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

Adipocytes isolated from the epididymal fat of hypophysectomized rats by digestion with collagenase failed to respond to insulin with an increase in glucose utilization. These cells also exhibited an anomalous response to insulin when added in the presence of epinephrine. While insulin antagonized the lipolytic actions of epinephrine in normal adipocytes or in segments of epididymal fat from normal or hypophysectomized rats, it potentiated lipolysis in adipocytes isolated from hypophysectomized rats. This anomalous effect was also evident when isoproterenol, ACTH, or glucagon was used as the lipolytic agent, but the expected antilipolytic response was obtained when theophylline served as the lipolytic agonist. The lipolytic effects of insulin were not seen until 4-7 days after hypophysectomy. Treatment of hypophysectomized rats with a combination of GH (100 micrograms/rat . day), cortisone acetate (1 mg/rat . day), and T3 (1 micrograms/rat . day) for 5 days restored the antilipolytic response to insulin in cells of hypophysectomized rats, but no one hormone alone was effective. The data indicate that adipocytes of hypophysectomized rats retain their ability to recognize and response to insulin, but the ability of insulin to stimulate glucose oxidation or antagonize epinephrine-induced lipolysis is abolished by the cell isolation procedure. The findings underscore the need to consider the impact of hormonal status on the ability of cells to retain normal responsiveness during the rigors of the cell isolation procedure and suggest that failure to do so might lead to erroneous interpretations of the physiological actions of hormones.
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PMID:Lipolytic effects of insulin in adipocytes isolated from hypophysectomized rats. 627 27

(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

The effects of Ca2+ and calmodulin inhibitors on lipolysis induced by epinephrine, norepinephrine, caffeine and ACTH in rat epididymal adipose tissue were investigated. 1. Omission of Ca2+ from the incubation medium slightly depressed lipolysis induced by epinephrine, norepinephrine and ACTH. Lipolysis induced by caffeine was significantly depressed. 2. Lipolysis induced by epinephrine, norepinephrine, caffeine and ACTH was strongly depressed when Ca2+-deficient tissue was incubated in Ca2+-free Ringer solution. 3. In Ca2+-deficient tissue, the addition of 0.75mM Ca2+ apparently restored lipolysis induced by epinephrine, norepinephrine and ACTH, whereas that by caffeine was restored to only approximately 89%. 4. The addition of La3+ markedly inhibited lipolysis induced by each agonist. 5. The Ca2+ antagonists such as verapamil and diltiazem dose-dependently inhibited lipolysis induced by each agonist. 6. The specific calmodulin inhibitors such as chlorpromazine, trifluoperazine and W-7 markedly inhibited lipolysis induced by each agonist. These results strongly support the possible key role that the redistribution and influx of Ca2+ may play in lipolysis induced by epinephrine, norepinephrine, caffeine and ACTH, and further suggest that calmodulin may affect lipolysis.
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PMID:[Effects of Ca2+ and calmodulin inhibitors on lipolysis induced by epinephrine, norepinephrine, caffeine and ACTH in rat epididymal adipose tissue]. 630 33

The activity of adipose tissue hormone-sensitive lipase in animals with hyperinsulinemia has been reported to be increased compared with that in control animals. We examined whether this results from a direct effect of insulin on the tissue and whether it is accompanied by alteration in the regulation of lipolysis. When rat epididymal fat pads are incubated in culture medium with bovine serum albumin for 2-4 h with 2 ng/ml or 50 microU/ml of insulin, hormone-sensitive lipase activity in the postmicrosomal supernatant fraction after acid precipitation and activation with ATP-Mg2+ increases significantly compared with preparations from tissues incubated with the vehicle. The specific activities of hormone-sensitive lipase in sonicates of adipocytes after primary culture with insulin at concentrations from 10 to 4000 ng/ml (250 microU to 100 mU/ml) increase in an insulin-dose-related manner. Lipolysis in response to 10(-7) M isoproterenol also increases in an insulin-dose-dependent manner. Enhancement of isoproterenol-mediated lipolysis is not attributable to a difference in the triglyceride content of the cells. Lipolysis caused by the beta-agonist could be completely blocked by the simultaneous presence of insulin in both control and insulin-treated cells reflecting normal responsiveness of both types of cells to the acute effect of insulin. Although an increase in lipolysis is seen with norepinephrine and growth hormone after insulin treatment, other lipolytic agents such as ACTH, thyrotropin, and glucagon evoke similar responses in insulin-treated and control cells. The simultaneous presence of growth hormone and insulin during the 16-h culture results in additive effects on the subsequent response of the cells to 10(-7) M isoproterenol compared with the responses of the cells cultured with each hormone alone. beta-Agonist-mediated cAMP accumulation in the presence of Ro-20.1724, a specific phosphodiesterase inhibitor, is significantly higher in cells cultured in the presence of insulin than in control cells. Forskolin (1-25 microM) increases the lipolytic responses of insulin-treated cells compared with control cells, but the maximal response of the insulin-treated cells to forskolin is lower than that to isoproterenol. We conclude that changes produced by chronic insulin treatment involve more than one site along the lipolytic cascade.
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PMID:Chronic exposure of rat fat cells to insulin enhances lipolysis and activation of partially purified hormone-sensitive lipase. 839 27

Short day photoperiod promotes thermogenesis and extensive weight loss in Siberian hamsters (Phodopus sungorus sungorus). To determine whether a change in hormone-sensitive lipolysis occurs after short-photoperiod exposure, some lipolytic responses were measured on white adipocytes isolated from animals exposed in warm conditions to short or Long daylight photoperiod. The body mass of male Siberian hamsters exposed during 11 weeks to short days (SD; light: dark, 6:18 hr) reached only 50% of those kept in long days (LD; 16: 8 hr). In SD-hamsters, adipose depot mass also represented approximately 50% of the LD group. A lower DNA content was observed in intra-abdominal fat pads of SD-hamsters. Lipolytic responses to noradrenaline, adrenaline, isoproterenol and ACTH were unchanged. However, sensitivity to the beta-3 adrenergic agonist, BRL 37344, was moderately increased. The major component of the adrenergic control of lipolysis was mediated by beta-3 adrenoceptors in both LD- and SD-Siberian hamsters. The limited antilipolytic effect of alpha-2 adrenergic agonists, PYY or insulin was rather surprising in Siberian hamsters since these inhibitory systems are efficient in hibernants and other photoperiod-sensitive rodents. Our results show that, after short photoperiod exposure, white adipose tissue mass and DNA content are reduced, especially in the epididymal fat pad, with only minor changes in the adipocyte sensitivity to lipolytic hormones.
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PMID:Lipolytic and antilipolytic responses of the Siberian hamster (Phodopus sungorus sungorus) white adipocytes after weight loss induced by short photoperiod exposure. 1124 94

We assessed the effects of peripheral leptin on anxiety and exploratory behaviour in the elevated plus-maze and in the four-hole box or Y-maze tests, in rats fed 80% of normal daily food intake and rats fed ad libitum. In the Y-maze test, i.p. injection of 0.4 or 1 mg/kg leptin into rationed rats significantly decreased the percentage of spontaneous alternation behaviour and increased the number of visits. In the elevated plus-maze test, rationed rats spent significantly more time in the open arms (aversive part of the maze) than did rats fed ad libitum. This difference in behaviour was abolished by injecting 0.4 mg/kg leptin. In the four-hole box test, i.p. administration of 1 mg/kg leptin significantly reduced the duration and number of hole visits in rationed and ad libitum fed rats. As with leptin inhibition of food intake, these behavioural changes caused by leptin were prevented by a CCK(1) receptor antagonist (L364,718), at a dose that had no effect by itself. Finally, a 20-min stress that increased corticosterone and ACTH levels had no effect on circulating leptin levels and on the leptin content of epididymal fat tissue, stomach and brain. Thus, leptin induces hypoexploration and decreases spontaneous alternation in rats and these effects are partly dependent on nutritional status. These results also suggest that the CCK system may be involved in the induction of these behavioural changes in rats by leptin, via the CCK(1) receptor.
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PMID:Leptin decreases feeding and exploratory behaviour via interactions with CCK(1) receptors in the rat. 1136 35

Neonatal manipulations (10 min of maternal separation plus s.c. sham injection, daily for the first 21 d of life) determine overweight in male adult mice. In this work, we investigated the mechanisms underlying mild obesity and the alteration of caloric balance. Neonatally manipulated mice become overweight after onset of maturity, showing increased fat tissue and hypertrophic epididymal adipocytes. Increase in body weight occurs in the presence of a small increase in daily food intake (significant only in the adult period) and the absence of a decrease in spontaneous locomotor activity, while the calculated caloric efficiency is higher in manipulated mice, especially in adulthood. Fasting adult animals show hyperglycemia, hyperinsulinemia, hypertriglyceridemia, hypercholesterolemia, and hyperleptinemia. Soon after weaning and in the adulthood, plasma corticosterone and adrenocorticotropin (ACTH) are also significantly increased. Thus, neonatal manipulations in nongenetically susceptible male mice program mild obesity, with metabolic and hormonal alterations that are similar to those found in experimental models of diabetes mellitus, suggesting that this metabolic derangement may have at least part of its roots early on in life and, more interestingly, that psychological and nociceptive stimuli induce these features.
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PMID:Overweight and metabolic and hormonal parameter disruption are induced in adult male mice by manipulations during lactation period. 1632 92

This study shows the characteristics of hormone-dependent lipolysis in white adipose tissues from corpulent spontaneously hypertensive rats (SHR/NDmc-cp(cp/cp)). The glycerol-releasing activity on addition of norepinephrine (NE) and corticotropin (ACTH) was diminished in slices of epididymal, retroperitoneal, and mesenteric adipose tissues from cp/cp rats compared with those from Wistar Kyoto rats and lean spontaneous hypertensive rats (SHR/NDmc-cp(+/+)). 8-Bromo-cyclic adenosine monophosphate had a slight effect on lipolysis in epididymal, retroperitoneal, and mesenteric adipose tissues from cp/cp rats, and addition of NE and ACTH resulted in a slight accumulation of cyclic adenosine monophosphate in epididymal adipose tissue from cp/cp rats. Therefore, the alteration of hormone-dependent lipolysis-related genes was analyzed using quantitative real-time polymerase chain reaction. It was found that the expression of beta(3)-adrenergic receptor, melanocortin 2 receptor, hormone-sensitive lipase, and perilipin messenger RNAs was limited in epididymal, retroperitoneal, mesenteric, and subcutaneous adipose tissues from cp/cp rats compared with +/+ rats. These results indicate that in white adipose tissue from cp/cp rats, the diminished lipolytic response to NE and ACTH may be caused by impaired expression of beta(3)-adrenergic receptor, melanocortin 2 receptor, hormone-sensitive lipase, and perilipin.
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PMID:Characteristics of lipolysis in white adipose tissues of SHR/NDmc-cp rats, a model of metabolic syndrome. 1751 19

Cocaine- and amphetamine-regulated transcript (CART) has been implicated in the feeding behavior and the regulation of hypothalamic-pituitary-adrenal axis activity. In this study we investigated the expression of CART mRNA in the hypothalamus at several intervals after adrenalectomy or sham surgery in basal conditions or after a fasting-refeeding regimen. Male Wistar rats, with free access to food and drinking, were subjected to bilateral adrenalectomy (ADX) or sham surgery. Plasma corticosterone, ACTH, and leptin levels, epididymal and perirenal fat content, and CART expression were determined 1, 3, 7 and 14 days after surgery. Another set of rats was subjected to a 48-h fasting period followed by refeeding during 4 h on the 7th day after ADX or sham surgery. On the day of the experiment, rats were anesthetized and perfused and the brain was processed for CART mRNA in situ hybridization. We observed that long-term but not short-term adrenalectomy decreased leptin plasma levels and CART expression in the arcuate and paraventricular nuclei. Furthermore, we showed that CART expression was reduced by fasting and it was increased after refeeding in the sham group, however, CART expression was not changed by fasting or refeeding after ADX. In conclusion, the present data indicate that following long-term ADX, under freely feeding conditions, there is a decrease of CART expression in the hypothalamus that is associated with a decrease of leptin secretion. CART expression induced by feeding seems to be modulated by glucocorticoid.
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PMID:Time course effects of adrenalectomy and food intake on cocaine- and amphetamine-regulated transcript expression in the hypothalamus. 1766 77

Ghrelin, an endogenous ligand for the growth-hormone-secretagogue receptor, is a 28-amino acid peptide with a post-translational acyl modification necessary for its activity. It has central nervous system actions that affect appetite, body mass and energy balance. An intracerebroventricular (ICV) injection protocol of sub-nanomolar doses of ghrelin, known to alter the morphology of ACTH and GH producing pituicytes and plasma levels of these hormones, was used to provide an overview of metabolic changes linked to energy metabolism. Variables measured were: food intake (FI), water intake (WI), fecal mass, urine volume, body weight (BW), retroperitoneal (RP) and epididymal (EPI) white adipose tissue (WAT), and changes in serum leptin, insulin, triglycerides, cholesterol, and glucose. Five injections of rat ghrelin or PBS (n=8 per group) were given ICV every 24 h (1 microg/5 muL PBS) to adult male rats. Ghrelin had a positive and cumulative effect on FI, WI and BW (p<0.05), but not feces mass or urine volume (p>0.05). Centrally applied ghrelin clearly increased RP WAT (by 235%, p<0.001), EPI WAT (by 85%, p<0.05) and serum insulin levels (by 43%, p<0.05), and decreased serum leptin levels (by 77%, p<0.05) without (p>0.05) evoking changes in blood triglyceride cholesterol, or glucose levels. These data and the available literature clearly document that exposure of the brain of normal rats, over time, to sub-nanomolar doses of ghrelin results in metabolic dysregulation culminating in increased body mass, consummatory behavior, and lipid stores as well as changes in blood leptin/insulin levels. Thus, modulation of central ghrelin receptors may represent a pharmacological approach for controlling multiple factors involved in energy balance and obesity.
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PMID:Consummatory behavior and metabolic indicators after central ghrelin injections in rats. 1828 May 92


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