Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to investigate fat metabolism and the regulation of lipolysis and blood fuel metabolites by insulin, nine patients with chronic obstructive pulmonary disease (COPD) with chronic hypoxaemia and seven healthy control subjects of similar age were investigated by determination of the turnover rate of free fatty acids (TOR), using 1-14C-oleic acid as a tracer, and arterial concentrations of FFA, glycerol and 3-hydroxybutyrate. The measurements were performed in the basal state and during insulin and glucose infusion, aiming at euglycaemia at insulin levels of 50 and 100 mU l-1. The subjects' ages were 64 +/- 2.7 and 66 +/- 1.1 (mean +/- SEM) years in the COPD and control groups, respectively. TOR was 0.73 +/- 0.06 and 0.52 +/- 0.02 mmol min-1 (P < 0.05) in the basal state, 0.33 +/- 0.04 and 0.30 +/- 0.02 at an insulin level of 50 mU l-1 and 0.32 +/- 0.08 and 0.24 +/- 0.02 at an insulin level of 100 mU l-1, in the COPD and control groups, respectively. Arterial FFA concentration was 0.98 +/- 0.08 and 0.75 +/- 0.06 mmol l-1 (P < 0.05) in the basal state in the COPD and control groups, respectively. During the clamp, the decrease in FFA mirrored that in TOR. The results show that the state of lipolysis is increased in severe COPD patients with chronic hypoxaemia. Furthermore, the results suggest a reduced effect of insulin in lipolysis.
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PMID:Fat metabolism and its response to infusion of insulin and glucose in patients with advanced chronic obstructive pulmonary disease. 755 66

Lactate and glycerol turnover is enhanced in obesity and NIDDM. To evaluate the influence of NIDDM on subcutaneous adipose tissue metabolism microdialysis combined with 133Xe clearance and measurements in arterialized plasma were carried out using samples of subcutaneous abdominal fat from nine obese NIDDM subjects (glucose, 7.9 +/- 0.7 mmol L-1) (mean +/- SEM) and nine obese non-diabetic subjects (glucose, 4.9 +/- 0.1) matched for age, BMI and body fat. After an overnight fast arterialized plasma levels were 1145 +/- 110 vs. 876 +/- 59 mumol L-1 (P < 0.05) for lactate and 75 +/- 10 vs. 66 +/- 8 mumol L-1 for glycerol in the diabetic and control group, respectively. The corresponding abdominal subcutaneous interstitial lactate and glycerol concentrations were 1278 +/- 63 vs 1107 +/- 64 mumol L-1 and 314 +/- 28 vs. 311 +/- 17 mumol L-1, respectively. However, adipose tissue blood flow in the same region was lower in NIDDM subjects (1.5 +/- 0.2 vs 2.4 +/- 0.3 mL 100 g-1 min-1) (P < 0.05). Consequently, apparent subcutaneous lactate and glycerol release, estimated according to Fick, were not statistically different in the two groups (1.8 +/- 0.4 vs 2.4 +/- 0.8 and 2.1 +/- 0.4 vs 3.1 +/- 0.5 mumol kg-1 min-1 in NIDDM and control subjects, respectively). Thus, in the post-absorptive state apparent lactate and glycerol release by the abdominal subcutaneous tissue in obese NIDDM subjects was similar to that in a matched group of obese non-diabetic controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Microdialysis assessment of adipose tissue metabolism in post-absorptive obese NIDDM subjects. 758 14

Alkaline phosphatase (AP) is required for the proper mineralization of cartilage and bone. The enzyme is localized to the outer surface of cells through a phosphatidylinositol-glycolipid anchor, which is covalently attached to the carboxyl terminus of the protein. In calcifying cartilage, AP-rich matrix vesicles (MVs) are released into the matrix from chondrocytes, and apatite formation is initiated within and around these particles. In this paper we examine the role of the AP glycolipid anchor using an in vitro mineralization assay system. AP was purified to homogeneity, and the purified enzyme was used to drive mineral formation in vitro with and without the anchor. Mineral formation was initiated through phosphate release from beta-glycerol phosphate (beta-GP). The amount of PO4(-3) released was similar whether the anchor was present or absent. However, SEM and X-ray microanalysis revealed that the mineral produced by anchored AP was indistinguishable from that produced by MVs and that both of those minerals were more apatite-like than mineral formed by soluble AP or through spontaneous precipitation. Taken together, the data suggest that in addition to providing PO4(-3) to drive mineralization, AP influences the nature of the mineral formed. Further, AP containing its glycolipid anchor produces mineral comparable with that formed by tissue-derived MVs. Thus, in the absence of extracellular matrix, MV mineralization in vitro can be emulated by glycolipid-anchor containing AP.
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PMID:The phosphatidylinositol-glycolipid anchor on alkaline phosphatase facilitates mineralization initiation in vitro. 761 Sep 27

1. Platelet-activating factor can be synthesized by two distinct biochemical pathways and is degraded by a number of enzymes, the first step of which is deacetylation by a specific acetyl hydrolase. 2. The biochemical pathway of platelet-activating factor synthesis de novo and the first step in platelet-activating factor degradation have been investigated for the first time in incubates of normal human colon mucosa and in inflamed mucosa from patients with inflammatory bowel disease. 3. In the presence of 100 mumol/l CDP-choline and 100 mumol/l hexadecyl acetyl glycerol, homogenates from inflamed mucosa synthesized significantly greater platelet-activating factor [851 +/- 574 pmol/mg of protein (mean +/- SEM) in 90 min incubation] than normal mucosa [105 +/- 61 pmol/mg of protein in 90 min incubation] (P < 0.05). 4. Under the same conditions of assay, the percentage turnover to inactive lyso-platelet-activating factor was similar in inflamed mucosa (35.5 +/- 9.4%) and normal mucosa (42.7 +/- 8.5%) in 90 min (P > 0.05). 5. The identity of platelet-activating factor was confirmed by HPLC, by its mobility on TLC and by the ability of WEB 2170, a selective platelet-activating factor receptor antagonist, to block its platelet-aggregatory action. 6. These findings confirm the presence of the pathway for the synthesis de novo of the potently proinflammatory platelet-activating factor in human colon mucosa in inflammatory bowel disease.
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PMID:Biosynthesis of platelet-activating factor in normal and inflamed human colon mucosa: evidence for the involvement of the pathway of platelet-activating factor synthesis de novo in inflammatory bowel disease. 763 57

The purpose of the present study was to compare the acute and delayed effects of low- and moderate-intensity exercise on serum lipoprotein concentrations. Twelve healthy volunteers (five men, seven women), aged 28 (2) years [mean (SEM)], maximal oxygen uptake (VO2max) 48 (3) ml.kg-1.min-1 walked on a treadmill for 90 min, on two separate occasions, in a balanced design. On one occasion walking was at a grade which elicited 32.1 (0.8)% of VO2max, i.e. low intensity, while on the other it elicited 60.1 (1.6)% of VO2max, i.e. moderate intensity (MI). Serum concentrations of total cholesterol (TC), triacylglycerol (TAG), high density lipoprotein cholesterol (HDL-C) and the subfraction HDL2-C free fatty acids (FFA) and free glycerol were measured in venous blood samples drawn before exercise (after a 12-h fast), during walking and after 1 h and 24 h of recovery. Serum TAG concentrations decreased as a result of the exercise bout over the period of observation (P < 0.05), but this decrease was not different between the two intensities. Changes in serum TC concentrations over time differed between trials (P < 0.05). Serum free glycerol and FFA concentrations increased during exercise bouts, these increases being (P < 0.05) greater with MI. The decrease in serum TAG concentrations during and after a single episode of either prolonged low or moderate intensity exercise may be associated with an increased clearance and/or a decreased secretion of TAG-rich lipoproteins.
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PMID:The influence of the intensity of treadmill walking upon changes in lipid and lipoprotein variables in healthy adults. 764 44

Type 2 diabetes is characterized by resistance to insulin action of glucose metabolism and lipolysis. First-degree relatives of diabetic patients are at increased risk of developing diabetes themselves and early metabolic abnormalities in these relatives may represent primary defects in the pathogenesis of diabetes. Our previous work has demonstrated impaired suppression of lipolysis after an oral glucose load in glucose-tolerant relatives of Asian origin, but not in European relatives. To investigate whether a more subtle defect exists in the European population we studied 8 first-degree relatives of European patients and 9 matched control subjects. All had normal glucose tolerance. Glycerol and glucose turnovers were measured using a primed constant infusion of the stable isotopic tracers [1,1,1,2,3(2)H5] glycerol and [6,6(2)H] glucose, basally and in response to a very low dose insulin infusion (0.005 units kg-1 h-1). The relatives had higher basal insulin concentrations (median (range): 49 (30 to 113) vs 28 (18 to 66) pmol 1(-1), p < 0.05) compared to controls, but basal glycerol and glucose turnovers and plasma concentrations of glycerol, glucose, and non-esterifed fatty acids (NEFA) were similar. Following insulin, the suppression of glycerol appearance in the circulation measured isotopically was significantly less complete in the relatives compared with controls (mean change +/- SEM: + 0.06 +/- 0.21 vs - 0.51 +/- 0.16 mumol kg-1 min-1, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin resistance with respect to lipolysis in non-diabetic relatives of European patients with type 2 diabetes. 771 8

The aim of this study was to compare the effects of drinking two carbohydrate (CHO) electrolyte solutions and water on marathon running performance. Seven endurance-trained runners completed three 42.2-km treadmill time-trials which were randomly assigned and 4 weeks apart. On each occasion the subjects ingested 3 ml.Kg-1 body weight of either water (W), a 6.9% CHO solution (O) or a 5.5% CHO solution (L) immediately prior to the start of the run and 2 ml.kg-1 body weight every 5 km thereafter. The total volume of fluid ingested [mean (SEM)] was 1112 (42), 1116 (44) and 1100 (44) ml, respectively. Running times for W, O and L trials were 193.9 (5.0), 192.4 (3.3) and 190.0 (3.9) min, respectively. Performance time for the L trial was faster (P < 0.05) compared with that of the W trial. Running speed was maintained in the L trial, whereas it decreased after 10 km (P < 0.05) in the W and after 25 km (P < 0.05) in the O trial. Blood glucose and lactate, and hormonal responses to fluid ingestion were similar in all three trials. Higher plasma free fatty acid and glycerol concentrations were observed at the end of the W trial compared with those obtained after the O and L trials, respectively (P < 0.05). Plasma ammonia concentration was higher (P < 0.01) at the end of the L trial compared with the W trial. Plasma creatine kinase concentration was higher (P < 0.05) 24 h after the completion of the L trial than after the W trial.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of carbohydrate-electrolyte drinks on marathon running performance. 776 38

Cryopreservation of sperm from transgenic mice would make possible the economical perpetuation of these genetic models. In order to design a protocol for this process, it was first necessary to determine the hydraulic conductivity, Lp, or water permeability, of the plasma membrane as a function of temperature to calculate its activation energy, Ea. This was done with sperm from the caudae epididymides of CD-1 mice, using the hyposmotic cell lysis method, in which the critical osmolality, Osmcrit, defined as the osmolality at which 50% of the cells lyse, was first determined, and then the time, t, to lysis of 50% of the cells in a medium of Osm < Osmcrit was obtained. Values (mean +/- SEM, n = 10) of Osmcrit at 37, 22, 4, and 0 degrees C were 32.1 +/- 2.7, 33.7 +/- 4.1, 30.8 +/- 3.4, and 101.0 +/- 10.8 mOsm, and of t in 17 mOsm medium were 40.6 +/- 2.4, 33.8 +/- 5.7, 25.0 +/- 4.4, and 4.7 +/- 1.2 s, respectively. Values of Lp were calculated from Osmcrit and t by two different algorithms, one based on the high-amplitude swelling model used with sperm from other mammalian species and the other based on a low-amplitude swelling model. Values of Lp in micron.min-1.atm-1 from the high-amplitude swelling model at 37, 22, 4, and 0 degrees C were 1.41 +/- 0.08, 1.88 +/- 0.35, 2.12 +/- 0.19, and 1.13 +/- 0.1, respectively. From the low-amplitude swelling model, the Lp values were 0.025 +/- 0.001, 0.040 +/- 0.008, 0.082 +/- 0.029, and 1.66 +/- 0.23. Examination of mouse sperm in hyposmotic media by microscopy revealed little swelling of the cells, indicating that the low-amplitude swelling model may be the one more applicable to these cells. The temperature dependence, and hence Ea, of Lp shows a marked discontinuity between 4 and 0 degrees C with values calculated from either model. This suggests a membrane phase transition to a more brittle structure in this temperature range, consistent with the observed marked increase in Osmcrit (P < 0.0003) and decrease in t (P < 0.0001) at 0 degrees C compared to the other temperatures. In the presence of 1 M glycerol, there was no discontinuity between 4 and 0 degrees C in the values of Osmcrit, consistent with the ability of glycerol to fluidize the membrane. Low hydraulic conductivity and low-temperature embrittlement of the plasma membrane are proposed as two factors leading to mouse sperm hypersensitivity to cryodamage.
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PMID:The temperature dependence in the hydraulic conductivity, Lp, of the mouse sperm plasma membrane shows a discontinuity between 4 and 0 degrees C. 778 26

A new isotope dilution mass spectrometric method for total glycerides and triglycerides in human serum is described. Total glycerides are defined as the sum of tri-, di-, and monoglycerides plus free glycerol; triglycerides are defined as the pure triglyceride species. In both determinations, serum samples are supplemented by addition of [13C3]tripalmitin, processed, derivatized, and the abundance ratios of selected ions are determined. Bias is investigated by quantifying the analyte in the same samples under different chromatographic and ionization conditions. The analytes were determined in two human serum pools. The CV for a single measurement ranged from 0.35% to 0.72%, and the relative SEM ranged from 0.10% to 0.34%; there was no significant bias in the measurements. The combination of high precision and absence of significant bias in the results qualify this method for consideration as a Definitive Method as defined by the National Committee for Clinical Laboratory Standards.
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PMID:Isotope dilution mass spectrometry as a candidate definitive method for determining total glycerides and triglycerides in serum. 788 15

Previous studies have demonstrated that prostaglandin E2 (PGE2) inhibits arginine vasopressin-(AVP)dependent adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in microdissected rat outer medullary collecting tubules (OMCD), by a mechanism unrelated to the inhibition of cAMP synthesis. The potential role of the activation of protein kinase C (PKC) to explain the negative regulation elicited by PGE2 was investigated in this study. Single OMCD samples were pre-incubated (10 min, 30 degrees C) in the presence or absence of either activators of PKC, phorbol 12-myristate 13-acetate (PMA), 1-oleoyl-2-acetyl-glycerol (OAG), dioctanoylglycerol (DOG) or an inhibitor of PKC, staurosporine (SSP). These compounds were present also with the agonists tested during the incubation period (4 min, 35 degrees C). In contrast to PGE2, activators of PKC did not decrease AVP-dependent cAMP accumulation (mean +/- SEM): 1 nM AVP = 47.1 +/- 6.8 fmol.mm-1 x 4 min-1; AVP+0.3 microM PGE2 = 20.1 +/- 2.7, P < 0.01 versus AVP; AVP + 10 nM PMA = 42.0 +/- 4.7, NS versus AVP; AVP + 50 micrograms/ml OAG = 44.1 +/- 4.8. NS versus AVP, N = 5 experiments. However, 10 nM PMA prevented PGE2-induced inhibition: AVP + PGE2 = 44.2 +/- 3.5% of the response to AVP and 90.3 +/- 3.2% without and with PMA respectively, N = 16. Similar results were obtained with either 50 micrograms/ml OAG or 25 micrograms/ml DOG (AVP + PGE2 + OAG = 92.9 +/- 6.6% of the response to AVP, N = 8; AVP + PGE2 + DOG = 94.1 +/- 5.3%, N = 7).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The activation of protein kinase C prevents PGE2-induced inhibition of AVP-dependent cAMP accumulation in the rat outer medullary collecting tubule. 790 84


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