PubMed Health⌕ Search

Biomedical subjects

J H Youn

Publications and source records attributed to J H Youn.

At least 19 recordsLinked to original sources
PubMed1992

Glucose transporters and maximal transport are increased in endurance-trained rat soleus.

Voluntary wheel running induces an increase in the concentration of the regulatable glucose transporter (GLUT4) in rat plantaris muscle but not in soleus muscle (K. J. Rodnick, J. O. Holloszy, C. E. Mondon, and D. E. James. Diabetes 39: 1425-1429, 1990). Wheel running also causes hypertrophy of the soleus in rats. This study was undertaken to ascertain whether endurance training that induces enzymatic adaptations but no hypertrophy results in an increase in the concentration of GLUT4 protein in rat soleus (slow-twitch red) muscle and, if it does, to determine whether there is a concomitant increase in maximal glucose transport activity. Female rats were trained by treadmill running at 25 m/min up a 15% grade, 90 min/day, 6 days/wk for 3 wk. This training program induced increases of 52% in citrate synthase activity, 66% in hexokinase activity, and 47% in immunoreactive GLUT4 protein concentration in soleus muscles without causing hypertrophy. Glucose transport activity stimulated maximally with insulin plus contractile activity was increased to roughly the same extent (44%) as GLUT4 protein content in soleus muscle by the treadmill exercise training. In a second set of experiments, we examined whether a swim-training program increases glucose transport activity in the soleus in the presence of a maximally effective concentration of insulin. The swimming program induced a 44% increase in immunoreactive GLUT4 protein concentration. Glucose transport activity maximally stimulated with insulin was 62% greater in soleus muscle of the swimmers than in untrained controls. Training did not alter the basal rate of 2-deoxyglucose uptake.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Enhanced glucose tolerance in spontaneously hypertensive rats. Pancreatic beta-cell hyperfunction with normal insulin sensitivity.

We used intravenous glucose tolerance tests in vivo and 3-O-methylglucose transport into skeletal muscle in vitro to assess glucose tolerance, pancreatic beta-cell function, and insulin action in 9- to 11-wk-old spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar Kyoto rats (WKY). Body weight was slightly higher in the WKY (P less than 0.001), while blood pressure was elevated in the SHR (P less than 0.001). Insulin responses to intravenous glucose after 4 or 12 h of fasting in SHR were 2-3 times the responses of WKY rats (P less than 0.001). The greater insulin responses in SHR were associated with accelerated glucose disappearance P less than 0.001 vs. WKY rats). A direct correlation (r = 0.49, P less than 0.05) between the peak plasma insulin responses to glucose and Kg values in SHR suggested that the exaggerated insulin responses contributed to the accelerated glucose disappearance in that group. 3-O-methylglucose transport rates into epitrochlearis muscles in vitro did not differ significantly between SHR and WKY groups in the absence of insulin (P less than 0.2) or in the presence of insulin at physiological (600 pM, P greater than 0.4) or pharmacological (120,000 pM, P greater than 0.9) concentrations. Thus, compared with WKY rats, SHR had exaggerated insulin responses to glucose, similar insulin-mediated glucose transport into skeletal muscle, and enhanced glucose tolerance. Our findings indicate that young, hypertensive SHR have hyperfunction of pancreatic beta-cells that is unrelated to insulin resistance. The resultant nutrient-stimulated hyperinsulinemia could play a role in the development or maintenance of elevated blood pressure in SHR.

3-O-Methylglucose↗
PubMed1992

Detection of antibodies in serum and cerebrospinal fluid to Toxoplasma gondii by indirect latex agglutination test and enzyme-linked immunosorbent assay.

Sensitivity of anti-Toxoplasma antibody (IgG) test by enzyme-linked immunosorbent assay (ELISA) was evaluated in comparison with indirect latex agglutination (ILA) using 2,016 paired human samples of serum and cerebrospinal fluid (CSF). The samples were collected from neurologic patients in Korea with mass lesions in central nervous system (CNS) as revealed by imaging diagnosis (CT/MRI). When the sera were screened for anti-Toxoplasma antibody by ILA, 76 cases(3.8%) were positive (1:32 or higher titers). In the paired samples of CSF, no positive reactions were observed. When ELISA was performed using PBS extract of Percoll purified tachyzoites as antigen, cut-off absorbance was determined as 0.40 for serum and 0.27 for CSF tests. The antibody positive rates by ELISA were 7.0% in serum and 5.6% in CSF. Of them, 40 cases (2.0%) showed positive reactions in both serum and CSF. The antibody positive rates were higher in groups older than 40 years. The rates were higher in male (4.7% by ILA, 8.3% by ELISA) than in female (2.2% by ILA, 5.0% by ELISA). The rates in CSF showed no such sex difference. ELISA showed twice higher positive rates when serum was tested, and was sensitive enough to detect specific antibodies in CSF. Etiologic relations between positive antibody tests and CNS lesions remained unknown.

Age Factors↗
PubMed1991

Prolonged incubation of skeletal muscle increases system A amino acid transport.

During the course of experiments involving prolonged incubation of skeletal muscle, we observed large increases in system A amino acid transport activity. System A activity was monitored with the nonmetabolizable amino acid analogue alpha-(methylamino)isobutyrate (MeAIB). When rat epitrochlearis muscles are incubated in Krebs-Henseleit buffer supplemented with 0.1% bovine serum albumin and 8 mM glucose, basal MeAIB transport doubles after 5 h and is elevated approximately sevenfold after 9 h compared with rates measured in muscles incubated for 1 h. Insulin-stimulated transport also doubles after 5 h and increases by fourfold after 9 h. The increases in basal and insulin-stimulated system A transport over time can be prevented by incubating muscles in the presence of cycloheximide. Addition of minimum essential medium essential amino acids (EAA) to the incubation medium blocks the increase in basal and insulin-stimulated MeAIB transport measured after 9 h by 85-90 and 60%, respectively. A single amino acid, glutamine, can account for half of the inhibitory effect of EAA on the time-dependent increase in basal system A transport. Amino acid metabolism is not necessary for inhibition of the rise in basal MeAIB transport. At concentrations normally present in minimum essential medium, nonessential amino acids are less effective (51% inhibition) in preventing the rise in basal transport occurring over 9 h. At three times normal concentrations, however, the ability of nonessential amino acids to prevent the time-dependent increases in basal and insulin-stimulated MeAIB transport is comparable to that of EAA. These changes in MeAIB transport with prolonged incubation are not due to muscle deterioration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1991

Calcium stimulates glucose transport in skeletal muscle by a pathway independent of contraction.

In this study we investigated the possibility that an increase in cytoplasmic Ca2+ concentration that is too low to cause muscle contraction can induce an increase in glucose transport activity in skeletal muscle. The compound N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), which induces Ca2+ release from the sarcoplasmic reticulum (SR), caused a dose-dependent increase in tension in rat epitrochlearis muscles at concentrations more than approximately 200 microM. Although 100 microM W-7 did not increase muscle tension, it accelerated loss of preloaded 45Ca2+. Glucose transport activity, measured with the nonmetabolizable glucose analogue 3-O-methylglucose, increased sixfold in muscles treated for 100 min with 50 microM W-7 (P less than 0.001) and eightfold in response to 100 microM W-7 (P less than 0.001). The increase in glucose transport activity was completely blocked with 25 microM cytochalasin B. There was no decrease in ATP or creatine phosphate concentrations ([approximately P]) in muscles incubated with 50 microM W-7. Dantrolene (25 microM), which blocks Ca2+ release from the SR, blocked the effects of W-7 both on 45Ca2+ release and on glucose transport activity. 9-Aminoacridine, another inhibitor of Ca2+ release from the SR, also blocked the stimulation of hexose transport by W-7. Caffeine, a compound structurally unrelated to W-7 that also releases Ca2+ from the SR, also increased glucose transport activity. Incubation of muscles with 3 mM caffeine for 30 min, which did not cause contraction or lower [approximately P], induced a threefold increase in 3-O-methylglucose transport (P less than 0.001). These results provide evidence suggesting that an increase in cytoplasmic Ca2+ too low to cause contraction or [approximately P] depletion can bring about an increase in glucose transport activity in skeletal muscle.

3-O-Methylglucose↗
PubMed1991

Conversion of oral glucose to lactate in dogs. Primary site and relative contribution to blood lactate.

We evaluated the relative contribution of oral glucose to arterial lactate and the relative role of the splanchnic bed in converting glucose to lactate in normal healthy dogs. After an oral glucose load (1.2 g/kg) spiked with [U-14C]glucose (16.9 muCi/kg; protocol 1, n = 7), arterial blood lactate increased from 0.43 +/- 0.03 mM at basal to a peak of 1.04 +/- 0.07 mM at 45 min and then slowly decreased to 0.47 +/- 0.07 mM at 240 min. Arterial blood [14C]lactate peaked at 60 min and then decreased slowly to approximately 35% of the peak at 4 h. When arterial blood lactate peaked at 45 min, the proportion of arterial lactate that was derived from oral glucose was 34 +/- 3%. The integrated area under the curve of lactate derived from exogenous glucose was 40 +/- 2% of that of total lactate. The splanchnic bed released lactate and [14C]lactate during the initial 2 h after oral [14C]glucose. Thus, the splanchnic bed apparently contributed to the conversion of exogenous glucose to lactate. In the matched experiments (protocol 2, n = 5), dogs were given the same amount of oral glucose but no [14C]glucose, and [U-14C]lactate was infused into the right atrium to match the splanchnic [14C]lactate release from the first experiment. Despite a well-matched splanchnic [14C]lactate contribution, arterial concentrations of [14C]lactate were markedly lower in protocol 2 compared with protocol 1. The integrated area under the [14C]lactate profile in protocol 2 was only 11 +/- 1% of that in protocol 1. These results indicate that the splanchnic bed is responsible for only 11% of arterial blood lactate that was derived from oral glucose. We concluded that 1) after oral glucose loading, a major portion of circulating lactate has its origin not in exogenous glucose but in endogenous sources, and 2) the splanchnic bed is not the major site of oral glucose conversion to lactate after glucose ingestion.

Administration, Oral↗
PubMed1991

Cell cycle-dependent entry of Toxoplasma gondii into synchronized HL-60 cells.

The degree of attraction of Toxoplasma gondii to vertebrate cells varies with cell type and cell phase. Human promyelocytic leukemia cells, HL-60, were synchronized by double thymidine block method and co-cultured with Toxoplasma for 1 hr at each cell stage to investigate the cell cycle specific susceptibility of parasites to host cells. For 30 hr the average number of Toxoplasma that invaded was a little changed except at 3 hr from G1/S phase boundary which concurred with the peak point of DNA synthesis. At 3 hr which is a relatively short interval compared to whole S phase, modification of cells by parasitic invasion was most remarkable. The number of Toxoplasma that penetrated was increased to more than six times. The shape of the cells became sludgy and almost indiscernible by strong accessibility of parasites only for an hour of mid-S phase. The same fluctuation was also observed at the second peak of S phase but weakly. This suggests that there be surface molecules concerning with the attachment of Toxoplasma to the host cells, which is expressed at special point of S phase. Further studies on the specific protein or similar molecules related could be carried out using synchronized HL-60 cells.

Animals↗
PubMed1990

Enhancement of hepatic glycogen by gluconeogenic precursors: substrate flux or metabolic control?

After a meal or glucose load, most carbons of hepatic glycogen are derived from gluconeogenesis. In vitro, hepatic glycogen accumulation is sluggish with glucose alone but markedly enhanced in the presence of gluconeogenic substrates. These findings conflict with the classical view that glucose is the major precursor of hepatic glycogen and have been termed the "glucose paradox." In this review, we attempt to elucidate the central mechanism underlying the glucose paradox by critically examining the in vitro data of hepatic glycogen accumulation. Our analysis is inconsistent with the current hypothesis that glucose phosphorylation is rate limiting for hepatic glycogen accumulation from glucose and that gluconeogenesis enhances glycogen accumulation primarily by increasing substrate flux to the hepatic glucose 6-phosphate pool. Instead, our analysis leads us to the conclusion that the rate-limiting step is the net incorporation of glucose 6-phosphate into glycogen, which is synergistically facilitated with glucose and gluconeogenic substrates. Thus gluconeogenic substrates are involved in the regulation of key enzyme(s) of glycogen metabolism. In addition, in the livers from fasted rats there is substantial cycling through glycogen, and that suppression of glycogen degradation may be a major mechanism in the enhancement of glycogen accumulation by gluconeogenic substrates. Thus we propose a specific hypothesis of the role of gluconeogenic substrates in glycogen metabolism (i.e., inhibition of phosphorylase), which can be tested by future studies.

Animals↗
PubMed1990

The effect of cyclic AMP on the growth of Toxoplasma gondii in vitro.

To assess the role of cAMP on the growth and proliferation of Toxoplasma in HL-60 cells we tested the effect of exogenous cAMP and cAMP analogues to the co-culture system of Toxoplasma and HL-60 cells. cAMP, dbcAMP, and br-cAMP stimulated the growth of Toxoplasma at a specific concentration, i.e., 10(0) mM, 10(0) mM, and 10(-1) mM, respectively. There were differences in growth induction kinetics and in the rate of promotion. These results were further verified by treating the co-culture with adenylate cyclase activator, pNHppG, cAMP phosphodiesterase activators, imidazole and A23187, and cAMP phosphodiesterase inhibitors, IBMX, compound 48/80, and theophylline, separately. When the cytosolic cAMP levels increased by the reagents mentioned above, Toxoplasma in the cytoplasm of HL-60 cells stimulated to proliferate more rapidly with concentration-dependent modes compared to the control, and vice versa. It is suggested that some mechanisms are activated by the high levels of cAMP in the cytoplasm, which result in the stimulation of Toxoplasma proliferation.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1990

Effects of pyrimidine salvage inhibitors on uracil incorporation of Toxoplasma gondii.

Metabolic inhibitors which act in the process of pyrimidine salvage influenced on the uracil incorporation into nucleic acids of Toxoplasma. Inhibitors of dihydrofolate reductase, pyrimethamine and methotrexate, and inhibitors of thymidylate synthase, fluoro-uridine, fluoro-dUMP and fluoro-uracil, diminished isotopic uracil uptake in dose-dependent manners. Azauridine which suppresses de novo pyrimidine biosynthesis did not affect the salvage even in a relatively high dose. These results suggested that the activation of uracil salvage should be closely related with the function of TMP biosynthetic enzymes. The pattern of thymidine uptake had no differences between control HL-60 cells and Toxoplasma infected cells, which did not reflect the specific proliferation of Toxoplasma. It can be exploited to characterize the effects of various compounds related with the proliferation of Toxoplasma, especially its DNA synthesis.

Animals↗
PubMed1990

Tight junctional inhibition of entry of Toxoplasma gondii into MDCK cells.

Various conditions of cultures were performed to investigate the role of tight junctions formed between adjacent MDCK cells on the entry of Toxoplasma. When MDCK cells were cocultured with excess number of Toxoplasma at the seeding density of 1 x 10(5), 3 x 10(5), and 5 x 10(5) cells/ml for 4 days, the number of intracellular parasites decreased rapidly as the host cells reached saturation density, i.e., the formation of tight junctions. When the concentration of calcium in the media (1.8 mM in general) was shifted to 5 microM that resulted in the elimination of tight junction, the penetration of Toxoplasma increased about 2-fold (p less than 0.05) in the saturated culture, while that of non-saturated culture decreased by half. Trypsin-EDTA which was treated to conquer the tight junctions of saturated culture favored the entry of Toxoplasma about 2.5-fold (p less than 0.05) compared to the non-treated, while that of non-saturated culture decreased to about one fifth. It was suggested that the tight junctions of epithelial cells play a role as a barrier for the entry of Toxoplasma and Toxoplasma penetrate into host cells through membrane structure-specific, i.e., certain kind of receptors present on the basolateral rather than apical surface of MDCK cells.

Animals↗
PubMed1989

Glucose phosphorylation is not rate limiting for accumulation of glycogen from glucose in perfused livers from fasted rats.

Incorporation of Glc and Fru into glycogen was measured in perfused livers from 24-h fasted rats using [6-3H]Glc and [U-14C]Fru. For the initial 20 min, livers were perfused with low Glc (2 mM) to deplete hepatic glycogen and were perfused for the following 30 min with various combinations of Glc and Fru. With constant Fru (2 mM), increasing perfusate Glc increased the relative contribution of Glc carbons to glycogen (7.2 +/- 0.4, 34.9 +/- 2.8, and 59.1 +/- 2.7% at 2, 10, and 20 mM Glc, respectively; n = 5 for each). During perfusion with substrate levels seen during refeeding (10 mM Glc, 1.8 mumol/g/min gluconeogenic flux from 2 mM Fru), Fru provided 54.7 +/- 2.7% of the carbons for glycogen, while Glc provided only 34.9 +/- 2.8%, consistent with in vivo estimations. However, the estimated rate of Glc phosphorylation was at least 1.10 +/- 0.11 mumol/g/min, which exceeded by at least 4-fold the glycogen accumulation rate (0.28 +/- 0.04 mumol of glucose/g/min). The total rate of glucose 6-phosphate supply via Glc phosphorylation and gluconeogenesis (2.9 mumol/g/min) exceeded reported in vivo rates of glycogen accumulation during refeeding. Thus, in perfused livers of 24-h fasted rats there is an apparent redundancy in glucose 6-phosphate supply. These results suggest that the rate-limiting step for hepatic glycogen accumulation during refeeding is located between glucose 6-phosphate and glycogen, rather than at the step of Glc phosphorylation or in the gluconeogenic pathway.

Animals↗
PubMed1989

Characterization of proteases of Toxoplasma gondii.

The proteases of Toxoplasma gondii were purified partially and characterized for some biochemical properties including various chromatographic patterns, major catalytic classes, and conditions to promote the activity of these enzymes. When Toxoplasma extract was incubated with 3H-casein at various pH, peak hydrolysis of casein was observed at pH 6.0 and at pH 8.5. Proteases working at pH 6.0 and at pH 8.5 were purified partially by conventional methods of chromatographies of DE52 anion exchange, Sephadex G-200 gel permeation, and hydroxylapatite chromatography. Partially purified enzymes were tested by site-specific inhibitors and promotors. The protease working at pH 6.0 was inactivated by iodoacetamide with LD50 of 10(-3) M and promoted by dithiothreitol, while the protease working at pH 8.5 was inhibited by phenylmethylsulfonyl fluoride with LD50 of 10(-5) M and was promoted by ATP (excess ATP beyond 2 mM inhibited the activity reversely). The protease of pH 8.5 had the activity of ATPase which might exert the energy to its action. Therefore the former was referred to as a cysteinyl acid protease and the latter, ATP-dependent neutral serine protease.

Adenosine Triphosphate↗
PubMed1989

Toxoplasma antibody titers by indirect latex agglutination test in patients of Kangnam St. Mary's Hospital and Cheju Medical Center.

Total 2,829 persons consisted of 1,019 general patients and 1,030 asthma-suspected patients who visited Kangnam St. Mary's Hospital and 780 general patients who visited Cheju Medical Center were examined for the antibody titers of Toxoplasma by indirect latex agglutination (ILA) test. Nineteen out of 1,019(1.86%) cases in general patients group, 11 out of 1,030(1.07%) cases in asthma patients group, and 45 out of 780(5.77%) cases in Cheju patients group showed positive ILA titers. Concerned with the age and ILA positive cases, general and asthma patients expressed more cases at thirties to sixties while Cheju patients showed high incidence at children and adolescents in addition to the above mentioned ages. Frequencies of ILA positive titers were highest in 1:32 and 1:64, and some cases showed 1:2,048 or higher titers.

Adolescent↗
PubMed1989

Scanning electron microscopic observations of Thelazia callipaeda from human.

Four females and a male nematode isolated from 2 patients who visited eye clinics in Seoul were identified as Thelazia callipaeda and their ultrastructures were observed by scanning electron microscopy (SEM). General features of the worms were slender and attenuated at both ends. Vaginal opening was located at 0.27 mm from the anterior end, and in front of the esophago-intestinal junction. In the body cuticle transverse striations varied characteristically through the body. The number of cuticular transverse striations was 400-650/mm at head portion, 250/mm at middle portion and 300-350/mm at tail portion. The SEM observation of the mouth part of the females showed 6 cord-like cuticular thickenings in hexagonal arrangement and an amphid was observed. A lateral line, a vaginal opening, a pair of phasmids, and an anus were identified in the body portion. A pair of papillae and 6 cord-like cuticular thickenings were on the mouth part of the male. It was difficult to observe structures at the tail of the male except wrinkle-like structures. Most of the larvae isolated from the uterus of a female worm were sheathed and thus cuticular striations were not seen. Others were un-sheathed and revealed cuticular striations. The oval membrane which encysted sheathed larvae was also observed. These are the 18th and 19th record of human thelaziasis in Korea as the literature are concerned.

Animals↗
PubMed1988

Regulation of glycogen synthase in muscle and adipose tissue during fasting and refeeding.

Using immunoblot analysis, we examined the electrophoretic mobility of glycogen synthase from rat skeletal muscle and adipose tissue. Extracts from muscle freeze clamped in situ contained at least three forms of synthase with different electrophoretic mobilities. Extracts from adipose tissue also contained multiple forms but lacked the form with greatest mobility found in the muscle extracts. Phosphorylation at multiple sites of glycogen synthase is known to deactivate the enzyme and retard its electrophoretic mobility in sodium dodecyl sulfate gels. These results suggest that there is very little or no dephosphorylated glycogen synthase in adipose tissue and that phosphorylated forms of glycogen synthase synthesize adipose tissue glycogen. Relative to control, it is known that fasting decreases and refeeding increases glucose incorporation into glycogen in rat epididymal adipose tissue but not skeletal muscle incubated in vitro in the presence of insulin. Fasting did not change the electrophoretic pattern of muscle synthase but decreased the relative amount of adipose tissue forms with greater mobility. Refeeding increased above control the relative amount of adipose tissue synthase with greater mobility. These results indicate that changes in the phosphorylations that retard mobility contribute to the effects of fasting and refeeding on adipose tissue glycogen metabolism.

Adipose Tissue↗
PubMed1988

Response to deep hypoglycemia does not involve glucoreceptors in carotid perfused tissue.

In the present study we examined whether the magnified hormonal counter-regulatory response seen during deep hypoglycemia (40 mg/dl) could be attenuated by supplying the forebrain with glucose furnished through carotid infusion. Two protocols were performed in conscious dogs. In the first protocol we infused glucose bilaterally into the carotid circulation to produce a forebrain glycemia of 55 +/- 1 mg/dl (as reflected in the jugular vein), whereas systemic glycemia declined to 39 +/- 2 mg/dl. In the second protocol as a control we infused glucose into the systemic circulation at a rate matched to protocol 1 so that both systemic and jugular plasma glucose concentrations were equivalent to the systemic glucose concentrations in protocol 1 (jugular, 41 +/- 3 mg/dl; systemic, 40 +/- 2 mg/dl; P greater than 0.9). In spite of a substantial difference in forebrain glycemia (55 mg/dl compared with 41 mg/dl) there were no differences in the counter-regulatory responses of catecholamines or glucagon. In addition, through the use of radiolabeled microspheres, we defined the precise regions of the forebrain irrigated during bilateral intracarotid glucose infusions. The concentration of microspheres was high in the forebrain but very low in the hindbrain. Our results indicate that glucoreceptor cells in tissues perfused by carotid arteries may play a tautological role in the sympathetic response to hypoglycemia and imply that glucose-sensitive receptors must also be located elsewhere in the central nervous system or in the periphery.

Animals↗