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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Very small fat cells (less than 35 micron diameter) and normal large fat cells (greater than 40 micron diameter) were isolated from adult Fischer 344 rat epididymal adipose depots. These very small fat cell preparations were free from normal, large fat cells (40-130 micron diameter) and stromal-vascular elements. Examination by electron microscopy and lipid analysis showed a similarity in overall organization and composition to normal, large fat cells. Incubations with [U-14C]glucose showed that the very small fat cell preparations oxidized glucose in proportion to both cell number and time. These preparations also responded to insulin, increasing [U-14C]glucose oxidation in a manner similar to normal large fat cell preparations (i.e., 2- to 4-fold increases in CO2 production with insulin stimulation). The very small fat cells also incorporated radiolabeled glucose into lipids; but, unlike normal large fat cells, insulin failed to stimulate this process. Glycerol release from very small fat cells was stimulated by lipolytic hormones in a manner similar to these responses in co-isolated large fat cells.
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PMID:Very small fat cells. II. Initial observations on basal and hormone-stimulated metabolism. 388 21

The hormonal regulation of GH binding and the effects of GH on glucose metabolism were studied in hypophysectomized rats. Male rats (130-140 g) were hypophysectomized and on the day after the operation treatment with one or a combination of two hormones was started and continued for 7 days. The different hormonal treatments were cortisone acetate, insulin, insulin plus cortisone acetate, thyroxine, thyroxine plus cortisone acetate and GH. Glucose metabolism was studied by determining the production of CO2 from [14C]glucose in epididymal fat pads and adipocytes and the incorporation of [14C]glucose into lipids in adipocytes. Binding of GH was measured in cell aliquots using 125I-labelled human GH. In hypophysectomized control animals, GH binding was decreased to approximately 25% of the binding observed in adipocytes of normal rats. Insulin treatment increased GH binding by approximately 100% and the response to GH was markedly increased. Similar effects were achieved by thyroxine treatment. Basal levels of glucose oxidation were markedly decreased after hypophysectomy but were increased towards normal by insulin or thyroxine treatment. Neither cortisone nor GH treatment had any effect on GH binding or glucose metabolism. The results show that insulin and thyroxine may be important for the GH receptor and the insulin-like effect of GH in adipocytes.
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PMID:Hormonal regulation of growth hormone binding and responsiveness in adipose tissue and adipocytes of hypophysectomized rats. 388 9

There is a 'futile' cycle of unknown significance operating at a very rapid rate (about 40 percent that of the total central fat droplet's daily turnover rate) in white adipose tissue of normal mice. The futile cycle may be measured and studied because it occurs in a region of the adipose tissue that has poor anatomical contact with the capillaries coupled with a high affinity of the adipocytes, plasma membranes for the FFA in the ECF. The cycle is drastically inhibited in mice bearing the Ehrlich ascites carcinoma, a transplantable tumor; the inhibition is associated with a 20-fold increase in the FFA pool size of the epididymal fat pad (measured directly) and a 70 percent reduction in the TGFA pool that is involved in the cycle (estimated indirectly from kinetic measurements). However, the mass of TGFA in the central lipid droplet was being conserved in the tumor-bearing mice during this study. The TGFA pool involved in the cycle represents only about 1 percent of the total adipose tissue TGFA. The relation of this futile cycle to adipose TGFA turnover, plasma FFA turnover and oxidation to CO2, dietary sources of TGFA, and the loss (and preservation) of body fat in cancer-bearing animals was considered in terms of a simple model. Although the significance of the altered futile cycle is unknown, the new approach described here, coupled with other quantitative tracer and non-tracer measurements, may prove useful in understanding factors that lead to obesity or body fat loss.
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PMID:In vivo tracer studies of perturbed fatty acid transport and metabolism in adipose tissue. 406 21

Compound LY104119, [R-(R*,S*)]-4-[3-[(2-hydroxy-2-phenylethyl)amino]butyl]benzamide monohydrochloride, was found to be a potent beta-agonist in the mouse. Its Ki for displacing the binding of (-)-3H-dihydroalprenolol to beta-receptors on the lung membranes from either viable yellow obese mice (VY/WfL-Avy/a) or their corresponding normal controls (VY/WfL-a/a) was 3 X 10(-7) M, comparable to that of isoproterenol which was 2 X 10(-7) M. LY104119 increased the concentration of cyclic AMP in adipose tissue, stimulated lipolysis in vitro and in vivo and the expiration of CO2 in vivo. When given s.c. or p.o., LY104119 reduced the body weight of Avy/a mice without altering the food consumption. The loss of triacylglycerol accounted for a major portion of the weight loss and the weight was recovered after the treatment was withdrawn. When fed in the diet, LY104119 reduced the weight of Avy/a mice and caused a moderate increase of food intake. Thermogenesis (whole body heat production) of the treated mice increased. An elevated level of hepatic glucokinase activity regularly found in these mice was almost normalized to the level measured in normal mice. The kinetic properties of the beta-receptors were not altered, but the number of beta-receptors on lung membranes was reduced about 25 percent. The lipolytic response of epididymal adipose tissue to LY104119 or isoproterenol, however, was not changed. When slightly overweight a/a mice were treated with LY104119 in the diet, they lost weight, but a similar treatment of normal-weight a/a mice caused a loss of only a small amount of carcass triacylglycerol without affecting the body weight. These normal-weight a/a mice were able to maintain their weight by an exorbitant increase of food intake. When this large increase of food consumption was not allowed, ie by being restricted to normal amounts of food intake, normal-weight a/a mice fed LY104119 did lose weight. Thermogenesis increased in all LY104119-treated a/a mice. However, the increase in the LY104119-treated but diet-restricted a/a mice was smaller than that in the LY104119-treated a/a mice fed ad libitum. We conclude from these observations that: Compound LY104119 was able to decrease weight in Avy/a mice apparently through the stimulation of the beta-adrenergic system. The metabolic responses to LY104119 were not different in obese Avy/a mice and normal a/a mice. The difference between the Avy/a mice and the a/a mice was in their ability to increase their food consumption to compensate for the energy loss caused by LY104119.
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PMID:Thermogenesis and weight control. 615 57

It has been proposed that the lipolytic effect of serum is based on the presence of either lipoproteins or catecholamines. To test these hypotheses, pieces of epididymal fat pads from fed rats were incubated in the presence of albumin and glucose for 120 min. The addition of rat serum (5 mul/vial) enhanced the rates of both glycerol release to the media and [U-14C] glycerol utilization by the tissue. Heparin did not alter these parameters or the response produced by serum. VLDL from rat plasma also enhanced glycerol release and utilization for the formation of CO2 and lipids, and heparin significantly augmented these effects. Neither of the conditions studied affected the percentual distribution of 14C-lipid fractions in the tissues. It is known that in similar conditions to those used in the present study, adrenaline produces a decrease in the utilization of glycerol. Thus our findings do not support the proposed hypothesis explaining the fat-mobilizing action of serum, the mechanism of which remains to be determined.
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PMID:Effect of rat serum on glycerol metabolism in adipose tissue in vitro. 616 15

[U-14C] glucose utilization by pieces of epididymal fat-pad was studied in streptozotocin-diabetic rats, food-restricted animals, and normal controls. Both CO2 and fatty acids formation were greatly reduced in tissues from the diabetic animals treated or not with insulin and this change was milder in tissues from food-restricted rats. A positive correlation was found between [14C] glucose utilization in vitro and plasma RIA-insulin levels when values from all animals were pooled. The percentual response to high doses of insulin was small in adipose tissue from streptozotocin-diabetic animals for CO2 and total lipids formation, but it was high for fatty acids synthesis; the response in food-restricted animals was high and was greatly augmented in tissues from the streptozotocin-diabetic rats treated with insulin. Results indicate that in adipose tissue from streptozotocin-diabetic animals the alteration of insulin responsiveness occurs distal to the receptor events and that impaired basal glucose metabolism is a direct consequence of their hypoinsulinemia.
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PMID:Effects of streptozotocin diabetes and insulin treatment on adipose tissue glucose utilization in the rat. 620 55

(1) In order to assess the possible role of 3',5'-(cyclic)adenosine monophosphate (cAMP) in the control of glucose transport, the effect of the nucleotide or agents known to increase its intracellular concentration on sugar transport or 45Ca2+ washout were characterized in epididymal fat pads, free fat cells and soleus muscles of the rat. (2) When added to the incubation medium, cAMP (0.1-2.0 mM) stimulated 3-O-[14C]methylglucose washout from fat pads. This effect was abolished by cytochalasin B, and additive to that induced by submaximal (10-25 microU/ml), but not by supramaximal (10 microU/ml) concentrations of insulin. (3) cAMP (2 mM) stimulated the conversion of [U-14C]glucose into CO2 and triacylglycerols. This effect was additive to that of insulin (100 microU/ml). (4) ACTH, glucagon, adrenaline, noradrenaline and salbutamol, which are all known to increase the cAMP content of adipose tissue, stimulated the washout of 3-O-[14C]methylglucose and 45Ca2+ from preloaded fat pads. The fractional losses of the two isotopes were significantly correlated (P less than 0.001, r = 0.73). (5) In free fat cells, adrenaline (10(-6) M) and salbutamol (10(-5) M) stimulated the uptake of 3-O-[14C]methylglucose, and salbutamol (10(-5) M) did not interfere with the stimulating effect of insulin (25 microU/ml) on sugar uptake. (6) In rat soleus muscles, adrenaline and salbutamol produced a dose-dependent stimulation of the washout of 3-O-[14C]methylglucose and 45Ca2+. The effect of adrenaline on sugar efflux was abolished by propranolol. (7) It is concluded that the activation of the glucose transport system by insulin is unlikely to be mediated by a drop in the cellular concentration of cAMP. An increase in cAMP brought about by beta-adrenoceptor agonists or lipolytic hormones may induce a mobilization of calcium ions from cellular pools into the cytoplasm, which in turn leads to the activation of the glucose transport system demonstrated in the present as well as in several earlier studies.
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PMID:The stimulating effect of 3',5'-(cyclic)adenosine monophosphate and lipolytic hormones on 3-O-methylglucose transport and 45Ca2+ release in adipocytes and skeletal muscle of the rat. 629 57

To explore the short term effects of endogenous GH on body growth, glucose metabolism, and insulin responsiveness in adipose tissue, 35- to 40-day-old male rats were treated with a potent goat antiserum against rat GH (ArGHS). The administration of ArGHS, but not normal goat serum, caused a dose-dependent decrease in body weight gain and longitudinal bone growth, as measured by the tetracycline method. Glucose metabolism was measured by determining the production of CO2 from [14C]glucose in epididymal fat pad. Treatment with ArGHS (0.05-0.5 ml, ip, twice daily for 6 days) resulted in increased insulin sensitivity, as determined by the ED50 values for the effect of insulin. An increased response to a submaximal concentration of insulin was observed 3 h after the administration of 0.5 ml ArGHS. Basal levels were not consistently affected by ArGHS treatment. The maximal response to insulin was significantly increased after treatment with low doses of ArGHS (0.1-0.2 ml/day) and was decreased after treatment with high doses of ArGHS (0.8-1 ml/day) for 6 days. The magnitude of the response, as determined by the percent increase in response to 10 mU/ml insulin, was, however, not different compared to that observed in adipose tissue of normal goat serum-treated rats. These results demonstrate that elimination of endogenous GH results in retarded growth in the rat within 24 h. Moreover, the results suggest that GH is important in insulin sensitivity.
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PMID:Effects of in vivo administration of antiserum to rat growth hormone on body growth and insulin responsiveness in adipose tissue. 633 8

Glucose oxidation to CO2 was investigated in isolated perifused rat epididymal fat cells. Insulin stimulated rates of oxidation up to 30-fold. Multiple pulses of insulin or prolonged perifusion with the hormone led to a time-dependent desensitization of the cells. The action of insulin could be mimicked by H2O2. Reversal of H2O2 effects was associated with a damped oscillation of large initial amplitude. Initiation of perifusion with insulin induced rates of glucose oxidation that oscillated around a mean elevated rate with an amplitude of about +/- 4% of the mean, significantly larger than the measurement error. Basal rates did not show clear oscillations. The oscillations after insulin had a statistically significant period of around 14 min. The results were the same with C1- or C6-labeled glucose and occurred in the presence of both 0.275 and 5.5 mM glucose in the perifusion medium. The oscillations were interpreted as the result of insulin- or H2O2-induced synchronization of oscillatory glycolysis by individual fat cells. The similarity of the observed oscillatory period with the period of oscillatory insulin secretion by pancreatic beta cells suggests that oscillatory glycolysis may constitute the internal pacemaker for the latter process.
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PMID:Dynamic aspects of insulin action: synchronization of oscillatory glycolysis in isolated perifused rat fat cells by insulin and hydrogen peroxide. 634 Jul 30

Copper deficiency was induced in rats by feeding sucrose or starch diets deficient in copper. Copper-deprived rats fed either diet exhibited decreased plasma ceruloplasmin concentration and increased plasma cholesterol. Glucose homeostasis and utilization was impaired both in vivo and in vitro. Oral glucose tolerance was impaired, insulin binding decreased, and CO2 formation and lipogenesis from [U-14C]glucose were decreased. Feeding sucrose but not starch diets deficient in copper magnified the copper deficiency and resulted in 60% mortality. Although both deficient diets contained the same concentration of copper, the hepatic copper concentration of rats fed sucrose was reduced nearly threefold compared to rats fed starch. Reduced epididymal fat pad, increased liver weight, reduced blood hemoglobin and a marked hypertrophy of the heart with gross deformities as well as histopathologic changes were noted only in those rats fed the copper-deficient sucrose diet. The biochemical lesions induced by deprivation of copper can be suppressed by feeding diets containing starch or can be magnified by high sucrose intake.
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PMID:Effect of copper deficiency on metabolism and mortality in rats fed sucrose or starch diets. 634 33


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