STUDIES ON THE NUMBER AND VOLUME OF FAT CELLS IN ADIPOSE TISSUE

1962 ◽  
Vol 40 (4) ◽  
pp. 437-442 ◽  
Author(s):  
W. Zingg ◽  
A. Angel ◽  
M. D. Steinberg
Keyword(s):  
Adipose Tissue ◽  
Cell Volume ◽  
Histological Examination ◽  
Cell Number ◽  
Fat Content ◽  
Fat Cells ◽  
Desoxyribonucleic Acid ◽  
Fat Depots ◽  
Perirenal Fat

The changes in number and volume of fat cells accompanying changes in the size of the perirenal fat depots of rats induced by dietary and other means have been investigated by direct histological examination and by estimation of the total desoxyribonucleic acid (DNA) and fat content. With both methods, an increase in cell volume and in cell number was found to accompany an increase in depot volume.

STUDIES ON THE NUMBER AND VOLUME OF FAT CELLS IN ADIPOSE TISSUE

1962 ◽  
Vol 40 (1) ◽  
pp. 437-442 ◽  
Author(s):  
W. Zingg ◽  
A. Angel ◽  
M. D. Steinberg
Keyword(s):  
Adipose Tissue ◽  
Cell Volume ◽  
Histological Examination ◽  
Cell Number ◽  
Fat Content ◽  
Fat Cells ◽  
Desoxyribonucleic Acid ◽  
Fat Depots ◽  
Perirenal Fat

The changes in number and volume of fat cells accompanying changes in the size of the perirenal fat depots of rats induced by dietary and other means have been investigated by direct histological examination and by estimation of the total desoxyribonucleic acid (DNA) and fat content. With both methods, an increase in cell volume and in cell number was found to accompany an increase in depot volume.

scholarly journals Changes in adipose tissue of the rat due to early undernutrition followed by rehabilitation

1980 ◽  
Vol 43 (1) ◽  
pp. 27-31 ◽  
Author(s):  
Patricia M. Harris
Keyword(s):  
Adipose Tissue ◽  
Wistar Rats ◽  
Cell Number ◽  
Fat Cells ◽  
Stock Diet ◽  
Fat Cell ◽  
Black And White ◽  
Fat Depots ◽  
Male Wistar Rats ◽  
Number Of Cells

1. Male Wistar rats were allocated at birth to foster mothers in litters of three, nine or sixteen. At weaning animals from each litter size were ad lib.-fed on a stock diet. Further animals from litters of nine and sixteen were fed on the stock diet in restricted amounts until 12 weeks of age and then rehabilitated by being allowed ad lib. access to the stock diet.2. Five animals from each group were killed at 24 weeks of age and the size and number of cells determined in four specific fat depots.3. Animals reared in litters of sixteen and further undernourished from 3 to 12 weeks (group L16/U) had significantly fewer fat cells at all sites studied than animals reared in litters of three and ad lib.-fed. Group L16/U animals also had significantly fewer observable fat cells at the epididymal site than ad lib.-fed animals reared in litters of nine. These results differ from those found in the Black and White Hooded rat where, after similar treatments, no significant differences in observable fat cell number were found.

Adipose tissue blood flow and cellularity in the growing rabbit

1975 ◽  
Vol 229 (1) ◽  
pp. 107-112 ◽  
Author(s):  
M Digirolamo ◽  
J Esposito
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Cell Volume ◽  
Cell Number ◽  
Tissue Blood Flow ◽  
Tissue Composition ◽  
Fat Cell ◽  
Fat Depots ◽  
Wide Range ◽  
Definition Of

Resting blood flow was measured in isolated, innervated, epigastric fat-pads of 27 male rabbits during growth in the 1st yr of life and found to vary widely in range (7.6-28.1 ml/100 g tissue per min). Definition of adipose tissue composition and of fat-cell size and number made it possible to explain the wide range of flow and to identify two types of relationships between adipose blood flow and tissue constituents. Expressed in the usual manner (ml/100 g tissue per min), adipose blood flow declined with increasing adiposity of the fat depots, and a negative correlation was found between flow and fat-cell volume (r equals -.571, P less than .01). In contrast, when blood flow was expressed on the basis of fat-cell number (ml/108 fat cells/min), a positive and highly significant correlation was found between blood flow per fat cell and fat-cell volume (r equals .842, P less than .001). In the rabbit tissue the relationship of blood flow to fat-cell number and size was more predictable than the usual expression of flow in terms of tissue wet weight. Food deprivation for 18-24 h did not significantly alter these relationships. The results indicate that changes in adipose tissue composition and cellularity, resulting from growth and from accumulation of lipid in enlarging adipocytes, are important determinants of blood flow regulation to adipose tissue.

Water content of rat adipose tissue and isolated adipocytes in relation to cell size

1976 ◽  
Vol 231 (5) ◽  
pp. 1568-1572 ◽  
Author(s):  
M DiGirolamo ◽  
JL Owens
Keyword(s):  
Adipose Tissue ◽  
Water Content ◽  
Cell Volume ◽  
Cell Size ◽  
Intracellular Water ◽  
Male Rats ◽  
Fat Cells ◽  
Fat Cell ◽  
Tissue Water ◽  
Adipose Mass

Epididymal adipose tissue composition and adipocyte water content were studied in male rats during growth and development of spontaneous obesity. The data show that a highly significant positive correlation exists between fat-cell volume and intracellular water space (IWS) (r=.967, P less than .001). Intracellular water, expressed as picoliters per fat cell, varied from 1.5-2 in small fat cells (mean vol, 30-50 pl) to 9-10 in large cells (800-1,000 pl). When expressed as percent of fat-cell volume, IWS varied from 5-7% in the small fat cells to 1-1.3% in the large ones. Total adipose tissue water continued to increase with increasing adipose mass. Similarly, total adipocyte water increased with enlarging cell size and tissue mass. The contribution of total adipocyte water (as contrasted to that of nonadipocyte water) to total tissue water, however, was found to be limited (less than 23%) and to decline progressively with adipose mass expansion.

scholarly journals Genetic and Pharmacological Inhibition of PAPP-A Protects Against Visceral Obesity in Mice

Endocrinology ◽  
2020 ◽  
Vol 161 (10) ◽  
Author(s):  
Akhila Ramakrishna ◽  
Laurie K Bale ◽  
Sally A West ◽  
Cheryl A Conover
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Liver Lipid ◽  
Protein A ◽  
Visceral Obesity ◽  
Cell Number ◽  
Metabolic Effects ◽  
Adipocyte Size ◽  
Fat Depots ◽  
Mesenteric Fat

Abstract Pathogenicity of visceral adipose tissue (VAT) has been linked to the metabolic stress of enlarging mature adipocytes and a limited ability to recruit new adipocytes. One of the major distinguishing features of VAT preadipocytes is the high expression of the zinc metalloprotease, pregnancy-associated plasma protein-A (PAPP-A), when compared to subcutaneous adipose tissue (SAT). In this study we used 2 different approaches to investigate the effect of PAPP-A inhibition on different fat depots in mice on a high-fat diet (HFD) for 15 weeks. Conditional knockdown of PAPP-A gene expression in female adult mice resulted in significant decreases of 30% to 40% in adipocyte size in VAT (mesenteric and pericardial depots) compared to control mice. There was no effect on SAT (inguinal) or intra-abdominal perigonadal fat. Liver lipid was also significantly decreased without any effect on heart and skeletal muscle lipid. We found similar effects when using a pharmacological approach. Weekly injections of a specific immunoneutralizing monoclonal antibody (mAb-PA 1/41) or isotype control were given to male and female wild-type mice on HFD for 15 weeks. Adipocyte size was significantly decreased (30%-50%) only in VAT with mAb-PA 1/41 treatment. In this model, cell number was significantly increased in mesenteric fat in mice treated with mAb-PA 1/41, suggesting hyperplasia along with reduced hypertrophy in this VAT depot. Gene expression data indicated a significant decrease in F4/80 (macrophage marker) and interleukin-6 (proinflammatory cytokine) and a significant increase in adiponectin (anti-inflammatory adipokine with beneficial metabolic effects) in mesenteric fat compared to inguinal fat in mice treated with mAb-PA 1/41. Furthermore, there was significantly decreased liver lipid content with mAb-PA 1/41 treatment. Thus, using 2 different models systems we provide proof of principle that PAPP-A inhibition is a potential therapeutic target to prevent visceral obesity and its metabolic sequelae, such as fatty liver.

scholarly journals Adenosine and the control of lipolysis in rat adipocytes during pregnancy and lactation

1983 ◽  
Vol 216 (1) ◽  
pp. 121-128 ◽  
Author(s):  
R G Vernon ◽  
E Finley ◽  
E Taylor
Keyword(s):  
Adipose Tissue ◽  
Cell Volume ◽  
Adenosine Deaminase ◽  
Stromal Cells ◽  
Male Rats ◽  
Fat Cells ◽  
Pregnant Rats ◽  
Mean Cell Volume ◽  
Pregnancy And Lactation ◽  
Adenosine Analogue

The rate of noradrenaline-stimulated lipolysis is lower in fat-cells from lactating than from pregnant rats; this difference is eliminated by the addition of adenosine deaminase [Aitchison, Clegg & Vernon (1982) Biochem. J. 202, 243-247]. The activity of 5′-nucleotidase, and hence the capacity of the cells to synthesize adenosine, was the same in fat-cells and also stromal cells of adipose tissue from pregnant, lactating and male rats. The response and sensitivity of fat-cells to the anti-lipolytic effects of adenosine were measured by incubating cells in the presence of noradrenaline, adenosine deaminase (to remove endogenous adenosine) and various concentrations of the adenosine analogue N6-phenylisopropyladenosine (PIA). PIA caused a greater inhibition of the rate of noradrenaline-stimulated lipolysis in adipocytes from lactating than from pregnant rats. The concentration of PIA required to inhibit by 50% the rate of noradrenaline-stimulated lipolysis fell from over 100 nM for fat-cells from pregnant rats to 30 nM for fat-cells from lactating rats. The decreased rate of noradrenaline-stimulated lipolysis during lactation was not due to the smaller mean cell volume of adipocytes during this state.

Adipose tissue metabolism and cell size: variation between subcutaneous sites and the effect of copper supplementation

1987 ◽  
Vol 45 (1) ◽  
pp. 75-80 ◽  
Author(s):  
P. A. Sinnett-Smith ◽  
J. A. Woolliams
Keyword(s):  
Adipose Tissue ◽  
Cell Volume ◽  
Lipolytic Activity ◽  
Subcutaneous Fat ◽  
Size Variation ◽  
Tissue Cell ◽  
Fat Depots ◽  
Adipose Tissue Cell ◽  
Proportional Increase ◽  
Effect Of Copper

AbstractAdipose tissue cell volume, lipolytic rates, Iipoprotein lipase (LPL) and acetyl CoA carboxylase (ACC) activities were determined in biopsy samples taken from the back, shoulder, rump and groin subcutaneous fat depots of 17-month-old female sheep (no. = 24). Half of the sheep had received a copper (Cu) supplement at 6 weeks of age. Biopsy samples were taken after fasting overnight.Differences in cell volume and ACC activity were apparent between sites. Supplementation with Cu at 6 weeks of age led to a proportional increase of between 0·24 and 0·45 in adipose cell volume and a proportional increase in lipolysis which varied from 0·70 to 2·27 depending on site and hormone addition. Correlations between sites for cell volume and lipolytic activity were not high in general but those for ACC and LPL activities were higher (for ACC r = 0·40 to 0·79). Overall the best correlations were between the back and rump sites. Correlations between the various metabolic measurements and cell volume were not apparent within treatment groups.

Qualitative regional differences in adipose tissue growth and cellularity in male Wistar rats fed ad libitum

1998 ◽  
Vol 274 (5) ◽  
pp. R1460-R1467 ◽  
Author(s):  
M. DiGirolamo ◽  
J. B. Fine ◽  
K. Tagra ◽  
R. Rossmanith
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Regional Differences ◽  
Wistar Rats ◽  
Cell Number ◽  
Tissue Growth ◽  
Fat Cell ◽  
Fat Depots ◽  
Male Wistar Rats ◽  
Ad Libitum

Adipose tissue grows primarily by a combination of increases in fat cell volume (hypertrophy) and in fat cell number (hyperplasia), but the regional growth pattern of white adipose tissue depots in animal species and in the human is still unclear. In this study we characterized fully the age-related changes in adipose tissue growth, composition, and cellularity of four fat depots of male Wistar rats that varied in age from 7 wk to 15 mo and in body weight from 178 to 808 g. Body weight and the weight of each of the four adipose depots studied (epididymal, mesenteric, subcutaneous inguinal, and retroperitoneal) increased progressively with age and ad libitum feeding. Comparison of the cellularity of the four adipose depots, however, showed remarkable and significant differences in the pattern of growth within the same animals. The cumulative growth of the two intra-abdominal fat depots (mesenteric and epididymal) was due mostly to hypertrophy (increases in cell volume of 83 and 64%, respectively), whereas the growth of the other two depots (retroperitoneal and inguinal) was due predominantly to hyperplasia (increases in cell number of 58 and 65%, respectively). These findings uncover major and unexpected regional differences in the modulation of adipose tissue growth within aging animals fed ad libitum and suggest local, region-specific regulatory controls of this growth.

Resistance to adipocyte hyperplasia in ground squirrels given high-fat diets

1987 ◽  
Vol 253 (4) ◽  
pp. R576-R579 ◽  
Author(s):  
I. M. Faust ◽  
N. Mrosovsky
Keyword(s):  
Weight Gain ◽  
Cell Number ◽  
Ground Squirrels ◽  
Fat Cells ◽  
High Fat ◽  
Fat Cell ◽  
Fat Depots ◽  
Body Weights ◽  
Fat Diets ◽  
Adipocyte Hyperplasia

Mammalian hibernators prepare for the winter by depositing fat in existing fat cells. There is little, if any, production of new fat cells. This is curious because equivalent fat deposition in rats is associated with substantial fat cell production. To determine whether degree of weight gain, diet composition, or some special mechanism militating against adipocyte hyperplasia may underlie the absence of adipocyte hyperplasia in hibernators, male Richardson's ground squirrels, Spermophilus richardsonii, were fed a fattening high-fat diet for either 5 mo or 1 yr. The 5-mo high-fat feeding period caused peak body weights to increase 36% relative to the peak body weights seen in control animals fed ordinary chow. Despite this increase, there was no apparent increment in fat cell number in any of the major fat depots. Animals fed the diet for 1 yr reached body weights similar to those of the 5-mo group but showed significant adipocyte hyperplasia in all fat depots studied. Thus adult ground squirrels are clearly capable of enlarging their pool of mature fat cells, but they fail to do so, at least at certain times, in response to conditions of weight gain that cause considerable adipocyte hyperplasia in rats.

scholarly journals Histone Carbonylation Is a Redox-Regulated Epigenomic Mark That Accumulates with Obesity and Aging

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1210
Author(s):  
Amy K. Hauck ◽  
Tong Zhou ◽  
Ambuj Upadhyay ◽  
Yuxiang Sun ◽  
Michael B. O’Connor ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Disease ◽  
Adipose Tissue ◽  
Fat Depots ◽  
Michael Adducts ◽  
Lipid Aldehydes ◽  
Visceral Adipose ◽  
Fat Feeding

Oxidative stress is a hallmark of metabolic disease, though the mechanisms that define this link are not fully understood. Irreversible modification of proteins by reactive lipid aldehydes (protein carbonylation) is a major consequence of oxidative stress in adipose tissue and the substrates and specificity of this modification are largely unexplored. Here we show that histones are avidly modified by 4-hydroxynonenal (4-HNE) in vitro and in vivo. Carbonylation of histones by 4-HNE increased with age in male flies and visceral fat depots of mice and was potentiated in genetic (ob/ob) and high-fat feeding models of obesity. Proteomic evaluation of in vitro 4-HNE- modified histones led to the identification of both Michael and Schiff base adducts. In contrast, mapping of sites in vivo from obese mice exclusively revealed Michael adducts. In total, we identified 11 sites of 4-hydroxy hexenal (4-HHE) and 10 sites of 4-HNE histone modification in visceral adipose tissue. In summary, these results characterize adipose histone carbonylation as a redox-linked epigenomic mark associated with metabolic disease and aging.

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