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T Goda

Publications and source records attributed to T Goda.

At least 55 records · Page 3Linked to original sources
PubMed1995

Dietary regulation of sucrase-isomaltase gene expression in rat jejunum.

We have previously demonstrated that intake of fat as well as carbohydrate affects the activity and immunoreactive amount of sucrase-isomaltase (S-I) in rat jejunum. To examine whether diet-related changes in sucrase and isomaltase activities are accompanied by the variations of sucrase-isomaltase mRNA levels, 7-week-old rats were fed either a high-long-chain triacylglycerols diet (73 energy% as corn oil), a high-medium-chain triacylglycerols (MCT) diet (66 energy% as MCT, 7 energy% as corn oil) or a high-carbohydrate diet (70 energy% as corn starch) for 7 days. Northern blot analysis revealed that S-I mRNA levels were abundant in the jejunum of rats fed the high-MCT diet; the levels were similar to those in the rats fed the high-carbohydrate diet. Force-feeding a high-sucrose diet (40 energy% as sucrose) brought about a parallel rise in both S-I mRNA and sodium/D-glucose cotransporter (SGLT1) mRNA levels within 12 h. Force-feeding the high-MCT diet also produced an elevation of S-I mRNA and SGLT1 mRNA. However, force-feeding a diet containing alpha-methylglucoside, a non-metabolizable but actively transported sugar, did not increase S-I mRNA or SGLT1 mRNA level; sucrase activity was nevertheless elevated by feeding alpha-methylglucoside diet. These results suggest that not only carbohydrate intake but also MCT intake might influence S-I mRNA and SGLT1 mRNA levels in the jejunum, presumably through common metabolite(s) of carbohydrates and MCT, and that carbohydrate may play another role in enhancement of the sucrase activity through modulation of translation and/or posttranslational modifications of the sucrase-isomaltase complex.

Animals↗
PubMed1995

Alterations in coagulation and fibrinolysis after surgery for aortic aneurysm.

We investigated the alterations in the coagulation and fibrinolysis systems after aortic aneurysm surgery under cardiopulmonary bypass (CPB) while using newly developed "molecular markers". Fibrinogen and antithrombin III (AT-III) decreased after surgery but returned to normal values within three days. The thrombin-antithrombin III complex (TAT) and plasmin-alpha-2-plasmin inhibitor complex (PIC) both showed increased values even preoperatively, which indicated that coagulation and fibrinolysis were activated in some patients with an aortic aneurysm. Both markers maintained a high level for at least 14 days after surgery. The fibrin degradation product (FDP) also showed an increased value before and after surgery. These results apparently showed that coagulation/fibrinolysis had already been activated in some patients and maintained such a state for at least 14 days after surgery. The relation of activated system and postoperative organ dysfunction as well as the means to suppress such activation are also discussed.

Aged↗
PubMed1995

Preoperative disseminated intravascular coagulation (DIC) associated with aortic aneurysm--does it need to be corrected before surgery?

Disseminated intravascular coagulation (DIC) is one of the complications accompanying aortic aneurysm. We herein report four patients with aortic aneurysm who had DIC preoperatively. In all four cases, DIC was corrected immediately after surgery; however, in two cases, DIC could not be corrected preoperatively. This prompted us to reconsider the importance of correcting DIC before surgery. Of the four cases reported in this paper, DIC existed even at the time of surgery in two cases, in spite of meticulous treatment with heparin and/or protease inhibitor; however, the DIC could be removed postoperatively even in these two cases. Surgeons should not waste time with intensive DIC treatment preoperatively. If the DIC cannot be corrected within more than 2 weeks of meticulous treatment, surgeons should then perform surgery on the patient. In addition, it is also essential to ensure that the DIC is due to the aneurysm itself and that no other disease processes have been overlooked.

Aged↗
PubMed1995

Dietary maltitol increases calcium content and breaking force of femoral bone in ovariectomized rats.

Maltitol is a disaccharide alcohol generated by hydrogenation of maltose and exhibiting resistance to intestinal disaccharidases. We demonstrated previously that maltitol stimulates transepithelial transport of calcium in the ileum, accompanied by an elevation of intestinal calcium absorption as well as calcium retention in the body. In this study, we examined whether the maltitol-induced increase in intestinal calcium absorption leads to an alteration of the physical properties of bones in rats subjected to ovariectomy. We used this study as a simulation model for postmenopausal females who are at risk for osteoporosis. Following the intake of a low-calcium diet for 28 d ovariectomized rats were fed diets containing either 10% maltose (control) or 10% maltitol, together with increased amounts of calcium (0.3% in Experiment 1 and 1.2% in Experiment 2) for 21 d. Balance studies performed during the final 5-d (Experiment 1) or 2-d (Experiment 2) period of the experiments showed that maltitol increased intestinal calcium absorption and retention. The breaking force of femoral bones was significantly elevated (by 5-7%) in animals fed the maltitol diet compared with that in rats fed the maltose diet. The calcium content in the femoral bones as well as the mineral bone density of the tibial metaphysis was also elevated in rats fed the maltitol diet. These results indicate that maltitol stimulates the intestinal absorption of dietary calcium leading to an increase in calcium content in the bone, and coinciding with the elevation of the breaking strength of the bone in ovariectomized rats.

Analysis of Variance↗
PubMed1995

Unsaturated fatty acids regulate gene expression of cellular retinol-binding protein, type II in rat jejunum.

We have shown that cellular retinol-binding protein, type II (CRBP II) mRNA and its protein levels are elevated in the jejunum of rats fed a diet rich in long-chain triacylglycerols. In the present study, we explored which types of fatty acids modulate CRBP II gene expression. Rats previously fed a low fat, high starch diet were force-fed a basal fat-free diet or the diet supplemented with 0.21 mol/L of various fatty acids (i.e., caprylic, palmitic, stearic, oleic, linoleic and alpha-linolenic acids). Force-feeding a diet containing linoleic acid produced an elevation of CRBP II mRNA levels in rats in both a dose-dependent (0.053-0.21 mol/L) and time-dependent (up to 6 h) manner. Among fatty acids tested, all unsaturated fatty acids (oleic, linoleic and alpha-linolenic acids) were able to enhance CRBP II mRNA levels by 54-63% within 6 h, whereas a medium-chain fatty acid (caprylic acid) and a saturated fatty acid (stearic acid) elicited little effect on the CRBP II mRNA levels; palmitic acid produced only a small elevation (16%) of the CRBP II mRNA level. Transcripts of both retinoid X receptor alpha and peroxisome proliferator-activated receptor (PPAR), which are thought to interact as a heterodimer with the cis-element located in the CRBP II promoter and to be activated by 9-cis retinoic acid and long-chain fatty acids, respectively, were constitutively expressed in the rat jejunum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Consumption of excess vitamin A, but not excess beta-carotene, causes accumulation of retinol that exceeds the binding capacity of cellular retinol-binding protein, type II in rat intestine.

We assessed the effects of excess dietary vitamin A or beta-carotene on the cellular retinol-binding protein, type II [CRBP(II)] level and activities of lecithin: retinol acyltransferase (LRAT) and acyl-CoA:retinol acyltransferase (ARAT) in rat intestine. Male rats were fed for 7 d diets containing amounts of retinyl acetate or beta-carotene that were 1 (control), 10, 100 and 1000 times the NRC recommended requirement. No responses of the jejunal CRBP(II) level to an intake of excess vitamin A or beta-carotene were observed. The unesterified retinol and retinyl palmitate concentrations in the jejunum were small in rats fed 10 times the vitamin A requirement but they were significantly greater in rats fed 100 and 1000 times the vitamin A requirement than in controls. The molar ratio of unesterified retinol/CRBP(II) was < 1 for the controls and the group fed 10 times the vitamin A requirement, but > 3 for the group fed 100 times the requirement and > 19 for the group fed 1000 times the requirement. The LRAT activity was significantly greater in rats fed 1000 times the vitamin A requirement compared with all other groups, but ARAT activity was unaffected. Consumption of excess beta-carotene did not alter LRAT or ARAT activity, and led to a very small deposition of unesterified retinol and retinyl palmitate in the jejunum. Because CRBP(II) may play an important role in preventing the toxic effect of unbound retinol in the small intestine, consumption of excess vitamin A in amounts < 10 times the NRC recommended requirement may not cause a disturbance of the absorptive cell function.(ABSTRACT TRUNCATED AT 250 WORDS)

Acyltransferases↗
PubMed1995

Diet-induced changes in gene expression of lactase in rat jejunum.

To explore the mechanisms by which jejunal lactase activity is modified by carbohydrate and/or fat intake, mRNA levels and the absolute synthesis rate of lactase-phlorizin hydrolase (LPH) were determined in 6-wk-old rats that were fed either low-starch diets containing long-chain triacylglycerol (LCT, 73% energy as corn oil) or medium-chain triacylglycerol (MCT, 66% energy as MCT, 7% energy as corn oil), or a high-starch diet (70% energy as cornstarch) for 7 days. LPH mRNA levels in the jejunum were similar between LCT-fed and MCT-fed rats, but animals fed the high-starch diet exhibited a greater (2x) LPH mRNA level than other groups. The absolute synthesis rate of LPH, estimated by the flooding dose technique using [3H]phenylalanine, was greater (2.4x) in rats fed the high-starch diet than in other groups. A short-term force-feeding experiment revealed that sucrose was able to evoke LPH mRNA levels within 12 h but that a nonmetabolizable sugar (alpha-methylglucoside) was unable to enhance it. By contrast, animals fed the high-LCT diet showed a lower (by 30%) lactase activity than rats fed the low-starch, high-MCT diet, which was accompanied by not only a reduction of immunoreactive LPH in brush-border membranes but also a reduction in lactase activity per unit weight of immunoreactive LPH. These results suggest that both gene expression and posttranslational events of LPH might be influenced by dietary manipulations; carbohydrate intake primarily increases LPH mRNA levels, and LCT accelerates inactivation and/or degradation of lactase.

Animals↗
PubMed1994

Dietary fat regulates cellular retinol-binding protein II gene expression in rat jejunum.

Cellular retinol-binding protein II (CRBP II) is an abundant cytosolic protein of intestinal absorptive cells. In this study, we examined whether dietary fat modulates the expression of CRBP II in the small intestine. In the rats fed a diet rich in long-chain triacylglycerols (LCT), both CRBP II mRNA and CRBP II protein levels in the jejunum were more than two-fold greater than in the rats fed a low fat diet and a diet rich in medium-chain triacylglycerols (MCT). The mRNA abundance of a retinoid X receptor (RXR alpha), which is thought to interact with the cis-element located in the CRBP II promoter, was elevated in the jejunum of rats fed high-LCT and high-MCT diets as compared with that of animals fed a low-fat diet, but the levels of RXR alpha mRNA of the LCT diet group was similar to that of MCT diet group. These results suggest that the expression level of the CRBP II gene is not directly related to the RXR alpha expression, and that it might be modulated by long-chain fatty acids or their metabolites.

Animals↗
PubMed1994

Dietary carbohydrate and fat independently modulate disaccharidase activities in rat jejunum.

The role of carbohydrate and fat in diet-induced modifications of jejunal disaccharidase activities was evaluated with an isoenergic diet containing a nonmetabolizable sugar, alpha-methylglucoside. Rats previously fed a high fat, low starch diet or a high starch low fat diet were force-fed three times over 12 h isoenergic high fat diets with or without alpha-methylglucoside, or a low fat diet containing alpha-methylglucoside. Regardless of the previous diet fed, force-feeding the high fat, alpha-methylglucoside diet produced significantly greater sucrase and lactase activities in the upper jejunum than force-feeding the high fat diet without alpha-methylglucoside; comparable or only slightly greater sucrase and lactase activities were seen in the lower jejunum. The animals fed the low fat, alpha-methylglucoside diet exhibited significantly greater sucrase and lactase activities in the lower jejunum than did the rats fed the high fat, alpha-methylglucoside diet; a less marked difference (< 30%) was observed between these two groups for disaccharidase activities in the upper jejunum. The lower sucrase and lactase activities observed in the jejunum of animals force-fed the high fat diet after consuming the high starch, low fat diet were accompanied by greater trypsin activity in the lumen of the upper and lower jejunum, suggesting that proteolytic degradation of sucrase and lactase might be stimulated in rats fed the high fat diets. These results suggest that both dietary carbohydrate and dietary fat independently and by different mechanisms modulate jejunal disaccharidase activities.

Animals↗
PubMed1994

Effect of dietary fat content on microvillus in rat jejunum.

To examine whether dietary manipulation of isoenergic diets might affect microvillar structure of small intestinal epithelial cells, morphological parameters of enterocytes and microvilli in the mid-villus portion of jejunum were determined in the rats fed either high-starch (70 energy %), low-fat (7 energy %) diet or high-fat (73 energy %), low-starch (5 energy %) diet for 7 days. Feeding the high-fat diet produced an increase in the height of villus, in accordance with the elevated jejunal mucosal weight and total protein contents as compared with the high-starch diet. No appreciable change in crypt depth occurred. Scanning electron microscopy of jejunal epithelial cells revealed that the morphometrical parameters of the villus cells were unchanged by the diets, but the microvillar structure of each villus cell was influenced by the diets; the animals fed the high-fat diet exhibited a reduced length (28%) of microvillus with a slight increase (12%) in diameter, showing a significantly reduced surface area of microvilli per enterocyte. The reduction in microvillar surface area of animals fed the high-fat diet was accompanied by the decrease in total proteins of the brush border membranes as well as the decrease in the activities of microvillar stalked disaccharidases, i.e., sucrase-isomaltase and lactase. These results provide an evidence that dietary manipulation, even when diets are "complete" in terms of the content of energy, protein, and other micronutrients, can modify the microvillar structure of small intestinal epithelial cells, leading to alterations in the digestive/absorptive surface area of villus cells.

Animals↗
PubMed1994

Monostearoylglycerol-starch complex: its digestibility and effects on glycemic and lipogenic responses.

We examined whether a modification of a starch into an alpha-amylase resistant form can lead to a reduction of postprandial glucose and insulin responses, and consequently to a change of lipid metabolism in liver and adipose tissue. For this purpose, a processed starch was prepared using a cornstarch (70% amylose and 30% amylopectin) and monoacylglycerol (monostearate; MS), forming monostearate-starch complex (MS-treated cornstarch). When we determined in vitro hydrolysis of MS-treated cornstarch using alpha-amylase and intestinal microvillar alpha-glucosidases, the glucose production rate of the MS-treated cornstarch was slower than the non-treated cornstarch. Measurement of a transmural potential difference (delta PD) evoked by the MS-treated cornstarch in everted rat jejunum showed that the absorption rate of glucose released from the MS-treated cornstarch was also remarkably slower than that from the non-treated cornstarch. The postprandial plasma insulin response to the MS-treated cornstarch was reduced, although plasma glucose response was unchanged. In a feeding study, two groups of five or six male Wistar-strain rats were fed defined diets containing 61.1% MS-treated cornstarch or 58.2% non-treated cornstarch ad libitum for 14 days. Food intakes during the period were similar between the two groups. Feeding the MS-treated cornstarch resulted in a significantly lower maltase activity in upper jejunum than did the non-treated cornstarch feeding. The activities of lipogenic enzymes--fatty acid synthetase (FAS), malic enzyme (ME), and glucose-6-phosphate dehydrogenase (G-6-PDH)--significantly decreased in epididymal adipose tissue of rats fed the MS-treated cornstarch. In the liver, FAS activity was lower in the MS-treated cornstarch group. The results indicated that MS-treated cornstarch was digested less rapidly, and lowered blood insulin response, consequently leading to a declined lipogenesis of adipose tissue and liver. This study suggests that the rate of intestinal hydrolysis of starch is an important determinant of metabolic responses such as glycemic and lipogenic responses to diets.

Adipose Tissue↗
PubMed1994

[A case of aortic valve replacement and aorto-coronary bypass with left lung collapse due to thoracoplasty].

A 64-year-old woman was attacked cardiac and respiratory failure in 3 times within a year. Aortic regurgitation (III degrees) and left anterior descending coronary artery 90% stenosis was recognized. %VC: 33% and %FEV1.0 75% were established. Aortic valve replacement (SJM 23 nm) and coronary arterial bypass grafting (SVG) were performed with cardiopulmonary bypass. Post operative course was no trouble and patient was discharged within 60 days.

Aortic Valve↗
PubMed1994

[A case of perforated mitral valve aneurysm following aortic valve replacement associated with infective endocarditis].

A case of perforated mitral valve aneurysm following aortic valve replacement associated with infective endocarditis was reported. The patient was a 29-year-old man, who was suffering from high fever, Osler's nodules and headache. A brain abscess was recognized in a computed tomography and 3rd grade aortic regurgitation was recognized in echocardiogram and aortography. Hematological studies suggested the inflammation and gram-positive cocci was incubated from his arterial blood. Then infective endocarditis with aortic regurgitation was diagnosed. AVR was performed following 8 weeks treatment with antibiotics, when he had negative CRP and his blood culture. After the operation, he was received the intravenous antibiotic therapy for 6 weeks and oral antibiotic drugs was given following his hospital discharge. At 6 months after AVR, mitral valve aneurysm was recognized in his echocardiogram. At 30 months after AVR, the perforation of it was revealed and mitral valve replacement was performed with his negative blood culture. The patient was discharged 28th day after MVR. There has been no active inflammation from his first hospital discharge and following days, the mitral valve aneurysm and the perforation was caused by weakened tissue of the anterior mitral leaflet due to sibilant inflammatory change.

Adult↗
PubMed1994

[Acute dissection of the interatrial septum after re-replacement of the mitral valve--a case report].

A 64-year-old man who had received a Carpentier-Edward mitral valve replacement seven years earlier was seen with dyspnea on exertion. After re-replacement of the mitral valve with SJM prosthesis, the patient developed acute left-sided heart failure on the third postoperative day. Transesophageal echocardiography revealed abnormal lumen posterior to the left atrium with regurgitant flow from the left ventricle. Right and left atriotomy revealed dissection of the interatrial septum and after removal of the prosthesis, communication between the left ventricle and the dissected lumen was recognized. After closing the communicating orifice, SJM prosthesis was again sutured on the mitral annulus with sub-annular pledgets to reinforce the annular attachment. Excessive debridement of the annular tissue was thought to be a causative factor to develop the dissection of the interatrial septum after mitral valve replacement.

Acute Disease↗
PubMed1993

Dietary vitamin A modulates lecithin-retinol acyltransferase activity in developing chick intestine.

Retinol absorbed and generated from beta-carotene requires to be esterified by lecithin-retinol acyltransferase (LRAT) in intestinal absorptive cells. To characterize developmental changes in retinol absorptive capability in intestine, we determined LRAT activity and the amount of its retinol donor, cellular retinol-binding protein, type two (CRBP(II)) in the duodenum of developing chicks. The LRAT activity in duodenal microsomes was very low at 18- and 20-day chick embryo, but exhibited a rapid (15-fold) increase during 48 h around hatching, which occurred in parallel with the abrupt elevation of the content of CRBP(II) in chick duodenum. To examine whether dietary vitamin A affects the developmental change in LRAT activity and CRBP(II) content, 1-day-old chicks were pair-fed vitamin A-depleted or vitamin A-supplemented diet for 14 days. The chicks fed vitamin A-depleted diet showed significantly reduced LRAT activity and CRBP(II) in duodenum as early as 3 days after the start of the vitamin A-depleted diet. Changing the diet from vitamin A-depleted to vitamin A-supplemented diet led to an increase in duodenal LRAT activity within 24 h, while serum retinol concentration remained unchanged. These results suggest that duodenal LRAT activity and CRBP(II) are modulated by dietary vitamin A during the perinatal period.

Acyltransferases↗
PubMed1993

Adaptive changes of intestinal cellular retinol-binding protein, type II following jejunum-bypass operation in the rat.

To examine whether the amount of intestinal cellular retinol-binding protein, type II (CRBP(II)) exhibits an adaptive change in a shortened jejunum, the distal end of 5-cm proximal-jejunal segment of 2-mth-old rats was joined to the proximal end of the ileum by an end-to-end anastomosis (jejunum-bypass operation). Three weeks after the operation, the amounts of CRBP(II) in proximal jejunum, proximal ileum and distal ileum were determined using a monospecific antiserum by enzyme-linked immunosorbent assay. The jejunum-bypass operation led to a 2-fold increase in the total amounts of CRBP(II) in proximal ileum where hyperplasia occurred; this elevation was in parallel to the increase of total proteins and DNA contents. in the proximal jejunum preceding the bypassed segment, the CRBP(II) level per unit DNA increased by 80%. The jejunum-bypass operation changed neither hepatic total retinol content, nor serum concentrations of retinol and retinol binding protein as compared with the sham-operation, suggesting that retinol absorption was elevated in the shortened small intestine. These results suggest that the increase in CRBP(II) content following jejunum-bypass might be an adaptive response to an enhancement of retinol absorption.

Adaptation, Physiological↗
PubMed1993

Feeding medium-chain triglycerides to rats decreases degradation of sucrase-isomaltase complex in the jejunum.

We demonstrated previously that feeding a diet containing medium-chain triglycerides (MCT) to rats causes an increase in the sucrase activity in jejunum relative to diets containing long-chain triglycerides (LCT). To explore the mechanism whereby MCT affect jejunal sucrase activity, 7-wk-old rats were fed a high LCT diet for 7 d, and then they were force-fed either the high LCT diet, a high MCT diet or a high carbohydrate (alpha-methylglucoside) diet for the subsequent 12 h. Feeding the high carbohydrate diet produced significantly greater sucrase and isomaltase activities in both upper and lower jejunum than feeding the LCT diet. Feeding the high MCT diet led to significantly greater sucrase activity in the lower jejunum, but isomaltase activity was not elevated. Rocket immunoelectrophoresis revealed that in the lower jejunum of the rats fed the high MCT diet the proportion of sucrase-isomaltase complex to its degradation product (i.e., isomaltase monomer) was elevated, suggesting that dietary MCT affects sucrase activity by retardation of degradation of sucrase-isomaltase. Because the amounts of total bile acids in the upper jejunum were 50% lower in rats fed the high MCT diet relative to animals fed the high LCT diet, it is likely that MCT feeding decreases secretion of bile into the lumen, which in turn decreases degradation of the sucrase subunit of the sucrase-isomaltase complex.

Animals↗