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Biomedical subjects

T Murakami

Publications and source records attributed to T Murakami.

At least 595 records · Page 33Linked to original sources
PubMed1997

Inhibition of sarcolemmal Na+,K+-ATPase activity reduces the infarct size-limiting effect of preconditioning in rabbit hearts.

BACKGROUND: The inhibition of sarcolemmal Na+,K+-ATPase activity is closely related to ischemic myocardial cell injury. However, the involvement of this enzyme in preconditioning has not been determined. METHODS AND RESULTS: We assessed the effect of ischemia on sarcolemmal Na+,K+-ATPase activity. Control and preconditioned rabbits were subjected to 0, 10, 20, 30, and 60 minutes of coronary occlusion. Ten to 60 minutes of ischemia reduced Na+,K+-ATPase activity, whereas preconditioning preserved the activity of this enzyme only during the first 20 minutes of ischemia. To determine whether the preservation of Na+,K+-ATPase activity in the early phase of ischemia contributed to limiting the infarct size, additional rabbits underwent 30 minutes of occlusion followed by 3 hours of reperfusion with or without pretreatment with digoxin, an inhibitor of Na+,K+-ATPase. Infarct size in animals pretreated with digoxin in the absence of preconditioning did not differ from that in controls. It was markedly reduced by preconditioning, whereas digoxin reduced the infarct size-limiting effect. Moreover, preconditioning increased sarcolemmal Na+-Ca2+ exchange activity in rabbits subjected to 20 minutes of ischemia, whereas digoxin diminished this increase. CONCLUSIONS: Preconditioning preserves the ischemia-induced reduction in sarcolemmal Na+,K+-ATPase activity in the early phase of ischemia in rabbit hearts. Inhibition of Na+,K+-ATPase activity reduces the infarct size-limiting effect of preconditioning with a loss of increased Na+-Ca2+ exchange activity, implying that this preservation is responsible for the cardioprotective effect of preconditioning.

Animals↗
PubMed1997

Extracellular signal-regulated kinase and c-Jun NH2-terminal kinase activities are continuously and differentially increased in aorta of hypertensive rats.

We first examined the activities of extracellular signal-regulated kinases (ERKs) and c-Jun NH2-terminal kinases (JNKs) in the aorta of hypertensive rats. In Dahl salt-sensitive (DS) rats, chronic hypertension caused by a high-salt diet was followed by sustained activation of aortic p42ERK and p44ERK. p46JNK and p55JNK activities were also increased in hypertensive DS rats, but returned to control levels earlier than ERKs, suggesting that ERKs and JNKs may be independently activated in hypertensive rats. In stroke-prone spontaneously hypertensive rats (SHRSP) which spontaneously develop hypertension under a low salt-diet, aortic p42ERK and p44ERK activities were progressively increased with the development of hypertension, compared with control normotensive rats. p46JNK and p55JNK activities in SHRSP were increased, with a different time course from ERKs. Thus, we first demonstrated that ERKs and JNKs activities are chronically and differentially increased in the aorta of hypertensive rats, suggesting the involvement of these kinases in hypertensive vascular diseases.

Animals↗
PubMed1997

Leptin suppresses basal insulin secretion from rat pancreatic islets.

The effects of leptin on insulin secretion from pancreatic islets of Sprague-Dawley rats were examined in vitro. In a basal glucose medium (5.5 mM), insulin secretion from isolated islets was significantly decreased after addition of a recombinant leptin (80 nM) (3.20+/-0.14 nmol/10 islets/h) compared with that before the addition (4.41+/-0.30 nmol/10 islets/h). Although significant leptin suppression of insulin secretion was not observed under a glucose-stimulated (11.1 mM) condition, these results suggest that a negative feedback system may exist between leptin and insulin, which increases the production of leptin from adipose tissues.

Animals↗
PubMed1997

Genomic structure and expression of the human heme A:farnesyltransferase (COX10) gene.

Charcot-Marie-Tooth disease type 1A (CMT1A) is associated with a 1.5-Mb tandem DNA duplication in chromosome 17p11.2-p12, while hereditary neuropathy with liability to pressure palsies (HNPP) is associated with a 1.5-Mb deletion at this locus. The 1.5-Mb CMT1A monomer unit duplicated in CMT1A and deleted in HNPP is flanked by two 24-kb direct repeats termed the CMT1A-REPs. Recently, sequence analysis of the CMT1A-REPs revealed that they contain an internal exon of the COX10 gene. To characterize COX10, encoding human heme A:farnesyltransferase, the genomic region was isolated and the gene structure and expression profile were determined. COX10 spans approximately 135 kb and consists of seven exons. Exons I-V are telomeric to the 1.5-Mb CMT1A monomer unit, whereas exon VII is located within this 1.5-Mb region. Exon VI is contained within the distal CMT1A-REP. All splice sites conform to the GT/AG rule. Analysis of the putative promoter region of the COX10 gene indicates that it lacks conventional TATA and CAAT boxes, but it does have several potential transcription factor-binding sites. This gene is expressed in multiple tissues with highest expression observed in the heart, skeletal muscle, and testis.

Alkyl and Aryl Transferases↗
PubMed1997

A short form of leptin receptor performs signal transduction.

The obese (ob) gene product, leptin, a peptide hormone, which is synthesized in adipocytes, is a satiety factor and is involved in the control of body weight via the regulation of energy homeostasis. Several alternate spliced isoforms (a-e, as well as others) of the leptin receptor (OBR) have been cloned, all of which, except for OBRe (soluble form), contain a single transmembrane domain. They share the same extracellular domain, with homology to the class I cytokine receptor family. The OBRb, which has longest cytoplasmic domain, is expressed in high levels in the hypothalamus and is thought to be the only isoform capable of signal transmission. Herein, we report the mRNA expression of immediate early genes, c-fos, c-jun and jun-B, which are induced by leptin addition, not only in CHO cells expressing the OBRb, but also in cells expressing one of the short form receptors, OBRa.

Animals↗
PubMed1997

V3 loop of human immunodeficiency virus type 1 suppresses interleukin 2-induced T cell growth.

We tested the effect of three linear or two loop peptides derived from the V3 region of the HTLV-III BH10 clone or the SF2 strain of human immunodeficiency virus type 1 on IL-2-driven T cell proliferation. V3-BH10, which consists of 42 amino acids and has a loop structure, suppressed IL-2-driven proliferation of all IL-2-dependent cells [Kit225, ED-40515(+), KT-3, 7-day PHA-blasts, and fresh peripheral blood mononuclear cells] tested, whereas it did not suppress the cell growth of IL-2-independent cell lines (Hut102, Molt-4, and Jurkat). This suppressive effect was also seen in IL-2-driven cell growth of CD8-positive lymphocytes purified from 7-day PHA-blasts, indicating that CD4 molecules were not required for the suppression. The treatment with anti-V3 loop monoclonal antibody (902 antibody) completely abolished the suppressive effect of V3-BH10. In addition, V3-BH10 generated the arrest of Kit225 cells and also purified CD8-positive lymphocytes in G1 phase in the presence of IL-2. Neither chromatin condensation nor DNA fragmentation was detected in Kit225 cells cultured with V3-BH10 and IL-2. V3-BH10 neither blocked radiolabeled IL-2 binding to IL-2 receptors nor affected tyrosyl phosphorylation of several cellular proteins (p120, p98, p96, p54, and p38), which is immediately induced by IL-2 stimulation. However, V3-BH10 enhanced IL-2-induced mRNA expression of c-fos but not c-myc or junB. Thus, the binding of V3 loop of gp120 to the cell surface molecule(s) appears to affect intracellular IL-2 signaling, which leads to the suppression of IL-2-induced T cell growth.

Amino Acid Sequence↗
PubMed1997

Distinct roles of C2A and C2B domains of synaptotagmin in the regulation of exocytosis in adrenal chromaffin cells.

Synaptotagmin that contains two repeats of C2 regulatory domains is considered to be involved in neurotransmitter release. To reveal the roles of synaptotagmin in the regulation of exocytosis, we examined the effects of antibodies against C2A and C2B domains on Ca2+-evoked catecholamine (CA) release from digitonin-permeabilized adrenal chromaffin cells, resolving the Ca2+-evoked release into ATP-dependent priming and ATP-independent Ca2+-triggered steps. Anti-C2A antibody clearly reduced the ATP-independent release, suggesting that the C2A domain directly facilitate or promote Ca2+-triggered step, vesicular fusion. In contrast, anti-C2B antibody did not affect Ca2+-evoked release by itself, but significantly increased the spontaneous Ca2+-independent release. In addition, inositol high-polyphosphate series (IHPS) that bind the C2B domain inhibited both the ATP-independent Ca2+-evoked release and the spontaneous release in a dose-dependent manner. The inhibition by IHPS was totally reversed by anti-C2B antibody and significantly reversed by high concentration of Ca2+. These results suggest that IHPS binding to C2B domain arrests membrane fusion by presumably preventing interaction of synaptotagmin with phospholipids or with proteins of plasma membrane. Thus, IHPS binding to the C2B domain might keep the docked or primed vesicles away from spontaneous fusion at resting level of intracellular Ca2+. Binding of the increased intracellular Ca2+ to the C2A domain may facilitate or trigger the vesicular fusion by releasing this suppression by IHPS.

Adenosine Triphosphate↗
PubMed1997

Isolation of novel genes from the CMT1A duplication/HNPP deletion critical region in 17p11.2-p12.

Charcot-Marie-Tooth disease type 1A (CMT1A) is associated with a 1.5-Mb tandem DNA duplication in chromosome 17p11.2-p12, while hereditary neuropathy with liability to pressure palsies (HNPP) is associated with a 1.5-Mb deletion at this locus. The 1.5-Mb CMT1A monomer unit duplicated in CMT1A and deleted in HNPP is flanked by low-copy repeats termed CMT1A-REPs. Both diseases appear to be caused by an altered copy number of the peripheral myelin protein 22 gene (PMP22), which lies within the critical region. To identify additional genes rapidly, we used a cosmid contig of this region and reciprocal probing of arrayed chromosome 17-specific cosmid and cDNA libraries. Three cDNA clones were identified within the CMT1A duplication/HNPP deletion region and one just proximal to the critical region. The cDNA for human heme A:farnesyltransferase (COX10) mapped 10 kb centromeric to the distal CMT1A-REP. The other two cDNA clones from within the critical interval mapped to cosmid 126D1 at the mfd41 (D17S261) DNA marker, and their conceptual translation showed homology to 60S ribosomal protein L9 (RPL9) and chromosomal protein RMSA-1 (RMSA-1). A gene that is homologous to human peroxisome proliferator activated receptor alpha (hPPARA) was identified near the proximal CMT1A-REP.

Alkyl and Aryl Transferases↗
PubMed1997

Cytometry in cell necrobiology: analysis of apoptosis and accidental cell death (necrosis).

The term cell necrobiology is introduced to comprise the life processes associated with morphological, biochemical, and molecular changes which predispose, precede, and accompany cell death, as well as the consequences and tissue response to cell death. Two alternative modes of cell death can be distinguished, apoptosis and accidental cell death, generally defined as necrosis. The wide interest in necrobiology in many disciplines stems from the realization that apoptosis, whether it occurs physiologically or as a manifestation of a pathological state, is an active mode of cell death and a subject of complex regulatory processes. A possibility exists, therefore, to interact with the regulatory machinery and thereby modulate the cell's propensity to die in response to intrinsic or exogenous signals. Flow cytometry appears to be the methodology of choice to study various aspects of necrobiology. It offers all the advantages of rapid, multiparameter analysis of large populations of individual cells to investigate the biological processes associated with cell death. Numerous methods have been developed to identify apoptotic and necrotic cells and are widely used in various disciplines, in particular in oncology and immunology. The methods based on changes in cell morphology, plasma membrane structure and transport function, function of cell organelles, DNA stability to denaturation, and endonucleolytic DNA degradation are reviewed and their applicability in the research laboratory and in the clinical setting is discussed. Improper use of flow cytometry in analysis of cell death and in data interpretation also is discussed. The most severe errors are due to i) misclassification of nuclear fragments and individual apoptotic bodies as single apoptotic cells, ii) assumption that the apoptotic index represents the rate of cell death, and iii) failure to confirm by microscopy that the cells classified by flow cytometry as apoptotic or necrotic do indeed show morphology consistent with this classification. It is expected that flow cytometry will be the dominant methodology for necrobiology.

Apoptosis↗
PubMed1997

Relation of iodine-123 metaiodobenzylguanidine myocardial scintigraphy to endomyocardial biopsy findings in patients with dilated cardiomyopathy.

BACKGROUND: Iodine-123 metaiodobenzylguanidine (123I-MIBG) concentrates in adrenergic neurons and has been developed for evaluation of the sympathetic nervous system. Recent studies have demonstrated that the normal heart is clearly visualized by 123I-MIBG cardiac scintigraphy, whereas abnormal 123I-MIBG myocardial uptake and washout have been demonstrated in patients after myocardial infarction and in patients with congestive cardiomyopathy, long QT syndrome, and ventricular tachycardia. HYPOTHESIS: Based on evidence from recent studies, it can be hypothesized that 123I-MIBG uptake is related to histopathologic changes in the myocardium. METHODS: The relation of 123I-MIBG uptake to the histologic findings for the heart was studied in 24 patients with dilated cardiomyopathy (DCM). The study group did not include patients with complicating disorders that primarily affect the adrenergic nervous system. The 123I-MIBG uptake was visually assigned one of four grades using the two criteria of the mean score for six regional uptake grades (mean score) and the global score obtained by visual evaluation of the entire image (global score). The 123I-MIBG uptake score was also determined for the region at which the biopsy specimen was obtained (biopsy region score). The histologic findings were evaluated by assigning one of four grades for each of the following five factors: myocyte hypertrophy, myocardial fibrotic change, myocyte degeneration and necrosis, mononuclear cell infiltration, and myocyte disarray. The sum for all grades was defined as the total score, and the global score was also assigned to the overall histologic findings. RESULTS: All of the global, mean, and biopsy region scores for 123I-MIBG uptake correlated significantly with the global and total scores for the histologic findings. Among the histologic factors, myocyte degeneration showed score correlated with all global, mean, and biopsy region scores for the uptake. Myocyte hypertrophy was associated weakly with the 123I-MIBG uptake scores. CONCLUSION: These results indicate that 123I-MIBG uptake imaging is associated with histopathologic abnormalities in patients with DCM.

3-Iodobenzylguanidine↗
PubMed1997

Analysis of genotypes and amino acid residues 2209 to 2248 of the NS5A region of hepatitis C virus in relation to the response to interferon-beta therapy.

In chronic hepatitis C virus (HCV) infection, genotypes other than genotype 1b of HCV (HCV-1b) and low serum HCV-RNA levels are known to be associated with favorable outcome of interferon alfa (IFN-alpha) therapy. In addition, we recently reported a close correlation between the number of mutations in amino acid sequences 2209 to 2248 of the nonstructual protein 5A gene (NS5A2209-2248) of HCV-1b and the response to IFN-alpha. In the present study, we analyzed these viral factors in relation to the efficacy to IFN-beta, another type I IFN. The pretreatment sera of 40 patients treated with IFN-beta intravenously at 6 MU daily for 42 days were studied. HCV genotypes, serum HCV-RNA levels, and the amino acid sequence of NS5A2209-2248 in HCV-1b were determined. A sustained complete response to IFN therapy occurred in none of the ten patients with the wild-type HCV-1b who had an NS5A2209-2248 sequence identical to the prototype HCV-1b and in none of the six patients with the intermediate-type HCV-1b that had 1 mutation. In contrast, complete responses occurred in the following: 4 of 6 patients with the mutant-type HCV-1b that had five to ten mutations; 6 of 13 patients with genotype 2a of HCV (HCV-2a); and 2 of 5 patients with genotype 2b of HCV (HCV-2b). Among patients with the mutant-type HCV-1b or genotype 2 of HCV (HCV-2) the rate of complete response was significantly higher (12 of 24 vs. 0 of 16 patients, P < .001) and HCV-RNA levels were significantly lower (4.5 [4.0-6.5] vs. 6 [4.5-6.5] log copies/mL, median [range]; P < .001) compared with patients with the wild- or the intermediate-type HCV-1b. Patients with the mutant-type HCV-1b or HCV-2 whose HCV-RNA levels were lower than 6 log copies/mL had a complete response rate of 75% (12 of 16 patients) in contrast to 0% (0 of 24 patients) of the others (P < .001). These results indicate that the mutant-type HCV-1b or HCV-2 are sensitive to IFN-beta as well as IFN-alpha. In conclusion, the determination of HCV genotypes, NS5A2209-2248 of HCV-1b and serum HCV-RNA levels may facilitate the selection of patients with a high likelihood of response to IFN-beta.

Amino Acid Sequence↗
PubMed1997

K(ATP) channels contribute to the cardioprotection of preconditioning independent of anaesthetics in rabbit hearts.

The contribution of ATP sensitive potassium (K(ATP)) channels to the infarct-size limiting effect of preconditioning is considered to be anaesthetic-dependent in the rabbit heart. It has previously been reported that ischaemic preconditioning prevents ischaemia-induced reductions in activities of sarcolemmal adenylate cyclase (AC) and Na+, K(+)-ATPase. Anaesthetic dependency of the role of K(ATP) channels in the preservation of these enzyme activities, induced by ischaemic preconditioning, as well as that induced by activation of A1-adenosine receptors, was examined in rabbits anaesthetized with either pentobarbital or ketamine-xylazine and subjected to 20 min of regional ischaemia. Adenylate cyclase and Na+, K(+)-ATPase activities were lower in the ischaemic than in the non-ischaemic region of the hearts in control rabbits, but not in animals subjected to ischaemic preconditioning, or those pretreated with the A1-adenosine receptor agonist R(-)-N6-(2-phenylisopropyl) adenosine. The protective effects of both ischaemic preconditioning and A1-adenosine receptor activation were prevented by 6 mg/kg, but not 3 mg/kg, of the K(ATP) channel blocker, glibenclamide, in rabbits anaesthetized with pentobarbital, while these effects were prevented by 3 mg/kg of the blocker in rabbits anaesthetized with ketamine-xylazine. Moreover, K(ATP) channel opener, cromakalim, prevented the ischaemia-induced decreases in enzymatic activities in rabbits subjected to either type of anaesthesia. Thus, although the antagonistic effect of glibenclamide is blunted under pentobarbital, compared to ketamine-xylazine anaesthesia, K(ATP) channels contribute to preservative actions independent of the type of anaesthesia in the rabbit heart.

Adenosine Triphosphate↗
PubMed1997

Iatrogenic paraplegia caused by surgicel used for hemostasis during a thoracotomy: report of a case.

A 46-year-old Japanese woman underwent a right lower lobectomy through a posterolateral incision made in the fifth intercostal space under general and epidural anesthesia on January 23, 1995. During the procedure, oxidized regenerated cellulose (Surgicel) was used to prevent postoperative rebleeding from the dorsal branch of the fifth intercostal artery. The following day it became evident that complete paraplegia had developed below the Th5 level, the cause of which was revealed by an emergency laminectomy, performed within 20 h after the thoracotomy, to be the Surgical treatment. By 50 days after the operation the patient had begun to show improvement, and was able to move her lower extremities against gravity. Her condition is continuing to improve.

Cellulose, Oxidized↗
PubMed1997

Localization of membrane-associated sialomucin on the free surface of mesothelial cells of the pleura, pericardium, and peritoneum.

Strong anionic sites, as recognized by deposition of cationic colloidal iron even at pH 1.5, were distributed on the free surfaces of the mesothelia of the mouse pleura, pericardium, and peritoneum. Methylation inhibited colloidal iron staining on the surface, and successive saponification restored it. Digestion with neuraminidase or hydrolysis of sialic acid with H2SO4 erased the colloidal iron staining. Lectin Limax flavus agglutinin (LFA), which is specific for sialic acid, labeled the free surface of the mesothelium. All these findings strongly suggested that the surface substance contained sialic acid. Moreover, prior treatment with LFA inhibited the mesothelial surface stain with colloidal iron. In transmission electron microscopy, the colloidal iron (pH 7.3)-stained substance took the shape of fine strands of 50-300 nm in length. These characteristics of the substance on the mesothelial surface correspond well with biochemical properties of membrane-associated sialomucin, whose strong and abundant negative charges produce repulsive forces between facing serosal surfaces. This may contribute to prevent serosal adhesion and to reduce friction during movements of organs.

Animals↗
PubMed1997

Increased secretion of hepatocyte growth factor by eutopic endometrial stromal cells in women with endometriosis.

OBJECTIVE: We evaluated the secretion of hepatocyte growth factor by eutopic endometrial stromal cells in vitro. DESIGN: Eutopic endometrial stromal cells were isolated and the culture supernatants were collected after 48 hours of incubation. The secretion of hepatocyte growth factor was analyzed by ELISA. SETTING: Department of Obstetrics and Gynecology of Tohoku University Hospital. PATIENT(S): Specimens of endometrium in the proliferative phase were excised from 11 patients who were undergoing laparoscopy for infertility. Six of the patients had endometriosis and five did not. None of the patients had received hormonal treatment before surgery. RESULT(S): Hepatocyte growth factor secretion was found to be increased significantly in cultured endometrial stromal cells from the infertile patients with endometriosis compared with those without endometriosis. CONCLUSION(S): The secretion of hepatocyte growth factor was up-regulated in eutopic endometrial stromal cells from patients with endometriosis. An increase in hepatocyte growth factor production may be characteristic of endometriosis and may be involved in the pathophysiology of this disease.

Adult↗
PubMed1997

Extrapancreatic action of truncated glucagon-like peptide-I in Otsuka Long-Evans Tokushima Fatty rats, an animal model for non-insulin-dependent diabetes mellitus.

To clarify the mechanism(s) of the antidiabetic effects of truncated glucagon-like peptide-1 (GLP-1) in diabetics, we examined its insulinotropic and extrapancreatic effects in a newly established strain of spontaneously non-insulin-dependent diabetic (NIDDM) rats, Otsuka Long-Evans Tokushima Fatty (OLETF) rats, that received a continuous infusion of truncated GLP-1 620 pmol/d/kg (G group, n = 12) or of vehicle (V group, n = 12) for 4 weeks by Alzet pump. Nonfasting plasma glucose levels were significantly lower (P < .05) in the G group than in the V group (7.0 +/- 0.67 v 9.1 +/- 1.7 mmol/L), and fasting plasma immunoreactive insulin (IRI) levels were lower in the former than in the latter (0.63 +/- 0.31 v 0.78 +/- 0.25 nmol/L). At day 15 of infusion, the G group showed an attenuated plasma glucose response to an oral glucose load, but had plasma IRI levels comparable to those in the V group. A long-term infusion of truncated GLP-1 increased the glucose infusion rate (GIR) significantly (P < .05) during a euglycemic-hyperinsulinemic clamp test (59.0 +/- 14.8 mumol/kg/min for group G v 38.9 +/- 12.2 for group V), but hepatic glucose output (HGO) did not differ significantly for either group. Uptake of 2-deoxy-D-glucose (2DG) by peripheral muscles in the G group was as much as 2.4-fold higher than in the V group (5.52 +/- 2.04 v 2.29 +/- 0.97 mumol/100 g muscle weight/min). We conclude from these data that truncated GLP-1, in addition to its well-known incretin effect, is capable of augmenting insulin action in peripheral tissues of diabetics, which can contribute, in part, to improve glucose intolerance in OLETF rats.

Administration, Oral↗
PubMed1997

Exercise training in Otsuka Long-Evans Tokushima Fatty rat, a model of spontaneous non-insulin-dependent diabetes mellitus: effects on the B-cell mass, insulin content and fibrosis in the pancreas.

The effects of exercise on alterations in the amount of B-cell mass, insulin content and fibrous tissue present in the pancreas were examined for a diabetic state induced by a 70% pancreatectomy and a prediabetic state in Otsuka Long-Evans Tokushima Fatty (OLETF) rat, a model for the spontaneous development of non-insulin-dependent diabetes mellitus (NIDDM). The rats (5-weeks old) were trained either by a 6-week running program or sedentary controls, and at 6-weeks of age, received either a 70% pancreatectomy or a sham-pancreatectomy (sham). As in our previous report, persistent hyperglycemia was detected after surgery for both trained pancreatectomized (Px) and sedentary Px groups. In the nondiabetic sham rats, exercise training resulted in a significantly smaller increase in body weight and beneficial effects on the pancreas as reflected by an increase in pancreatic volume, accompanied by increases in B-cell mass and insulin content as well as less connective tissue in the pancreas compared with the sedentary nondiabetic sham rats. The effect was not sufficient to improve sustained hyperglycemia in the trained diabetic Px rats. This is probably due to a decreased capacity for B-cell proliferation in response to an increased demand for insulin. Although exercise failed to improve this inherent defect in B-cell proliferation, it ameliorated the further deterioration of the pancreas which occurred with hyperglycemia, and resulted in a higher quantity of insulin stored per milligram of B-cell mass (as function of B-cell mass) and less fibrosis in the pancreas, compared with the sedentary diabetic Px rats. The findings of the present study suggest that exercise training has a beneficial effect on the pancreas in the nondiabetic state, and also exerts some positive effects in the diabetic state in this model rat.

Animals↗