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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism for the increased glucose transport response to insulin in adipose cells from chronically hyperinsulinemic rats was examined. Rats were infused with insulin s.c. for 2 wk. Isolated adipose cells were incubated with and without insulin, 3-O-methylglucose transport was measured, and glucose transporters in subcellular membrane fractions were assessed by cytochalasin B binding. Adipose cells from insulin-treated rats showed no change in basal but a 55% increase in insulin-stimulated glucose transport activity compared with those from control rats (7.1 +/- 0.8 vs. 4.6 +/- 0.5 fmol/cell per min, mean +/- SEM) and a corresponding increase in the concentration of glucose transporters in the plasma membranes (44 +/- 5 vs. 32 +/- 6 pmol/mg of membrane protein). In the low-density microsomes, glucose transporter concentrations in both basal and insulin-stimulated states were the same, but the total numbers were greater in cells from the insulin-treated rats because of a 39% increase in low-density microsomal protein. Therefore, chronic experimental hyperinsulinemia in the rat enhances the stimulatory action of insulin on glucose transport in the adipose cell by increasing the concentration of glucose transporters in the plasma membranes. This results from an enlarged intracellular pool due to increased intracellular protein and enhanced glucose transporter translocation in response to insulin.
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PMID:Mechanism for enhanced glucose transport response to insulin in adipose cells from chronically hyperinsulinemic rats. Increased translocation of glucose transporters from an enlarged intracellular pool. 302 79

The glucuronyl transferase activity was measured with 1-naphthol as a substrate in nuclear and microsomal fractions of the human intestinal mucosa. The mucosa was obtained from different parts of the intestine. The rate of 1-naphthol glucuronidation ranged between 0.70 and 1.26 nmol/mg/min (nuclear fraction) and 0.21 and 0.54 nmol/mg/min (microsomal fraction). The average (+/- SEM) of the nuclear/microsomal ratios of the glucuronyl transferase was 2.48 +/- 0.19. The epoxide hydrolase activity towards styrene oxide was measured in the same subcellular fractions; it was undetectable in the nuclear fraction, whereas it was 0.46 +/- 0.04 nmol/mg/min (mean +/- SEM) in the microsomal fraction. The glucuronyl transferase activity was also measured in nuclear and microsomal fractions of the human liver. The activity (mean +/- SEM) was 1.14 +/- 0.21 nmol/mg/min (nuclei) and 5.00 +/- 0.80 (microsomes). The average of the nuclear to microsomal ratios (mean +/- SEM) was 0.32 +/- 0.03.
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PMID:Glucuronidation of 1-naphthol in nuclear and microsomal fractions of the human intestine. 309 May 69

Osmotic water permeability of the apical membrane of toad urinary epithelium is increased greatly by vasopressin (VP) and is associated with exocytic addition of granules and aggrephores at the apical surface. To determine the physiological role of granule exocytosis, we measured the osmotic water permeability and membrane fluidity of isolated granules, surface membranes and microsomes prepared from toad bladder in the presence and absence of VP. Pf was measured by stopped-flow light scattering and membrane fluidity was examined by diphenylhexatriene (DPH) fluorescence anisotropy. In response to a 75 mM inward sucrose gradient, granule size decreased with a single exponential time constant of 2.3 +/- 0.1 sec (SEM, seven preparations, 23 degrees C), corresponding to a Pf of 5 x 10(-4) cm/sec; the activation energy (Ea) for Pf was 17.6 +/- 0.8 kcal/mole. Under the same conditions, the volume of surface membrane vesicles decreased biexponentially with time constants of 0.13 and 1.9 sec; the fast component comprised approximately 70% of the signal. Granule, surface membrane and microsome time constants were unaffected by VP. However, in surface membranes, there was a small decrease (6 +/- 2%) in the fraction of surface membranes with fast time constant. DPH anisotropies were 0.253 (granules), 0.224 (surface membranes) and 0.190 (microsomes), and were unaffected by VP. We conclude: (1) granules have among the lowest water permeabilities of biological membranes, (2) granule water permeability is not altered by bladder pretreatment with VP, (3) granule membrane fluidity is remarkably lower than that of surface and microsomal membranes, and (4) rapid water transport occurs in surface membrane vesicles. The unique physical properties of the granule suggests that apical exocytic addition of granule membrane may be responsible for the low water permeability of the unstimulated apical membrane.
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PMID:Very low osmotic water permeability and membrane fluidity in isolated toad bladder granules. 314 39

The influence of ranitidine on the pharmacokinetics and toxicity of doxorubicin was studied in six female New Zealand white rabbits. Plasma pharmacokinetic data were first obtained from rabbits given 3 mg/kg doxorubicin. After 1 month, the same rabbits were treated with ranitidine, 2.5 mg/kg or 25 mg/kg, before and during doxorubicin administration. The plasma doxorubicin assays to determine pharmacokinetic parameters were repeated. Drug toxicity was evaluated using complete blood counts, and hepatic function was measured using a 14C-aminopyrine breath test. High-dose ranitidine increased the total exposure to doxorubicin (area under the curve of doxorubicin alone = 1.44 +/- 0.88 microM.h/ml vs 4.49 +/- 2.35 microM.hr/ml for doxorubicin given with high-dose ranitidine; P = 0.06). Low-dose ranitidine did not alter doxorubicin pharmacokinetics. Exposure to doxorubicinol was altered by either high-dose or low-dose ranitidine. 14C-Aminopyrine half-life was altered by a ranitidine dose of 25 mg/kg (aminopyrine half-life after placebo control = 97 +/- 6 min as against aminopyrine half-life after ranitidine = 121 +/- 7 min; mean +/- SEM; P less than 0.02). Low-dose ranitidine did not exacerbate doxorubicin-induced myelosuppression. High-dose ranitidine enhanced doxorubicin-induced erythroid suppression while sparing the myeloid series. At cytochrome P-450-inhibitory doses, ranitidine's effects upon doxorubicin plasma pharmacokinetics are similar to those previously seen with cimetidine. These changes did not appear to alter drug detoxification and are not related to microsomal inhibition of doxorubicin detoxification. Low doses of ranitidine do not alter doxorubicin plasma pharmacokinetics or toxicity in rabbits.
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PMID:The influence of ranitidine on the pharmacokinetics and toxicity of doxorubicin in rabbits. 337 Jul 41

The effects of fasting and refeeding on the glucose transport response to insulin in isolated rat adipose cells have been examined using 3-O-methylglucose transport in intact cells and cytochalasin B binding and Western blotting in subcellular membrane fractions. After a 72-h fast, basal glucose transport activity decreases slightly and insulin-stimulated activity decreases greater than 85%. Following 48 h of fasting, insulin-stimulated glucose transport activity is diminished from 3.9 +/- 0.5 to 1.3 +/- 0.3 fmol/cell per min (mean +/- SEM). Similarly, the concentrations of glucose transporters are reduced with fasting in both the plasma membranes from insulin-stimulated cells from 38 +/- 5 to 18 +/- 3 pmol/mg of membrane protein and the low density microsomes from basal cells from 68 +/- 8 to 34 +/- 9 pmol/mg of membrane protein. Ad lib. refeeding for 6 d after a 48-h fast results in up to twofold greater maximally insulin-stimulated glucose transport activity compared with the control level (7.1 +/- 0.4 vs. 4.5 +/- 0.2 fmol/cell per min), before returning to baseline at 10 d. However, the corresponding concentration of glucose transporters in the plasma membranes is restored only to the control level (45 +/- 5 vs. 50 +/- 5 pmol/mg of membrane protein). Although the concentration of glucose transporters in the low density microsomes of basal cells remains decreased, the total number is restored to the control level due to an increase in low density microsomal protein. Thus, the insulin-resistant glucose transport in adipose cells from fasted rats can be explained by a decreased translocation of glucose transporters to the plasma membrane due to a depleted intracellular pool. In contrast, the insulin hyperresponsive glucose transport observed with refeeding appears to result from (a) a restored translocation of glucose transporters to the plasma membrane from a repleted intracellular pool and (b) enhanced plasma membrane glucose transporter intrinsic activity.
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PMID:Divergent mechanisms for the insulin resistant and hyperresponsive glucose transport in adipose cells from fasted and refed rats. Alterations in both glucose transporter number and intrinsic activity. 340 23

Estrogen 16 alpha-hydroxylase activity was measured in microsomes prepared from fetal tissues of first and second trimester human abortuses using [16 alpha-3H]estrone sulfate as substrate and NADPH as cofactor. Estrogen 16 alpha-hydroxylase activity was demonstrable in 13 of 14 fetal tissues examined in this study, viz. liver, adrenal fetal zone, adrenal neocortex, lung, kidney, intestine, heart, brain, skin, testis, spleen, pancreas, and stomach, and was either negligible or absent in placental tissue. The highest specific activity of the microsomal enzyme [pico-moles of product(s) formed per mg protein/h] was found in liver (mean +/- SEM, 338 +/- 62), and the next highest was found in the fetal zone of the adrenal cortex (70 +/- 20). The specific activities of estrogen 16 alpha-hydroxylase in adrenal neocortex, brain, skin, and testis were similar (25-53 pmol/mg protein X h) as were those in lung, kidney, intestine, heart, spleen and stomach (23-36 pmol/mg protein X h). The specific activity of the enzyme in the pancreas was 12 pmol/mg protein X h; the lowest specific activity, however, was in placental microsomes (0.2 +/- 0.1 pmol/mg protein X h).
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PMID:Estrogen 16 alpha-hydroxylase activity in human fetal tissues. 372 30

Antibody-dependent cell-mediated cytotoxicity (ADCC) is the process by which antibodies interact with killer cells to effect cell lysis, whereas natural killing (NK) refers to the ability of peripheral blood killer cells to lyse target cells in the absence of specific antibody. The purpose of the present study was to determine if either NK cells or ADCC might play a role in the development of Hashimoto's thyroiditis (HD) by testing the ability of killer cells to cause lysis of K562 erythroleukemia tumor cells and human thyrocytes in the presence and absence of serum from normal and HD patients. Using K562 target cells, NK activity was 70 +/- 4% (mean +/- SEM) for HD effector cells and 66 +/- 5% for normal effector cells at an effector to target ratio of 100:1. Similarly, with thyrocytes as targets, effector cells from HD patients (38 +/- 3%) and normal subjects (34 +/- 5%) caused comparable lysis (at an effector to target ratio of 100:1). Using K562 target cells, ADCC was 35% when effector cells from HD or normal subjects were coincubated with either normal or HD sera. Using thyrocyte target cells, lysis was about 25-30%, but, again, no differences were found between HD and normal effector cells or serum. There was a significant correlation between lysis for K562 and thyrocyte target cells, but there was no significant correlation between the titer of serum antithyroid microsomal antibodies and specific lysis. Intrathyroidal lymphocytes and peripheral lymphocytes from one patient with HD caused comparable lysis of labeled thyrocyte targets, as did normal peripheral lymphocytes. We conclude that ADCC and NK activities in peripheral lymphocytes were normal in HD patients and, therefore, may not have a primary role in mediating thyrocyte destruction in Hashimoto's thyroiditis.
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PMID:Killer cell activity and antibody-dependent cell-mediated cytotoxicity are normal in Hashimoto's disease. 375 62

The present work describes an accurate assay of the rate-limiting enzyme in bile acid synthesis, the cholesterol 7 alpha-hydroxylase, in human liver. The assay is based on isotope dilution-mass spectrometry, and endogenous microsomal cholesterol is used as the only substrate for the enzyme. Operative liver biopsies were obtained from patients undergoing elective cholecystectomy under highly standardized conditions. In ten gallstone patients, the enzyme activity of the microsomal fraction averaged 9.6 +/- 1.4 (mean +/- SEM) pmol X min-1 X mg protein-1 corresponding to a daily synthesis of about 0.5 mmol of bile acids. Three cholestyramine-treated patients displayed a four-fold higher enzyme activity. No evidence was obtained supporting the concept that the cholesterol 7 alpha-hydroxylase is modulated by phosphorylation-dephosphorylation.
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PMID:Bile acid synthesis in man: assay of hepatic microsomal cholesterol 7 alpha-hydroxylase activity by isotope dilution-mass spectrometry. 395 15

Studies were undertaken to determine if cholestasis in alcoholic or viral hepatitis is related to immunologic hyperreactivity as suggested for cholestasis due to type-II drug-induced hepatitis, and evaluate possible mechanisms involved in lymphokine-induced cholestasis. Results indicate that a cholestatic factor exists in alcoholic and acute viral hepatitis. Supernatants of lymphocytes from patients with alcoholic hepatitis stimulated by an extract of alcoholic hyalin evoked a 28% +/- 7.3 SEM reduction in rat bile flow (P less than 0.03). Supernatants of lymphocytes from patients with acute viral hepatitis activated by liver-specific protein caused a reduction in rat bile flow of 24% +/- 5.9 SEM (P less than 0.03). A decrease in bile flow also occurred following injections of sera from patients with alcoholic or acute viral hepatitis. In contrast, injection of supernatants of non-stimulated lymphocytes or those from chronic active hepatitis or healthy subjects did not produce a significant change in bile flow. Supernatants of stimulated lymphocytes from tuberculin-sensitized guinea pigs caused a similar decrease in rat bile flow and reduced excretion of human secretory immunoglobulin A (IgA). Despite reductions in rat bile flow there were no alterations in liver morphology, liver plasma membrane Na-K-ATPase activity, microsomal cholesterol-7 alpha-hydroxylase activity or low-dose indocyanine green clearance during the period of observation.
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PMID:Studies of the influence of immunological and serological factors from patients with cholestasis due to alcoholic or viral hepatitis on biliary function in the rat. 609 1

Iodized oil (1 ml im) was given to 58 goitrous patients from a mildly iodine-deficient area in Greece. Goiter size, urinary iodine, and serum T4, T3RU, T3, rT3, TSH, thyroxine-binding globulin (TBG), and thyroid autoantibodies were measured before and 1, 3, and 6 months after the injection. Goiter size decreased. Serum T4 remained relatively constant, but TBG decreased and therefore T3RU and FTI increased. Serum T3 and rT3 initially decreased (P less than 0.001) and then increased at the sixth month (P less than 0.001), both showing roughly parallel changes. Serum TSH, initially normal (1.42 +/- 0.11 (SEM) mU/liter), decreased to 0.65 +/- 0.01 and 0.76 +/- 0.05 mU/liter at the third and sixth month (difference from baseline P less than 0.001). Thyroid autoantibodies, both against thyroglobulin and the microsomal antigen, were undetectable before treatment, but became positive in 42.8% of the patients 3 and 6 months later. Three patients developed transient hyperthyroidism. This occurred 3 or 6 months after treatment, and was associated with high titers of thyroid autoantibodies. These results indicate that: 1) transient hyperthyroidism may occur after the administration of iodized oil, possibly because of thyroid tissue necrosis and leakage of hormones, and 2) serum TBG decreases after iodized oil, a finding not previously reported and one whose cause is not known.
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PMID:Thyroid hormone and immunological studies in endemic goiter. 630 89


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