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T Sugino

Publications and source records attributed to T Sugino.

At least 19 recordsLinked to original sources
PubMed2006

Mental fatigue-induced decrease in levels of several plasma amino acids.

To investigate the relation between plasma amino acid levels and mental fatigue, we measured the plasma concentrations of 20 amino acids in 9 healthy volunteers before and after a fatigue-inducing mental task session for 8 hr. As fatigue-inducing mental tasks, the subjects performed an advanced trail making test, a Japanese KANA pick up test, and a mirror drawing test. As a control, 8-hr relaxation session was performed in the same subjects at an interval of 4 weeks. Immediately after the fatigue session, the plasma levels of branched-chain amino acids, tyrosine, cysteine, methionine, lysine, and arginine were below those after a relaxation session. The values for other blood parameters including total protein, albumin, glucose, and total cholesterol did not show any differences between the 2 sessions. These results indicate that mental fatigue may be characterized by a decrease in the plasma level of these amino acids.

Adult↗
PubMed2006

Postprandial changes in plasma concentrations of growth hormone and ghrelin around weaning in the goat.

We measured and compared plasma levels of GH and ghrelin in response to feeding in 4-week-old (milk replacer-fed) and 13-week-old (alfalfa hay cube-fed) goats, in order to elucidate whether or not the postprandial regulation of these hormone levels changes around weaning. Furthermore, we examined the effects of suckling from the dam or intravenous glucose administration on both hormone and insulin levels in kids. In 4-week-old goats, feeding of a milk replacer diet significantly increased plasma GH levels without changing level of ghrelin. In contrast, in 13-week-old goats, feeding of hay cubes did not change the levels of either ghrelin or GH. Suckling of milk directly from the dams significantly increased the levels of GH and insulin, but not ghrelin, in kids. Finally, intravenous injection of glucose (0.625 mmol/kg BW) did not cause any significant increase in the levels of GH or ghrelin, despite a significant increase in the levels of insulin and glucose. From these results, we conclude that the regulatory system of the somatotropic axis is altered by weaning or weaning-associated processes, and that ghrelin levels may not be involved in this alteration in young goats.

Animals↗
PubMed2006

Ghrelin enhances glucose-induced insulin secretion in scheduled meal-fed sheep.

The purpose of this study was to investigate the effects of physiologic levels of ghrelin on insulin secretion and insulin sensitivity (glucose disposal) in scheduled fed-sheep, using the hyperglycemic clamp and hyperinsulinemic euglycemic clamp respectively. Twelve castrated Suffolk rams (69.8 +/- 0.6 kg) were conditioned to be fed alfalfa hay cubes (2% of body weight) once a day. Three hours after the feeding, synthetic ovine ghrelin was intravenously administered to the animals at a rate of 0.025 and 0.05 mug/kg body weight (BW) per min for 3 h. Concomitantly, the hyperglycemic clamp or the hyperinsulinemic euglycemic clamp was carried out. In the hyperglycemic clamp, a target glucose concentration was clamped at 100 mg/100 ml above the initial level. In the hyperinsulinemic euglycemic clamp, insulin was intravenously administered to the animals for 3 h at a rate of 2 mU/kg BW per min. Basal glucose concentrations (44+/- 1 mg/dl) were maintained by variably infusing 100 mg/dl glucose solution. In both clamps, plasma ghrelin concentrations were dose-dependently elevated and maintained at a constant level within the physiologic range. Ghrelin infusions induced a significant (ANOVA; P < 0.01) increase in plasma GH concentrations. In the hyperglycemic clamp, plasma insulin levels were increased by glucose infusion and were significantly (P < 0.05) greater in ghrelin-infused animals. In the hyperinsulinemic euglycemic clamp, glucose infusion rate, an index of insulin sensitivity, was not affected by ghrelin infusion. In conclusion, the present study has demonstrated for the first time that ghrelin enhances glucose-induced insulin secretion in the ruminant animal.

Animal Feed↗
PubMed2005

Role of nociceptin and opioid receptor like 1 on entrainment function in the rat suprachiasmatic nucleus.

The suprachiasmatic nucleus of the hypothalamus is the master circadian clock in mammals. Phase shifts in circadian locomotor activity occur when an animal is exposed to light during the subjective night. An endogenous ligand of opioid receptor like 1, nociceptin is reported to inhibit light-induced phase shifts in locomotor activity rhythm. However, little is known about the role of opioid receptor like 1 receptors in the entrainment. Therefore, we investigated the involvement opioid receptor like 1 and its endogenous ligand, intnociceptin, in the suprachiasmatic nucleus and in the entrainment of circadian rhythms in rats. In an in vitro experiment, glutamate (1 microM) -induced phase delay of suprachiasmatic nucleus neuronal activity rhythms was inhibited by nociceptin during the early subjective night. An opioid receptor like 1 antagonist, compound B (10 microM), induced a phase delay, and this effect was blocked by nociceptin (10 microM). Moreover, compound B (10 microM) potentiated the glutamate (1 microM) -induced phase delay. Fos expression in the suprachiasmatic nucleus of rats induced by photic stimulation (50 lux, 30 min) during the early subjective night was inhibited by treatment with nociceptin (0.5-10 nM, i.c.v.). The effect of nociceptin (10nM, i.c.v.) was blocked by pretreatment with compound B (30 mg/kg, i.p). In an in vivo experiment, nociceptin significantly inhibited a light-induced (300 lux, 1 h) phase delay of locomotor activity rhythms, and this effect was inhibited by Compound B. Compound B (30 mg/kg, i.p.) significantly potentiated the light-induced phase delay. Nociceptin induced a neuronal firing phase advance (in vitro) and locomotor activity rhythms (in vivo) in the daytime and this effect was blocked by Compound B. These results suggest that opioid receptor like 1 receptors have an inhibitory effect at night, and a facilitative effect in the day, on phase changes.

Action Potentials↗
PubMed2005

GH secretory responses to ghrelin and GHRH in growing and lactating dairy cattle.

Release of growth hormone (GH) is known to be regulated mainly by GH-releasing hormone (GHRH) and somatostatin (SRIF) secreted from the hypothalamus. A novel peripheral release-regulating hormone, ghrelin, was recently identified. In this study, differences of the GH secretory response to ghrelin and GHRH in growing and lactating dairy cattle were investigated and an alteration of plasma ghrelin levels was observed. The same amounts of ghrelin and GHRH (0.3 nmol/kg) were intravenously injected to suckling and weanling calves, early and mid-lactating cows and non-lactating cows. Plasma ghrelin levels were also determined in dairy cattle in various physiological conditions. The peak values of ghrelin-induced GH secretion were increased in early lactating cows compared to those in non-lactating cows. The relative responsiveness of GH secretion to ghrelin was also increased compared with that to GHRH in early lactating cows. GH secretory responses to GHRH were blunted in mature cows with and without lactation. Conversely, GHRH-induced GH secretory response was greater than that to ghrelin in calves, and also greater in calves than in mature cows. Plasma ghrelin concentrations were elevated in early lactating cows compared to those in non-lactating cows. Plasma GH concentrations were higher in suckling calves and early lactating cows compared with those in non-lactating cows. These results suggest that GHRH is an effective inducer of GH release in growing calves, and that the relative importance of ghrelin in contributing to the rise in plasma GH increases in early lactating cows.

Animals↗
PubMed2004

Effects of ghrelin on food intake and neuroendocrine function in sheep.

Ghrelin, a novel acylated peptide, is the endogenous ligand for growth hormone secretagogue (GHS) receptor. Ghrelin is produced mainly in the oxyntic glands of the stomach, but also produced in the intestines, kidneys, hypothalamus and pituitary gland. Circulating ghrelin levels have been shown to rise before a meal and fall afterwards, suggesting that anticipation of a meal may stimulate secretion. In some species, ghrelin administration has been shown to stimulate growth hormone (GH) secretion, and to cause weight gain by increasing food intake and reducing metabolic utilization of fat. Furthermore, intracerebroventricular and intravascular administration of ghrelin increases gastric acid output in a dose-dependent manner. Thus, ghrelin may play an important role in controlling feeding behavior and energy homeostasis. We have investigated the role of ghrelin in the control of feeding and neuroendocrine function in ruminants using sheep as an experimental model. This mini review describes mechanisms regulating ghrelin secretion at feeding time, and also focuses on the neuroendocrine functions of ghrelin.

Animals↗
PubMed2003

Circulating leptin response to feeding and exogenous infusion of insulin in sheep exposed to thermoneutral and cold environments.

Leptin has been shown to regulate feed intake and energy expenditure. Insulin stimulates leptin secretion in rodents, but its action on leptin secretion is still obscure in ruminants. If insulin stimulates leptin secretion in ruminants, circulating leptin concentrations may change during exposure to cold, because of fluctuating insulin secretion and action in the cold environment. The present experiment was designed to determine whether feeding or exogenous administration of insulin affects circulating leptin levels in sheep exposed to thermoneutral and cold environments. Suffolk rams that were shorn and fed a diet once daily were subjected to a thermoneutral (20 degrees C) or cold (0 degrees C) environment for at least 1 week. Overall mean concentrations of plasma leptin in the feeding experiment were lower (P<0.05) in the cold environment than in the thermoneutral environment. Plasma leptin levels remained relatively unchanged after feeding in both environments, though plasma insulin response to feeding in both environments increased (P<0.01). The euglycemic clamps (insulin infusion rate: 4 mUkgBW(-1)min(-1) for 2 h) increased (P<0.01) circulating leptin concentrations in the thermoneutral, but not in the cold environment. These results suggest that lower circulating leptin levels in ruminants exposed to the cold environment could be partly due to the depressed insulin action on leptin secretion.

Animals↗
PubMed2002

A transient ghrelin surge occurs just before feeding in a scheduled meal-fed sheep.

Ghrelin, a gastric-derived peptide, has recently been identified as an endogenous natural ligand for the growth hormone (GH) secretagogue receptor. However, secretory characteristics of ghrelin are still obscure in ruminants. To investigate the diurnal rhythm in ghrelin secretion and its relationship to GH secretion, plasma ghrelin and GH concentrations were determined in Suffolk rams fed with a roughage diet once daily (Experiment 1). Abrupt increases (P<0.05) in plasma ghrelin occurred just before a meal-feeding compared with that at 1h before feeding, then rapidly fell with a minimum during the feeding. A pulsatile surge (P<0.01) in plasma GH concentrations, which seemed to follow a single surge in plasma ghrelin, was observed during the feeding. In Experiment 2, plasma ghrelin and GH were determined in sheep subjected to a pseudo-feeding of 2h to determine whether feed ingestion itself influences ghrelin and GH secretions. Compared with those at 1h before feeding, a tendency of increases (P<0.1) in plasma ghrelin and significant increases (P<0.05) in GH occurred just before and during a pseudo-feeding, respectively. Plasma ghrelin temporally declined within 1h after the start of the pseudo-feeding, and increased again and maintained higher levels during the last period of the pseudo-feeding. These results suggest that the transient surge of ghrelin secretion just before a scheduled meal feeding would not be due to the ingestion of feed, and that a pulsatile increase in plasma GH during the actual- or pseudo-feeding could be induced by the transient ghrelin surge.

Animals↗
PubMed2001

Expression of glucose transporter-1 in human gastric carcinoma: association with tumor aggressiveness, metastasis, and patient survival.

BACKGROUND: Malignant cells show increased glucose uptake in vitro and in vivo, which is believed to be facilitated by glucose transporters (Gluts). Expression of Glut1, one of the Gluts, has been described in malignancies of the esophagus, colon, pancreas, lung, and brain, but to the authors' knowledge the significance of Glut1 expression in human gastric carcinoma has not been elucidated. The objective of the current study was to examine the expression and distribution of Glut1 and its relation to clinicopathologic parameters in patients with gastric carcinoma. METHODS: Immunohistochemistry with anti-Glut1 antibody was performed on 617 gastric carcinomas and 50 tubular adenomas of the stomach. Glut1-positive and Glut1-negative carcinomas were analyzed for their clinicopathologic characteristics including histologic subtype, depth of invasion, vascular permeation, lymph node and hepatic metastasis, peritoneal dissemination, and prognosis. RESULTS: None of the adenomas expressed Glut1, whereas 182 of 617 carcinomas (29.5%) were positive for the protein. Signet ring cell carcinoma and mucinous adenocarcinoma rarely were positive (2.0% and 6.3%, respectively) and papillary adenocarcinoma (44%) showed slightly higher positivity for Glut1 than tubular (32%) or poorly differentiated adenocarcinoma (28%). Glut1-positive tumor cells were localized mainly in the central part of tumor nests with or without peripheral distribution (92%) but peripheral distribution alone was very limited (8%) (P = 0.0001). Glut1 positivity was associated with depth of invasion (P = 0.0001), lymphatic permeation (P = 0.0001), venous invasion (P = 0.0001), lymph node metastasis (P = 0.0001), hepatic metastasis (P = 0.0001), and carcinoma stage (P = 0.0001). However, peritoneal dissemination was not found to be associated with Glut1 positivity (P = 0.0833). The survival of patients who had tumors that expressed Glut1 was significantly shorter than that of patients with Glut1-negative tumors (P = 0.0001). CONCLUSIONS: In human gastric carcinoma, Glut1 is expressed late in carcinogesis and increases with disease progression. Glut1 expression is associated with tumor aggressiveness and patient survival.

Adult↗
PubMed2001

Histone deacetylase inhibitors such as sodium butyrate and trichostatin A induce apoptosis through an increase of the bcl-2-related protein Bad.

The effects of sodium butyrate (SB) and trichostatin A (TSA) on cell proliferation andapoptosis against human glioma T98G, U251MG, and U877MG cells were investigated. Upon exposure to either SB or TSA, cell proliferation was reduced, and apoptosis detected by DNA fragmentation analysis and the cleavage of CPP32 was induced. Previously, we reported that SB increased the expression levels of p21 (WAF-1) and inhibited G1-S transition of the cell cycle. In this study, we showed that TSA also increased p21 expression, suggesting that histone deacetylase (HDAC) inhibitors may up-regulate p21 protein in common and thus arrest proliferation in the G1 phase of the cell cycle. To further determine the underlying molecular mechanisms of apoptosis with either SB or TSA treatment, we studied the expression levels of apoptosis-related proteins in human glioma cells. SB increased the expression of the Bad protein, although the expression of Bcl-2, Bcl-xL, Bax, and Fas was not changed by theaddition of SB. TSA treatment also up-regulated the expression of Bad protein. The results suggest that HDAC inhibitors such as SB and TSA induce apoptosis through an increase in Bad protein in human glioma cells in vitro.

Apoptosis↗
PubMed2001

Prognostic significance of apoptosis in squamous cell carcinoma of oral cavity with special reference to TNM stage, histological grade and survival.

Apoptotic count was assessed in 38 cases of squamous cell carcinoma of oral cavity by light microscopy and correlated with TNM stage, histological grade and survival. A direct correlation with the TNM stage (p = 0.0166) and an inverse correlation with the histological grade (p = 0.03) was found, however no correlation was found with the survival. Apoptotic count was significantly different between well and moderately differentiated carcinoma (p = 0.347) and well and poorly differentiated carcinoma (p = 0.0190). Thus apoptotic count may have prognostic value particularly in combination with staging and histological grade.

Adult↗
PubMed2000

Phosphorylation of c-Jun NH(2)-terminal kinase and p38 mitogen-activated protein kinase after transient forebrain ischemia in mice.

We investigated the activation of c-Jun NH(2)-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) during transient forebrain ischemia to clarify the roles of these stress kinases during brain ischemia. Mice were subjected bilateral common carotid artery (BCCA) occlusion for 20 min followed by reperfusion. Immunohistochemical analysis and Western blot analysis for active JNK and active p38 MAPK were performed at 0, 5, 10, 30 and 150 min after reperfusion. After 5 min of reperfusion, active JNK and p38 MAPK immunoreactivities were enhanced in neurons in the cerebral cortex and hippocampus; this activation peaked at 30 min of reperfusion. Stress kinases activation dominantly occurred in the similar regions, in which neurons with fragmented DNA were detected at 72 h after reperfusion. Western blot analysis indicated that JNK 1, JNK 2 and p38 MAPK were activated at 10 and 30 min after reperfusion. These findings indicate that JNK and p38 MAPK pathways may play important roles in neuronal death during brain ischemia.

Animals↗
PubMed2000

Activation of mitogen-activated protein kinases after transient forebrain ischemia in gerbil hippocampus.

We investigated the expression, activation, and distribution of c-Jun N-terminal kinases (JNKs), p38 mitogen-activated protein kinases (p38s) and extracellular signal-regulated kinases (ERKs) using Western blotting and immunohistochemistry in gerbil hippocampus after transient forebrain ischemia to clarify the role of these kinases in delayed neuronal death (DND) in the CA1 subfield. Immunoblot analysis demonstrated that activities of JNK, p38, and ERK in whole hippocampus were increased after 5 min of global ischemia. We used an immunohistochemical study to elucidate the temporal and spatial expression of these kinases after transient global ischemia. The immunohistochemical study showed that active JNK and p38 immunoreactivities were enhanced at 15 min of reperfusion and then gradually reduced and disappeared in the hippocampal CA1 region. On the other hand, in CA3 neurons, active JNK and p38 immunoreactivities were enhanced at 15 min of reperfusion and peaked at 6 hr of reperfusion and then gradually reduced but was continuously detected 72 hr after ischemia. Active ERK immunoreactivity was observed transiently in CA3 fibers and dentate gyrus. Pretreatment with SB203580, a p38 inhibitor, but not with PD98059, an ERK kinase 1/2 inhibitor, reduced ischemic cell death in the CA1 region after transient global ischemia by inhibiting the activity of p38. These findings indicate that the p38 pathway may play an important role in DND during brain ischemia in gerbil. Components of the pathway are important target molecules for clarifying the mechanism of neuronal death.

Animals↗
PubMed2000

Activation of mitogen-activated protein kinases in gerbil hippocampus with ischemic tolerance induced by 3-nitropropionic acid.

The present study investigated the activation of c-Jun NH2-terminal kinases (JNK), p38 mitogen-activated protein kinases (p38) and extracellular signal-regulated kinases (ERK) in the gerbil hippocampus by immunohistochemistry to clarify the role of these kinases in ischemic tolerance induced by3-NP. Intraperitoneal administration of 3-NP (3 or 10 mg/kg) caused the activation of JNK in CA1 subfield, which induced tolerance to subsequent ischemia and prevented delayed neuronal death (DND). As concerns p38 and ERK, no activation was induced by intoxication of 3-NP. Our results show the activation of JNK following chemical preconditioning with low dose of 3-NP is closely related to the acquisition of resistance to DND.

Animals↗
PubMed2000

Fatty acid synthase is expressed mainly in adult hormone-sensitive cells or cells with high lipid metabolism and in proliferating fetal cells.

Animal fatty acid synthase (FAS) is a homodimer protein which synthesizes long-chain fatty acids and is rich in liver, brain, breast, and lung. However, the precise cellular localization of FAS in human tissues has not been elucidated. Immunohistochemistry with a new antibody to human FAS revealed that in adult human tissues FAS is distributed mainly in cells with high lipid metabolism (adipocytes, corpus luteum, hepatocytes, sebaceous glands, and Type II alveolar cells), in hormone-sensitive cells (anterior pituitary, apocrine gland, breast, endometrium, prostate, seminal vesicle, and adrenal cortex), and in a subset of epithelial cells of duodenum and stomach, colon absorptive cells, cerebral neurons, basket cells of cerebellum, decidua, uroepithelium, and epidymis. In fetal cells at 20 weeks of gestation, FAS was mainly present in proliferative epithelial cells of the digestive and respiratory systems, proximal renal tubules, adrenocortical cells, and mesenchymal and hematolymphoid cells. Staining was significant in nonproliferating cells, as observed in adult, and in sympathetic ganglion cells, Leidig cells of testis, and Langhans cells of chorionic villi. FAS is maintained in hormone-sensitive cells and/or cells active in lipid metabolism in the adult and is expressed in proliferating cells in the fetus, suggesting active fatty acid synthesis for energy utilization or membrane lipids.

Adipocytes↗
PubMed2000

Intracranial hypotension due to cerebrospinal fluid leakage detected by radioisotope cisternography.

Seven patients, six females and one male aged 26 to 39 years old, presented with headache in the upright posture, which was completely relieved in the recumbent posture. Radioisotope cisternography with technetium-99m-human serum albumin detected cerebrospinal fluid (CSF) leakage at the cervicothoracic level in six patients, and at the high cervical level in one patient. The diagnosis was intracranial hypotension due to spontaneous CSF leakage. Complete bed rest for more than 2 weeks resulted in complete resolution of the headache in all patients, and follow-up cisternography showed no leakage. Radioisotope cisternography is useful for the diagnosis of spontaneous CSF leakage, and complete bed rest for more than 2 weeks may be the best method of treatment.

Adult↗
PubMed1999

Expression and distribution of redox regulatory protein, thioredoxin after metabolic impairment by 3-nitropropionic acid in rat brain.

Thioredoxin (TRX) is a small, multifunctional protein with a redox-active site and multiple biological functions that include reducing activity for reactive oxygen intermediates. We assayed TRX by immunohistochemical methods in the rat brain after intraperitoneal injection of 3-nitropropionic acid (3-NP), an irreversible inhibitor of succinate dehydrogenase. Systemic administration of 3-NP produced lateral striatal, hippocampal CA1 and CA3 lesions in the present study. The immunoreactivity for TRX was enhanced in hippocampal CA3, dentate gyrus and lateral striatum, but not detected in hippocampal CA1 subfield after 3-NP intoxication. The data suggest that TRX may play an important role in the pathogenesis of 3-NP neurotoxicity.

Animals↗