Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin was found to double the rate of incorporation of H14CO3- into protein by segments of rat epididymal adipose tissue provided the incubation medium contained a suitable energy substrate such as fructose. Overall protein synthesis was increased by insulin to a lesser extent, one-third as measured by tritiated water indicating that insulin also increased CO2 fixation into amino acids. The latter could be demonstrated only when the tissue amino acid pools were expanded by the addition of aspartate to the incubation medium. The pattern of labeling observed in the amino acids indicated that CO2 fixation occurred primarily at the pyruvate carboxylase step. Addition of pyruvate to the incubation medium also increased CO2 fixation and this effect was not additive with that of insulin, suggesting that insulin acted by increasing the availability of pyruvate to the carboxylase. No change in carboxylase activity could be measured. Mitochondria isolated from tissue exposed to insulin retained a higher capacity to fix CO2 into acid-soluble products provided they were not freeze-thawed or sonicated. Uptake of pyruvate by mitochondria incubated 1 min at 2 degrees C or 5 s at 15 degrees C was doubled by prior insulin treatment of the tissue. It is concluded that insulin increases the flux through pyruvate carboxylase in adipose tissue in part by increasing the transport of pyruvate through the inner mitochondrial membrane.
 ...
PMID:Effects of insulin on CO2 fixation in adipose tissue. Evidence for regulation of pyruvate transport. 640 Dec 94

Leucine is catabolized to ketone bodies in adipose tissue, but the contribution of this output to overall ketone metabolism is not known. The intent of the present study was to determine the capacity of different adipose tissues to synthesize ketone bodies from leucine. The amino acid was readily converted into acetoacetate in epididymal, perirenal, and omental fat tissues. In rats fed ad libitum, the rate of acetoacetate synthesis in omental fat (about 2 mumol g tissue-1h-1) was at least 8 times higher than in epididymal or perirenal fat. In omental fat, the rates of acetoacetate formation from alpha-ketoisocaproic acid were 47-55% lower than from leucine at all concentrations examined. There was no significant synthesis of beta-hydroxybutyrate from leucine or alpha-ketoisocaproic acid. After oxidative decarboxylation, a greater proportion (about three-fourths) of leucine in omental fat was metabolized to acetoacetate than to CO2 production through the Krebs cycle. Although addition of glucose, pyruvate, or carnitine did not affect the production of acetoacetate, fasting for 24 h stimulated acetoacetate synthesis from leucine and alpha-ketoisocaproic acid in omental fat. The high rate of leucine conversion to acetoacetate in omental fat was related to high activities of leucine aminotransferase and branched-chain alpha-keto acid dehydrogenase. Moreover, protein content and cytochrome c oxidase activity of omental mitochondria were, respectively, 13 and 12 times higher than in epididymal mitochondria. In contrast, fat content of epididymal adipose tissue was 21 times that of omental adipose tissue. Epididymal depot consisted of 2.0% protein and 75.8% fat, whereas omental depot contains 17.2% protein and 3.6% fat, resembling that of liver and muscle. The results suggest that the high ketogenic capacity of omental fat stems in part from an augmented mitochondrial mass and high activity of branched-chain alpha-keto acid dehydrogenase.
 ...
PMID:Ketone body synthesis from leucine by adipose tissue from different sites in the rat. 654 May 47

The potential for the chemosterilant 1,2-dibromo-3-chloropropane (DBCP) to reduce male fertility by acting at a site in the genital tract beyond the testis was evaluated in male, Fischer 344 rats. A single sc treatment with 100 mg/kg DBCP reduced fertility in male rats 2 to 7 days postexposure without affecting mating frequency. Doses of 10, 20, or 40 mg/kg DBCP given sc once daily for 7 days caused a dose-dependent reduction in the metabolism of glucose to CO2 by epididymal sperm, as measured in vitro. Conversion of glucose to lactate was not reduced, indicating inhibition of energy metabolism at a step post-glycolysis. No clinical signs of toxicity were observed in these studies. Direct addition of DBCP to epididymal sperm being incubated in vitro also inhibited the metabolism of glucose to CO2. Inhibition was concentration related, and the minimal inhibitory concentration was 0.316 mM. These data indicate that DBCP may cause a nearly immediate infertility via a direct effect on post-testicular sperm. A possible mechanism of this infertility is inhibition by DBCP of glucose metabolism in the ejaculated sperm.
 ...
PMID:1,2-dibromo-3-chloropropane (DBCP)-induced infertility in male rats mediated by a post-testicular effect. 663 94

Poor growth in uncontrolled experimental diabetes appears due in part to increased circulating inhibitor, a factor (or factors) that blocks stimulation of growing cartilage by somatomedins. To determine if the inhibitor has other antianabolic properties, we examined effects on insulin and insulin-like action on muscle and adipose tissue. Rat epididymal fat pads were exposed to normal rat serum, somatomedins (fraction from normal rat serum) or insulin, with or without added streptozotocin-diabetic rat serum or inhibitor (fraction from diabetic serum); insulin-like activity was assessed by glucose conversion to CO2. Diabetic rat serum alone lowered glucose utilization significantly below buffer levels (P less than .010), but inhibitor alone had no effect. However, stimulation by insulin, normal rat serum, or somatomedins was decreased significantly by both diabetic rat serum or inhibitor (P less than 0.01); Lineweaver-Burk analysis suggested that such inhibition was noncompetitive. In incubations with rat diaphragm, neither diabetic rat serum nor inhibitor alone lowered glucose incorporation into glycogen, but both inhibited muscle stimulation by insulin (P less than 0.01). In in vivo studies, rats given insulin with added diabetic rat serum exhibited decreased stimulation of glucose incorporation into muscle glycogen (P less than 0.01) and into adipose tissue total lipids. These observations indicate that an inhibitor in the serum of diabetic rats can brake anabolic processes is muscle (glycogen formation) and adipose tissue (glucose utilization, lipid formation). Such an inhibitor may therefore contribute to poor growth in diabetes by decreasing calorie storage due to insulin and insulin-like actions as well as skeletal elongation due to somatomedin action.
 ...
PMID:Nutrition and somatomedin. IX. Blunting of insulin-like activity by inhibitor in diabetic rat serum. 675 35

The metabolism of [14-14C]erucic acid and [U-14C]palmitic acid has been investigated in adipocytes isolated from rat epididymal fat. The rate of acylation of [14C]erucic acid in cellular lipids and oxidation to CO2 and acid-soluble activity was ca. 1/3 of the rate with [14C]palmitic acid as substrate. A maximal incorporation of fatty acids in triacylglycerol was found at a fatty acid concentration of 0.8 mM in the medium, both with [14C]erucic acid and [14C]palmitic acid as substrate. Glucose added to the medium increased the esterification and decreased the oxidation of both fatty acids. No significant chain-shortening of [14C]erucic acid to shorter monoenes was identified in the fat cells. Increasing concentrations of unlabeled palmitic acid in the incubation medium markedly inhibited the esterification of [14C]erucic acid, whereas unlabeled erucic acid had little effect on the rate of esterification of [14C]palmitic acid.
 ...
PMID:Metabolism of erucic acid in adipocytes isolated from rat epididymal fat. 684 2

Glucose utilization was studied in isolated adipocytes from rats fed a mixed (51% carbohydrate, 30% fat, 19% protein), high fat (81% fat, 19% protein) or high protein diet (30% fat, 70% protein). Despite similar food intake, rats on the high protein (HP) diet had smaller epididymal fat pads than the other two groups. The reduction in fat pad size was caused by small and variable reductions in both cell size and cell number. Fat cells from rats on the high fat (HF) diet had the previously reported reduction in pentose phosphate shunt activity in the absence and presence of insulin, and marked diminution of de novo fatty acid synthesis. Lactate release was elevated in the absence of insulin. There was no insulin stimulation of glucose uptake, CO2 production, glyceride-glycerol production or lactate release in these adipocytes. However, significant stimulation of fatty acid synthesis was seen. There was no impairment of glucose uptake or utilization in cells from rats on the HP diet despite the absence of dietary carbohydrate. Indeed, 14CO2 produced from glucose-l-14CO2 produced from glucose-1-14C was increased in these adipocytes. Thus the impaired glucose utilization in rats on the high fat, carbohydrate-free diet is due solely to the fat content of the diet.
 ...
PMID:Absence of impaired glucose utilization in adipocytes from rats fed a carbohydrate-free, high protein diet. 700 93

The mechanism(s) by which the oral sulfonylurea, tolazamide, exerts its extrapancreatic hypoglycemic effects was studied using rat epididymal adipose tissue maintained 20-44 h in the presence or absence of the drug. Insulin binding, hexose transport and glucose metabolism were compared in adipocytes isolated from the cultured tissue. In contrast to earlier reports that suggested that sulfonylureas alter the binding of insulin, neither receptor number nor affinity were changed by tolazamide treatment. The uptake of the glucose analogs 2-deoxyglucose and 3-0-methylglucose in the absence of insulin (i.e., basal) was also unchanged. However, exposure to tolazamide resulted in a potentiation of the stimulatory effects of insulin by approximately 30% at each hormone concentration assayed (0.4-40 ng/ml). This potentiation was dependent on the tolazamide concentration (0.003-0.30 mg/ml), with a maximal effect observed at therapeutic levels. A tolazamide analog hypoglycemic activity in vivo was found not to enhance either basal or insulin-stimulated uptake in vitro. Conversion of 0.1-5.0 mM glucose to CO2 and total lipids in the presence of insulin was also potentiated by tolazamide treatment. The inability of the drug to directly stimulate basal glucose uptake was paralleled by its lack of effect on glucose metabolism. At 50 mM glucose, where transport is no longer rate-limiting, tolazamide did not potentiate metabolism in the absence or the presence of insulin. These studies demonstrate that tolazamide in vitro alters postreceptor insulin action without influencing the receptor, and suggests insulin-stimulated hexose transport as the cellular process responsible for the hypoglycemic effect of sulfonyureas in adipose tissue.
 ...
PMID:In vitro effects of a sulfonylurea on insulin action in adipocytes. Potentiation of insulin-stimulated hexose transport. 701 48

The metabolic utilization of 14C-labelled acetate, pyruvate, lactate and glucose by isolated epididymal fat-cells was compared in two groups of rats fed ad libitum, one group young and lean (150-200 g body wt.), the other older and spontaneously obese (500-650 g body wt.). The influence of unlabelled glucose (6 mM) and insulin on substrate utilization by adipocytes was also studied. (1) Pyruvate and lactate were found to be good precursors for fatty-acid synthesis in small fat-cells, but not in larger fat-cells. On the other hand, lactate conversion into CO2 and the glycerol moiety of acylglycerols proceeded activity in both types of cells, and in some cases, it even exceeded the rates of glucose utilization. (2) The addition of glucose or glucose plus insulin, but not insulin alone, enhanced the metabolism of acetate, pyruvate and lactate in both types of fat-cells. (3) Fatty-acid synthesis de novo in large fat-cells was markedly decreased regardless of the substrate utilized. These findings point to lactate as a significant precursor for triacylglycerol synthesis in adipocytes. Furthermore, decreased fatty-acid synthesis de novo appears to be an acquired metabolic deficiency of enlarging adipocytes, independent of precursor substrate availability.
 ...
PMID:Alternative substrates for triacylglycerol synthesis in isolated adipocytes of different size from the rat. 703 Mar 17

Male Sprague-Dawley rats (125--150 g) were implanted intramuscularly with Walker 256 carcinoma. After 10--14 days, tumor-bearing rats, alone with controls, were killed and the ability of insulin to promote the in vitro utilization of glucose by epididymal adipose tissue was assessed. The sensitivity of free adipocytes and minced adipose tissue from tumor-bearing rats to insulin, as assessed by measurement of the incorporation of glucose into total lipids as well as into the triglyceride fraction of neutral lipids, was significantly less (P less than 0.01) as compared to control animals. Similarly, insulin was considerably less effective at enhancing glycogenesis in vitro in adipose tissue from animals bearing the tumor for 10 days compared to adipose tissue from controls. Adipose tissue from tumor-bearing animals tended to convert less glucose to CO2 in the presence of insulin than did adipose tissue from controls. That this decreased in vitro sensitivity to insulin of adipose tissue from tumor-bearing animals could be the result of simple down-regulation by high levels of circulating insulin can be ruled out by the fact that the presence of the tumor resulted in lower circulating insulin than that in control animals. Serum glucose levels were also lower in tumor-bearing rats than in corresponding control animals.
 ...
PMID:Insulin-stimulated glucose utilization in adipose tissue from rats bearing Walker 256 carcinoma. 703 69

Fat cells isolated from the epididymal (E) and dorsal subcutaneous (S) depots from 150g male Wistar rats were similar in size, but differed markedly in glucose metabolism. Retroperitoneal (RP) fat cells were slightly larger but were metabolically similar to epididymal fat cells. Basal incorporation of [1-14C] glucose into fatty acids was lower in S than E and RP, CO2 production and glyceride-glycerol synthesis were similar in all three; and lactate production was increased in RP and S compared to E. S adipocytes exhibited a blunted respond to both submaximally and maximally-stimulating concentrations of insulin compared to RP and E adipocytes in glucose incorporation into fatty acids, CO2 and lactate production, but not glyceride-glycerol. Maximally insulin-stimulated fatty acid synthesis by S fat cells was 19% and 29% of the values in E and RP fat cells respectively. Basal and maximally insulin-stimulated glucose transport (2-deoxy [14C] glucose uptake) was depressed by 30%-40% in S cells compared to E and RP. Thus, the decreased basal glucose utilization of S could be attributed primarily to a decreased glucose transport capacity. The markedly lower insulin-stimulated glucose metabolism in S fat cells, however, may be explained by alterations of the capacities for both transport and intracellular metabolism. Subcutaneous fat cells were also somewhat less sensitive to submaximal doses of insulin and this was reflected in rightward shift in the dose-response curves for 2-deoxyglucose uptake and fatty acid synthesis. The decreases in insulin stimulated glucose oxidation and fatty acid synthesis were paralleled by decreases in the major lipogenic enzymes. Although the reason for these variations in the capacity for glucose metabolism among depots is unknown, they are important in assessing the metabolic function of the whole adipose organ.
 ...
PMID:Variations of glucose metabolism by fat cells from three adipose depots of the rat. 712 Dec 59


<< Previous 1 2 3 4 5 6 7 8 9 Next >>