Ca2+, and are related to the movements of Ca2+ and cyclic AMP system in the cells.
Adipose Tissue, Brown↗
Interaction of thyroid hormones with human muscular tissue, leucocytes and adipose tissue in vitro.
The uptake of triiodothyronine (T3) and thyroxine (T4) by human leucocytes as well as by adipose and muscular tissues in vitro was markedly dependent on the extracellular protein concentration. The presence of extracellular protein was responsible for the difference in the uptake of T3 and T4 by leucocytes (the incorporation of T4 was significantly lower than that of T3), whereas its presence in the medium containing adipocytes did nto influence the incorporation values. In a protein-free medium, the muscular tissue uptake of T3 exceeded that of T4. In this tissue the deiodination of both hormones was likewise significantly different, that of T4 being higher. The conversion of T4 to T3 was also higher in the muscle cells, but represented only about 75% of the total deiodinated fraction. In the remaining tissues, no differences were observed in the uptake and deiodination of T3 and T4. The deiodination of T4 in human leucocytes was found to be considerably dependent of pH of the incubation medium (two deiodination optima, a higher one in acid region) whereas the deiodination of T3 was fairly indifferent to variations of pH (one flat deiodination optimum in the weakly alkaline region).
Adipose Tissue↗