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

Insulin stimulation of hydrogen peroxide production by rat epididymal fat cells was investigated by studying the oxidation of formate to CO2 by endogenous catalase. Under optimal concentrations of formate (0.1 to 1 mM) and glucose (0.275 mM), insulin stimulated formate oxidation 1.5- to 2.0-fold. Inhibitors of catalase activity, including nitrite and azide, inhibited both basal and insulin-stimulated formate oxidation at concentrations that did not interfere with insulin effects on glucose C-1 oxidation or glucose H-3 incorporation into lipids. The addition of exogenous catalase increased formate oxidation only slightly, while exogenous H2O2 (0.5 mM) stimulated formate oxidation by endogenous catalase strongly. These data indicate that the insulin-stimulated H2O2 production was intracellular. Insulin dose-response curves for formate oxidation were identical with those for glucose H-3 incorporation into lipids. The dependence of relative insulin effects on the logarithm of the glucose concentration was bell-shaped for formate oxidation and correlated highly with the coresponding dependences of glucose C-1 oxidation and glucose H-3 incorporation into lipids. This suggests that insulin stimulation of intracellular H2O2 production is linked to glucose metabolism. Since it is known that extracellular H2O2 can mimic insulin in several respects, these observations suggest that H2O2 may act as a "second messenger" for the observed effects of insulin.
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PMID:Insulin-stimulated intracellular hydrogen peroxide production in rat epididymal fat cells. 42 81

Spermatozoa were collected from the rete testis of conscious boars, from the cauda epididymidis by retro-flushing, and by ejaculation. Testicular spermatozoa showed no progressive motility, and that of ejaculated was greater than that of epididymal spermatozoa. Glycolysis and respiration of testicular spermatozoa, while lower than that of the more mature cells, were only slightly affected by the incubation conditions. Epididymal spermatozoa converted 83% of the glucose they utilized to CO2 or lactate, but testicular cells converted only 35% to these metabolites. Synthesis of lipid was greatest by testicular spermatozoa. With the more mature cells hyperosmolar conditions depressed CO2 production, but increased lactate production, and these changes were greater for ejaculated than for epididymal spermatozoa. Glycolysis plus respiration of these cells was related to their motility. These results were interpreted as showing increasing motility, glycolysis and respiration with maturation, but also decreased synthetic capacity and increased sensitivity to the environment.
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PMID:Effects of osmolality, bicarbonate and buffer on the metabolism and motility of testicular, epididymal and ejaculated spermatozoa of boars. 43 62

Crystalline insulin was extracted and purified from the pancreases of obese (BL/6J/-ob/ob) and lean mice (BL/6J and BL/6J-ob/+). The two insulin preparations were compared with respect to their radioimmunologic properties as well as their ability to stimulate glucose metabolism in rat epididymal adipocytes and epididymal adipose tissue from obese and lean mice. No significant differences could be seen between the two insulin preparations and thus an insulin of altered biological properties is not likely to be an adequate explanation for the symptoms observed in the obese mouse.
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PMID:Studies with crystalline insulin from obese and lean mice of the BL/6J strain. 44 99

Controlled perfusion through the lumen of the distal cauda epididymidis in the anaesthetized rat has been explored as a means of examining physiological exchanges from blood across the epididymal epithelium. The mean length of the perfused, sperm-free, tubule was 14.5 cm (+/- 1.5 s.e.m., n = 9). No cholesterol, protein or sialic acid was detected in the perfusate at flow rates exceeding 10 microliters/min, but at rates of 0.4--1.2 microliters/min, protein appeared at concentrations of 0.21--0.55 mg/ml (i.e. secretion rates of 0.21--0.83 micrograms/min; 3 rats). Glucose was detected at all perfusion rates (3--27 microliters/min) at concentrations of 0.06--0.58 mM (0.8--6.8% blood levels). During intravenous infusions of 3H2O, radioactivity in the perfusate rapidly attained 87% blood plasma concentrations; no radioactivity was detected when carboxy-E114C]dextran or methoxy-[3H]inulin were infused. Radioactivity appeared in the epididymal perfusate to 1--7% of blood levels during intravenous infusions of D-E1U-1RC]glucose or 3-O-methyl[1-3H]glucose. This evidence suggests that the preparation is physiological and could be used to explore the dynamics of exchanges between blood and epididymis.
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PMID:Investigation by luminal perfusion of the transfer of compounds into the epididymis of the anaesthetized rat. 46 37

The effects of adrenaline (0.5 microM) and the combination of adrenaline and insulin (1.7nM) on [6-14C]glucose metabolism were assessed in epididymal fat-pads from rats fed either a low- or high-fat diet. The response of lipolysis to adrenaline was clearly diminished in fat-fed rats. Insulin added to adrenaline inhibited the lipolysis by 50% regardless of the diet. Glucose utilization in adipose tissue of fat-fed rats was markedly stimulated by adrenaline (glucose uptake was increased 3-fold and the production of CO2 and the glycerol moiety of acylglycerol was increased 4-fold). However, adipose tissue from fat-fed rats was resistant to the effect of insulin to produce a further increase in adrenaline-stimulated glucose uptake. The intracellular capacity of lipogenesis on the one hand, and the production of CO2 and the glycerol moiety of acylglycerol on the other, are of prime importance in the action of insulin and adrenaline on glucose utilization in this model.
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PMID:Adrenaline responsiveness of glucose metabolism in insulin-resistant adipose tissue of rats fed a high-fat diet. 48 19

1. Evidence is presented that exposure of epididymal fat-pads from fed rats to insulin leads to a marked diminution in the Km for phosphoenolpyruvate of pyruvate kinase. Effects of insulin may be readily demonstrated in experiments both in vivo and in vitro and are not secondary to the activation by the hormone of glucose transport. No effect of insulin is apparent in tissues from 48 h-starved animals. 2. The mechanism of the effect of insulin on pyruvate kinase was not established. The observed changes in Km do not appear to be the result of alterations in the amounts of bound effectors such as fructose 1,6-bisphosphate and alanine. Rather, as the effect persists in incubated extracts, it appears that a change in the degree of phosphorylation or some other covalent modification of the enzyme may be involved.
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PMID:Acute regulation of pyruvate kinase activity in rat epididymal adipose tissue by insulin. 48 31

Disturbances in carbohydrate homeostasis are metabolic hallmarks in the host response to trauma. Since alterations in insulin responsiveness, especially insulin resistance, have been related to the metabolic sequelae of shock, the present study evaluated insulin responsiveness in traumatic shock. Injury (LD50) of fasted, male Holtzman rats (115 plus or minus 20 gm) by tumbling in the Noble-Collip drum resulted in hyperglycemia in spite of a concomitant hyperinsulinemia. The ability of insulin to lower plasma glucose was evaluated at either three hours or 24 hours post-trauma by means of glucose and insulin tolerance tests. The injured rats showed glucose intolerance and hyperinsulinemia three hours after injury but showed a normal glucose tolerance and hypoinsulinemia on the day after injury. Insulin was ineffective in lowering plasma glucose at both of these times. Noble-Collip tumbling trauma induced no systemic changes in insulin responsiveness in vitro at either time as evaluated by 1) epididymal fat pad glucose oxidation of U-D-14C-glucose to 14CO2 or 2) hemidiaphragm incorporation of U-D-14C-glucose into glycogen. The data suggest that insulin resistance is not due to a decreased capacity of various tissues to respond to insulin.
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PMID:Effect of traumatic injury on sensitivity to insulin. 49 33

The purpose of this study was to determine if the elevated concentration of norepinephrine in the hypothalamus of the obese-hyperglycemic mouse plays a role in the development of this syndrome. We treated normal and obese mice with the monoamine oxidase inhibitors pargyline or clorgyline for 25 weeks. This resulted in significant inhibition of monoamine oxidase in their hypothalamus, cerebral cortex, kidney, heart and epididymal fat. There was a significant increase in the norepinephrine concentration of the hypothalamus of the normal mice and the cerebral cortex of the obese mice. The obese mice receiving clorgyline had an increase in plasma glucose (313 +/- 9 mg/dl). However, the increase in tissue norepinephrine concentration did not result in increased weight gain or alterations in organ weights in the mice. Thus, the elevated hypothalamic norepinephrine concentration in obese mice is probably not the cause of their obesity.
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PMID:The role of altered tissue norepinephrine concentration in the hereditary obese-hyperglycemic syndrome of mice. 52 84

1. Adipocytes from rat epididymal fat-pads were incubated for 30 min with 5 mM-glucose and concentrations of lactate, pyruvate and amino acids typical of those found in rat plasma. 2. PDHa (active form of pyruvate dehydrogenase) activity was significantly increased after incubation of the cells with insulin (200 micro-i.u./ml), and decreased by incubation with palmitate (0.5--2 mM). 3. In the presence of insulin, palmitate did not decrease PDHa activity. 4. Dichloroacetate (1 mM) increased PDHa activity in the absence of palmitate to the same extent as did insulin. In the presence of dichloroacetate but the absence of insulin, palmitate decreased PDHa activity. In the presence of dichloroacetate and insulin, palmitate again did not decrease PDHa activity. 5. It is concluded that, in the presence of glucose, insulin has a strong protective action against inactivation of adipocyte PDHa by fatty acids.
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PMID:Inactivation of rat adipocyte pyruvate dehydrogenase by palmitate. Protection against this effect by insulin in the presence of glucose. 53 19

Metabolic adaptations to cyclic patterns of food intake were studied in genetically lean and obese Zucker rats. Twenty-four lean and 24 obese rats were exposed to 12 hours of light and 12 hours of dark and allowed food ad libitum. Both groups of rats ate more during the dark period of the cycle. The obese consumed nearly twice as much food as the lean during the light period of the cycle. At 4-hour intervals, rats were killed and liver and epididymal fat pads were removed for metabolic studies. Adipose tissue from lean rats demonstrated marked changes in rates of lipogenesis during the 24-hour cycle whereas adipose tissue from obese rats maintained a relatively steady rate of lipogenesis. Glucose incorporation into the glycerol moiety of triacylglycerol was nearly 3-fold higher in adipose tissue from obese rats. Liver lipogenesis in lean and obese rats followed their food intake pattern. Liver lipogenic rate (expressed per organ) was 3- to 5-fold higher in obese than lean rats during most of the 24-hour cycle. These data support the concept that the excessive fatty acids produced in the liver of obese rats are being esterified by adipose cells. Lipolytic response to glucagon was found in adipose tissue from obese rats during the dark and light periods, but only during the dark period for lean rats. These data suggest, in comparison to lean rats, that obese rats do not enter a relative catabolic state during a 24-hour cycle. A constant anabolic state in the genetically prone individual may lead to excessive lipid deposition and obesity.
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PMID:Diurnal changes in adipose and liver tissue metabolism of lean and obese Zucker rats. 57 Oct 11


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