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

Oxidation of [14C] glucose in isolated epididymal adipocytes from Golden hamsters was stimulated by isoproterenol, epinephrine and norepinephrine, which all interact with beta-adrenergic receptors and by adrenocorticotrophic hormone. In contrast alpha-receptor agonists, such as phenylephrine, methoxamine or clonidine did not increase basal glucose oxidation. The beta-adrenergic blocking drug propranolol inhibited both lipolysis and glucose oxidation when these had been stimulated by isoproterenol, epinephrine or norepinephrine. Conversely, the alpha-adrenergic blocking drugs phentolamine and phenoxybenzamine did not influence lipolysis or glucose oxidation when isoproterenol provided the stimulus and increased both lipolysis and glucose metabolism in the present of either epinephrine or norepinephrine. All alpha-adrenergic agonists tested (phenylephrine, methoxamine and clonidine) lowered lipolysis and glucose oxidation isolated adipocytes exposed to isoproterenol. However, when adrenocorticotropin provided the stimulus for glucose oxidation and lipolysis, only clonidine produced a significant reduction in lipolysis and glucose oxidation. None of the alpha-agonists influenced glucose metabolism which had been increased by insulin. These data confirm the presence of both alpha and beta adrenergic receptors on hamster epididymal adipocytes and suggest that they exert antagonistic influences on lipolysis and glucose oxidation. These data are also consistent with the view that adrenergic stimulation of glucose oxidation and lipolysis in adipocytes are both mediated through beta receptors.
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PMID:Roles of alpha and beta adrenergic receptors in control of glucose oxidation in hamster epididymal adipocytes. 17 71

Adipocytes were prepared by collagenase digestion of rat epididymal adipose tissue and incubated for 5, 15 or 30 minutes in Krebs-Ringer bicarbonate buffer containing albumin (40 mg/ml), glucose (1 mg/ml) and epinephrine. Calcium ion was present in some incubations at concentration of 2.5 mM and omitted from others; media with no added calcium contained 1.0 mM EGTA thereby producing a final calcium concentration of less than 10(-7) M. Glycerol release and accumulation of cyclic AMP were measured. Basal lipolysis and cell cyclic AMP levels were increased slightly but not significantly when adipocytes were incubated in calcium free media. Lipolysis could be activated with epinephrine in the absence of calcium but the sensitivity of the lipolytic response was greatly reduced; however, the maximum lipolytic response to epinephrine was not decreased in calcium free media. Similarly, incubation of adipocytes in calcium free media resulted in decreased accumulation of cyclic AMP in response to epinephrine but only when sub-maximum concentrations of the catecholamine were present. Varying the extracellular calcium concentration showed that a concentration of at least 10(-5) M was optimal for epinephrine activation of lipolysis. These observations are considered in accord with the view that activation of adenylate cyclase is facilitated by calcium ion.
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PMID:The role of calcium ion in epinephrine activation of lipolysis. 18 5

In non-obese but diabetic 15-week-old KK mice which showed fatty liver histopathologically, the content of liver lipids and the levels of blood glucose and plasma IRI were greater than those in the control ICR mice of the same age and were quite similar to those in GTG-obese mice. In 6-week-old KK mice which excreted no glycosuria and showed normal hepatic tissues, only plasma IRI level was slightly elevated as compared with that in the control mice. The cyclic 3',5'-AMP stimulators like epinephrine and theophylline exerted far less potent stimulatory effects on lipolytic activity in 6-week-old KK mice than in the control mice, as in diabetic 15-week-old KK mice and GTG-obese mice. Theophylline potentiated the lipolytic effect of epinephrine lineraly in KK mice, the tendency being different from that in the control mice, and only the submaximal rate was obtained. Furthermore, the inhibitory effect of theophylline on PDE from the epididymal adipose tissue was less potent in 6-week-old KK mice than in healthy ICR mice of the same age.
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PMID:Effects of epinephrine and theophylline on lipolytic response in hereditary diabetic mice. 18 66

The effects of two environmental temperatures (T; 16 degrees and 31 degrees), five diet dilutions (D; 0%, 12.5%, 25%, 37.5% and 50%), and five daily treadmill running periods (E; 10 minutes, 40 minutes, 70 minutes, 100 minutes, and 130 minutes) upon enzyme activities of liver and adipose tissue of male rats were observed. Liver enzymes studied were glucose-6-phosphatase (G6Pase), 6-P-gluconate dehydrogenase (6PGD), glucose-6-phosphate dehydrogenase (G6PD), fructose diphosphatase (FDPase), NADP-isocitrate dehydrogenase (ICDH), and malic enzyme (ME). Adipose tissue (epididymal fat) enzymes (6PGD, G6PD, and ME) were studied as well as the in vitro incorporation of the 14C of [U-14C] glucose into liberated 14CO2 and into the triglycerides, free fatty acids, and total lipids by adipose tissue slices. Equations describing regression surfaces for these responses (expressed as units/100 g body weight) could contain significant linear coefficients of the independent variables (T, D, and E), their first order interactions, and quadratic coefficients for D and E. Significnat regression coefficients for activities of liver enzymes associated with increased lipogenesis (6PGD, G6PD, and ME) produced response surfaces with conformations generally concave downward. All enzymes possessed positive and negative linear and quadratic coefficients for D which caused response surfaces to be concave downward with respect to that variable. Also, 6PGD and G6PD (positive linear and negative quadratic coefficients for E) exhibited response surfaces concave downward with respect to E. Additionally, 6PGD showed greater activity at 31 degrees than at 16 degrees while G6PD showed no effect of temperature on activity. Liver ICDH, probably important in supplying reducing equivalents for fatty acid synthesis, evidenced response surfaces almost identical to those for 6PGD. Significant regression coefficients for activity of liver enzymes associated with increased gluconeogenesis (FDPase and G6Pase) produced for FDPase a response surface concave downward with respect to both D and E with greater values at 31 degrees than at 16 degrees; but for G6Pase non-concave surfaces with lesser values at 31 degrees than at 16 degrees. Significant regression coefficients for activities of adipose enzymes associated with increased lipogenesis produced for 6PGD a response surface concave upward due to negative linear and positive quadratic coefficients for both D and E. For G6PD and ME regression surfaces were concave upward with respect to E, but these were modified by positive and negative linear coefficients, respectively, for D. Significant regression coefficients for incorporation of the 14C of glucose into triglycerides and free fatty acids of adipose tissue slices and their production of 14CO2 yielded response surfaces concave upward with respect to E (negative linear and positive quadratic coefficients). In addition, the surface for free fatty acids was concave upward with respect to D. The 14CO2 production was greater at 16 degrees than at 31 degrees...
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PMID:Effects in the rat of environmental temperature, diet dilution, and treadmill running on liver and adipose enzymes and metabolism of 14C-glucose: a multiple regression analysis. 18 37

In a first series of experiments, the effects of uridine and inosine on glucose metabolism in rat diaphragm muscle incubated in Krebs-bicarbonate buffer were studied. Uridine in concentrations of 10(-4) to 10(-6) M stimulated the uptake of glucose and increased the content of glycogen, but had no effect on the production of lactate. When diaphragm muscles were incubated in the buffer without glucose, uridine (10(-4)-10(-6) M) had no effects on the content of glycogen and on the production of lactate. On the other hand, inosine in concentrations of 10(-4) to 10(-6) M stimulated the uptake of glucose and the production of lactate, but had no effect on the content of glycogen in the muscle. In a second series of experiments, uridine (10(-4)-10(-5) M) and inosine (10(-4)-10(-7) M) inhibited the relase of glycerol from isolated rat epididymal adipose tissue in Krebs-bicarbonate buffer. Uridine and inosine in concentrations of 10(-4) M inhibited the epinephrine (10(-5) M)-, the norepinephrine (10(-5) M)- and the theophylline (10(-3) M)-stimulated lipolysis. Dibutyryl 3',5'-adenosine monophosphate-stimulated lipolysis was further activated in the presence of 10(-4) M uridine or inosine. Dose-response curves studies suggested that inosine, but not uridine, has a common receptor site with epinephrine in adipose tissue. These results demonstrated that both nucleosides stimulated the glucose uptake, but only uridine increased the synthesis of glycogen in the muscle. Both nucleosides also inhibited lipolysis in adipose tissue. The mechanism of antilipolytic action of these nucleosides is unknown, but one of the receptor sites for inosine might be adenylate cyclase.
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PMID:Effects of uridine and inosine on glucose metabolism in skeletal muscle and activated lipolysis in adipose tissue. 18 86

Normal male rats were made chronically diabetic by injection of alloxan or acutely diabetic by injection of anti-insulin serum. The concentration of cyclic AMP in epididymal adipose tissue was increased approximately 2 1/2-fold 24 h after alloxan administration and up to 7-fold 72 h post-alloxan. Treatment of alloxan-diabetic rats with insulin for 4 h completely suppressed lipolysis but only partially suppressed cyclic AMP levels; 6 h following insulin treatment cyclic AMP levels were normal. When segments of the epididymal fat bodies were incubated in vitro the high cyclic AMP levels were not maintained but instead decreased spontaneously. Addition of insulin to the incubation media decreased lipolysis in tissues of diabetic rats to levels measured in tissues of normal rats and accelerated the decline in cyclic AMP levels but did not return cyclic AMP levels to normal. Rats rendered acutely insulin deficient by injection of anti-insulin serum showed increased plasma glucose and free fatty acid levels and increased adipose tissue free fatty acid, and cyclic AMP levels 30 min following injection of the antiserum. Plasma glucagon levels increased but not until 2 h following anti-insulin serum, thereby excluding the possibility that an increment in plasma glucagon is the primary stimulus for the acceleration of lipolysis in diabetes. These data are consistent with the view that control of adipose tissue cyclic AMP levels in situ is an important physiologic action of insulin.
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PMID:Adenosine 3',5'cyclic monophosphate in adipose tissue of diabetic rats. 18 24

The effects of insulin and of two lipolytic hormones (epinephrine and ACTH1) on the rate and pattern of glucose metabolism were compared during incubation of isolated fat cells, obtained from epididymal fat pads of rats of varying age and degrees of adiposity. Glucose metabolism and the intracellular free fatty acid levels were expressed on a per cell basis and in relation to adipocyte size. The data for total glucose metabolism show that, in contrast to the declining insulin effect observed with adipocyte enlargement, the stimulation of glucose uptake and metabolism by these lipolytic hormones was significantly greater in the larger fat cells from the older fatter rats than in the smaller ones from the younger leaner rats. Lipolytic hormones suppressed, whereas insulin enhanced, fatty acid synthesis; moreover the lipolytic hormones stiumlated glucose ce effect of epinephrine on the intracellular free fatty acid levels was greater in the small fat cells than in the large ones; this effect of epinephrine was markedly curtained by the presence of glucose in the incubation medium, making it unlikely that acceleration of glucose metabolism by the lipolytic stimulus was mediated by an elevation of the intracellular free fatty acid level. The present results show a markedly enhanced capacity of the large adipocytes to accelerate glucose metabolism in response to these liplytic hormones. Thus, in contrast to prevailing notions of declining hormonal responsiveness with expanding fat cell size in older and more obese animals, this study documents an instance of increased hormonal response in enlarged adipocytes and points to the need for a more comprehensive reevaluation of the various hormonal effects in adipocytes of different size.
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PMID:Glucose metabolism in isolated fat cells: enhanced response of larger adipocytes from older rats to epinephrine and adrenocorticotropin. 18 34

The effect of cyclic adenosine 3':5'-monophosphate (cAMP) and caffeine on the motility of spermatozoa obtained in vivo by micropuncture from the rat rete testis, caput epidiymidis, and cauda epididymidis was studied. Spermatozoa from all sites were immobile in their native fluid. Rete testis spermatozoa were not motile under any experimental conditions. After dilution in salt solution, some caput sperm exhibited circular motion, whereas most cauda sperm swam progressively. Dextrose enhanced the motility of sperm from both epidiymal sites. Caffeine further increased the motility of epididymal sperm. Dibutyryl cAMP and cAMP stimulated caput spermatozoa but had no effect on cauda spermatozoa.
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PMID:Micropuncture studies of the motility of rete testis and epididymal spermatozoa. 18 86

The guanosine 3': 5'-monophosphate (cyclic GMP) level in isolated rat epididymal fat cells increased more than doubled 10 min after addition to the cells of carbamylcholine (10(-6) M) in the presence or absence of epinephrine (5 X 10(-7) M). Addition of carbamylcholine, cyclic GMP or dibutyryl cyclic GMP (10(-9) to 10(-5) M) did not affect glucose oxidation or epinephrine-stimulated lipolysis of the cells. No significant change in the cyclic GMP level was detected 2 min or 10 min after addition of insulin (1 mU/ml) to the cells, when glucose oxidation was stimulated and lipolysis induced by epinephrine was inhibited. These results indicate that the transient increase in the cyclic GMP level in the cells on treatment with carbamylcholine is not sufficient for expression of the effects of insulin.
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PMID:Effect of guanosine 3' : 5'-monophosphate on glucose oxidation and epinephrine-stimulated lipolysis in isolated rat epididymal fat cells. 18 2

To identify cells developing into adipocytes by accumulation of triglyceride, rat epididymal fat pad cells from small rats were exposed to (3)H-labeled chylomicron fatty acids in vivo and then liberated with collagenase. Tissue remnants were removed by filtration and mature fat cells by flotation. Aggregating cells were then removed by filtration through a 25- micro m nylon screen. Further purification of cells labeled in vivo was obtained by removing floating cells from those adhering to the bottom of a culture dish. The adhering cells multiplied to a confluent monolayer when cultured in Medium 199 containing serum, glucose, insulin, and a triglyceride emulsion. The cells then gradually enlarged due to granulation of the cytoplasm by a lipid-staining material. After about 2 weeks these granules had coalesced forming mature adipocytes of typical signet-ring appearance. Free adipocytes could then be recovered from the cultures by collagenase treatment. After about 2 weeks of culture these cells had the same size (about 30 micro m) as adipocytes recovered in the original collagenase preparation of the rat epididymal fat pad. They contained triglyceride lipase activity and incorporated glucose into triglycerides to the same extent as cells developed in vivo but had higher lipoprotein lipase activity. In vitro, heparin in a low concentration, prostaglandin E(1), isobutylmethylxanthine, and cholera toxin markedly promoted the development of these cells into adipocytes. This could be shown to occur almost completely indicating that this fraction of cells was homogeneous and consisted of cells with the capacity to form adipocytes. The duplication time was about 2 days and did not change with subculturing. Preadipocytes could be obtained by density gradient centrifugation, isolating triglyceride-containing cells either directly from the pad or after 3 days in culture. All of these cells developed into adipocytes as described above but did not multiply as readily. It was concluded that cells from the epididymal fat pad from small rats can be isolated in a homogenous fraction that develops in culture into cells of identical morphology and function as adipocytes formed in vivo. The differentiation of these cells into adipocytes may be manipulated in vitro.
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PMID:Isolation and characterization of cells from rat adipose tissue developing into adipocytes. 20 38


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