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.

scholarly journals Regulation of lipolysis during pregnancy and lactation in sheep. Response to noradrenaline and adenosine

1985 ◽  
Vol 230 (3) ◽  
pp. 651-656 ◽  
Author(s):  
R G Vernon ◽  
E Finley
Keyword(s):  
Adipose Tissue ◽  
Cell Volume ◽  
Milk Production ◽  
Early Lactation ◽  
Mean Cell Volume ◽  
Basal Rate ◽  
Adipose Tissue In Vitro ◽  
Pregnancy And Lactation ◽  
Adenosine Analogue

The effects of pregnancy and lactation on lipolysis in sheep adipose tissue in vitro were investigated. Neither pregnancy nor lactation altered the basal rate of lipolysis. The rate of noradrenaline-stimulated lipolysis was directly proportional to adipocyte mean cell volume. Lactation, but not pregnancy, increased the response to noradrenaline, but had no effect on the ED50 of noradrenaline. The adenosine analogue N6-phenylisopropyladenosine decreased the rate of lipolysis in the presence of noradrenaline; the effect was greater with adipose tissue from lactating than from control, unmated, sheep. Results are discussed in relation to the need of sheep to mobilize lipid during early lactation to support milk production.

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 Phosphatidic acid and phosphatidylinositol labelling in adipose tissue. The role of endogenously formed adenosine

1983 ◽  
Vol 212 (2) ◽  
pp. 499-506 ◽  
Author(s):  
R J Schimmel ◽  
T W Honeyman ◽  
K K McMahon
Keyword(s):  
Adipose Tissue ◽  
Phosphatidic Acid ◽  
Adenosine Deaminase ◽  
Prostaglandin E1 ◽  
Time Course ◽  
Fat Cells ◽  
Inhibitory Effects ◽  
Selective Agonist ◽  
Adenosine Analogue

Incorporation of [32P]Pi into phosphatidic acid and phosphatidylinositol of hamster epididymal adipocytes was partially inhibited by 3-isobutyl-1-methylxanthine. This effect of 3-isobutyl-1-methylxanthine was antagonized by isopropyl-N6-phenyladenosine but not by 2′,5′-dideoxyadenosine, prostaglandin E1 or clonidine. N6-Phenylisopropyladenosine did not affect incorporation of [32P]Pi into phosphatidic acid or phosphatidylinositol when 3-isobutyl-1-methylxanthine was not present. In contrast with 3-isobutyl-1-methylxanthine inhibition of [32P]Pi incorporation into phospholipids, which was blocked only by N6-phenylisopropyladenosine, accelerated lipolysis was blocked by prostaglandin E1, clonidine and 2′,5′-dideoxyadenosine as well as by N6-phenylisopropyladenosine. Phospholipid labelling was also decreased in the presence of adenosine deaminase, but not in the presence of isoprenaline (isoproterenol). The stimulatory effect of N6-phenylisopropyladenosine on [32P]Pi incorporation into phospholipids in cells exposed to 3-isobutyl-1-methylxanthine was evident as soon as 3 min after addition of the adenosine analogue and maximum 10 min after its addition. As observed by others, [32P]Pi incorporation into phospholipids was increased by the alpha 1-selective agonist methoxamine. The stimulatory effect of methoxamine occurred with a time course similar to that of N6-phenylisopropyladenosine and was present at nearly equal magnitude in the absence or presence of 3-isobutyl-1-methylxanthine. The inhibitory effects of 3-isobutyl-1-methylxanthine and adenosine deaminase on phospholipid labelling are attributed to blockade of the action, or to the enzymic removal, of adenosine formed in and released from the fat-cells during their incubation. Supporting this view is the selective reversal of the actions of 3-isobutyl-1-methylxanthine and of adenosine deaminase by N6-phenylisopropyladenosine. These findings suggest an important role for endogenous adenosine in regulation of phospholipid turnover in adipocytes.

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.

Androgen regulation and site specificity of angiotensinogen gene expression and secretion in rat adipocytes

2000 ◽  
Vol 279 (6) ◽  
pp. E1398-E1405 ◽  
Author(s):  
Valérie Serazin-Leroy ◽  
Mireille Morot ◽  
Philippe de Mazancourt ◽  
Yves Giudicelli
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Mrna Expression ◽  
Protein Secretion ◽  
Male Rats ◽  
Fat Cells ◽  
Intact Male ◽  
Rat Adipocytes ◽  
Fat Deposits

Adipose tissue is an important source of angiotensinogen (ATG), and hypertension is commonly associated with android obesity. Therefore, we tested the hypothesis that androgens may control ATG gene expression and secretion in rat fat cells. In intact male rats, ATG mRNA expression (Northern blot and co-reverse transcription-polymerase chain reaction analysis) and protein secretion were significantly higher in deep intra-abdominal (perirenal and epididymal) than in subcutaneous adipocytes. After castration, ATG mRNA was reduced almost 50% in the three fat deposits, with parallel changes in ATG protein secretion. Conversely, testosterone treatment fully restored the ATG mRNA decrease after castration, whatever the anatomical origin of the adipocytes. Finally, a 24-h in vitro exposure of perirenal fat cells or differentiated preadipocytes from castrated rats to testosterone or dihydrotestosterone (10 nM free hormone concentration) increased ATG mRNA expression by 50–100%, an effect that was prevented by the anti-androgen cyproterone acetate. These data, demonstrating both in vivo and in vitro androgen induction of ATG mRNA expression in rat adipocytes, add further weight to the hypothesis of a link between adipose tissue ATG production, androgens, and android obesity-related hypertension.

Comparison of the acute hematotoxicity of 2-butoxyethanol in male and female F344 rats

2000 ◽  
Vol 19 (3) ◽  
pp. 185-192 ◽  
Author(s):  
B I Ghanayem ◽  
S M Ward ◽  
B Chanas ◽  
A Nyska
Keyword(s):  
Body Weight ◽  
Cell Volume ◽  
Weight Ratio ◽  
Female Rats ◽  
Male Rats ◽  
Mean Cell Volume ◽  
Male And Female ◽  
Male And Female Rats ◽  
Butoxyacetic Acid ◽  
F344 Rats

Administration of 2-butoxyethanol (BE) to rodents causes acute hemolytic anemia, and metabolic activation of BE to butoxyacetic acid (BAA) is required for the development of this effect. Recent studies have shown that female rats treated with BE exhibit a variety of histopathologic lesions that are absent in males and many of these lesions are attributed to the hemolytic effects of BE. Current studies were designed to compare the acute hematotoxicity of BE in male and female F344 rats. Rats were treated with 250 mg BE/kg body weight or water (control; 5 ml/kg) by gavage. At 4, 8, or 24 h after dosing, rats were anesthetized, blood was collected by cardiac puncture, and various blood parameters were measured. BE resulted in a time-dependent swelling of erythrocytes as evidenced by an early increase in hematocrit (Hct) and mean cell volume (MCV) in male rats. In contrast, increased Hct in female rats did not accompany an increase in MCV. It is likely that hemolysis was so severe at 4 h that Hct exhibited a decline in female rats at that time point. Subsequently, red blood cell (RBCs), hemoglobin concentration (Hgb), and Hct declined as hemolysis progressed. However, the onset of BE-induced hemolysis was faster in female compared to male rats. These effects were also associated with a significant increase in the spleen weight to body weight ratio. Blood smears were also prepared and morphological changes evaluated by light microscopy included stomatocytosis, spherocytosis, and schistocytosis. Furthermore, aggregation of RBCs in female rats as evidenced by increased formation of rouleaux was observed at 24 h after BE administration. These effects were observed earlier and more frequently in female rats. No differences in the sensitivity of RBCs obtained from male and female rats and exposed to butoxyacetic acid (BAA) in vitro was observed as determined by measuring the packed cell volume. In conclusion, these data suggest that female rats are more sensitive to hemolysis and morphological alterations of erythrocytes induced by BE during the first 24 h after exposure compared to males. It is likely that the greater sensitivity of female rats to BE effects on RBCs may account for the reported development of thrombosis and tissue infarction in female rats.

Increased activities of mitochondrial enzymes in white adipose tissue in trained rats

1991 ◽  
Vol 261 (3) ◽  
pp. E410-E414 ◽  
Author(s):  
B. Stallknecht ◽  
J. Vinten ◽  
T. Ploug ◽  
H. Galbo
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Tricarboxylic Acid Cycle ◽  
Oxidative Capacity ◽  
Female Rats ◽  
Male Rats ◽  
Mitochondrial Enzymes ◽  
Fat Cells ◽  
Fat Cell ◽  
Respiratory Chain Enzyme

During earlier fat cell studies we noticed that homogenates of white fat cells became more brown with training, a fact that might reflect an increased content of mitochondria. This raised the question whether training (as is the case in muscle) increases the oxidative capacity in fat cells. Groups of 8-12 rats were swim trained for 10 wk or served as either sedentary, sham swim-trained, or cold-stressed controls. White adipose tissue was removed, and the activities of the respiratory chain enzyme cytochrome-c oxidase (CCO) and of the enzyme malate dehydrogenase (MDH), which participates in the tricarboxylic acid cycle as well as in the mitochondrial malate-aspartate and acetyl-group shuttles, were determined. The CCO and MDH activities expressed per milligram protein were increased in male rats 4.4- and 2.8-fold, respectively, in the swim-trained compared with the sham swim-trained rats (P less than 0.05). In female rats the CCO activity expressed per milligram protein was increased 4.5-fold in the trained compared with the sedentary control rats (P less than 0.01). Neither cold stress nor sham swim training increased CCO or MDH activities in white adipose tissue (P greater than 0.05). In conclusion, in rats, intensive endurance training induces an increase in mitochondrial enzyme activities in white adipose tissue as is seen in skeletal muscle.

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.

scholarly journals Protein restriction during early development enhances insulin responsiveness but selectively impairs sensitivity to insulin at low concentrations in white adipose tissue during a later pregnancy

1999 ◽  
Vol 81 (6) ◽  
pp. 481-489 ◽  
Author(s):  
M. J. Holness ◽  
L. G. D. Fryer ◽  
M. C. Sugden
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
G Protein ◽  
Glucose Utilization ◽  
Protein Restriction ◽  
Pregnant Rats ◽  
Early Protein ◽  
Low Concentrations ◽  
Pregnancy And Lactation

Poor early nutrition may elicit long-term detrimental effects on adult health, including susceptibility to non-insulin-dependent diabetes mellitus. We investigated the impact of moderate maternal protein restriction during pregnancy and lactation on the action of insulin on adipocyte glucose uptake in female offspring during their own pregnancies. Offspring of dams provided with diets containing either 200 g protein/kg or 80 g protein/kg during pregnancy and lactation (termed C and EPR groups respectively) were weaned on to 200 g protein/kg diet at 24 d of age. At 9–12 weeks of age both groups were time-mated and studied at day 19 of gestation. Rates of glucose utilization (assessed using the 2-deoxy-d-- [1-3H- ]glucose technique) measured in five distinct adipose tissue depots (parametrial (PM), mesenteric (MES), perirenal (PR), subcutaneous (SC), interscapular (IS)) in vivo in the post-absorptive state were consistently lower in early-protein-restricted (EPR) pregnant rats compared with control (C) pregnant rats. In C pregnant rats, insulin significantly increased glucose utilization only in the IS depot. In contrast, significantly increased glucose utilization rates in response to hyperinsulinaemia were evident in all five adipose-tissue depots of the EPR pregnant group. Consequently, glucose utilization rates in PM and SC depots during hyperinsulinaemia were significantly higher in EPR pregnant rats compared with C pregnant rats. Adipocytes were isolated from PM and MES depots to determine whether altered responses to insulin in vivo were retained in vitro. Rates of insulin-stimulated glucose uptake at sub-maximal (15 μU/ml) and maximal (15 mU/ml) insulin concentrations were significantly higher in both MES and PM adipocytes from EPR pregnant rats, but the sensitivity of glucose uptake to insulin at low concentrations was blunted compared with adipocytes from C pregnant rats. The results demonstrate that early protein restriction enhances the capacity for adipocyte glucose uptake at high insulin concentrations, but dampens the response to insulin at low physiological concentrations.

scholarly journals Supplemental vitamin A enhances the recovery from iron deficiency in rats with chronic vitamin A deficiency

1996 ◽  
Vol 75 (4) ◽  
pp. 623-636 ◽  
Author(s):  
AnnetJ.C Roodenburg ◽  
Clive E West ◽  
Robert Hovenierl ◽  
Anton C Beynen
Keyword(s):  
Vitamin A ◽  
Cell Volume ◽  
Packed Cell Volume ◽  
Binding Capacity ◽  
Vitamin A Deficiency ◽  
Haemoglobin Concentration ◽  
Erythrocyte Count ◽  
Male Rats ◽  
Mean Cell Volume ◽  
Supplemental Vitamin

Studies with anaemic children and pregnant women from areas where vitamin A deficiency is endemic have shown a beneficial effect on Fe status of supplemental vitamin A in addition to Fe supplementation. This suggests a relationship between vitamin Aand Fe status, which we attempted to mimic in rats with anaemia and chronic vitaminA deficiency. Male rats were fed on Fe-adequate diets (35 mg Fe/kg)containing different levels of vitamin A (1200,450,150,75 and 0 retinol equivalents (RE)/kg feed) until they were 5 weeks old. These diets wereidentical to the diets fed to their mothers. Then the young male rats were transferred to diets containing the same levels of vitamin A but no added Fe. After another 2 weeks the rats wererepleted with Fe (35 mg/kg feed) without or with vitamin A to a level of 1200 RE/kg feed. Increased vitamin A intake by the groups previously fed on diets with either 0 or 75 RE/kg produced a reduction in blood haemoglobin concentration, packed cell volume and erythrocyte count. In the group which had been fed on the diet without vitamin A, supplemental vitamin A raised mean cell volume, plasma Fe concentration and total Fe-binding capacity. Vitamin A supplementation during the period of Fe repletion produceda decrease in splenic and tibia Fe concentration, the effect being greater with increasing seventy of previous vitamin A deficiency. The paradoxical effect of supplemental vitamin A on haemoglobin, packed cell volume and erythrocyte count can be explained by a decrease in the degree of haemwoncentration. Thus, the positive effect of supplemental vitamin A seen in humans is also observed with rats under controlled experimental conditions. We speculate that supplemental vitamin A during Fe repletion contributes to optimum erythropoiesis and Fe mobilization when baseline vitamin A status is impaired

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