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Hiroaki Satoh

Publications and source records attributed to Hiroaki Satoh.

At least 37 records · Page 2Linked to original sources
PubMed2005

Radiologic findings in primary pulmonary plasmacytoma.

Plasmacytoma is an uncommon tumor and is rarely encountered as a primary pulmonary neoplasm. Herein we describe the conventional radiographic and computed tomographic findings in a patient with a primary pulmonary plasmacytoma.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2005

Histiocytoid breast carcinoma: solid variant of invasive lobular carcinoma with decreased expression of both E-cadherin and CD44 epithelial variant.

Histiocytoid breast carcinoma (HBC) is a rare type of breast carcinoma with morphologic characteristics resembling those of histiocytes. Described herein are cytological and histological findings in a case of HBC. Fine-needle aspiration cytology revealed numerous loosely cohesive tumor cells with abundant foamy to granular cytoplasm and bland-appearing nuclei. The resected tumor exhibited a solid growth pattern instead of classic invasive lobular patterns observed in most reported cases of HBC. However, distinct intracytoplasmic lumina and Pagetoid extension to ducts suggested that this tumor was a variant of invasive lobular carcinoma. To determine the cause of the loose cellular cohesiveness of this HBC, its expression of the epithelium-related cell adhesion molecules E-cadherin and CD44v8-10 (CD44 epithelial variant) was examined. Immunohistochemically, E-cadherin was not detected, similar to most lobular carcinomas. Furthermore, competitive reverse transcription-polymerase chain reaction (RT-PCR) analyses among alternatively spliced variants of CD44 revealed that the ratio of expression of CD44v8-10 to that of CD44v10 (dominant variant in leukocytes) was lower than that for the reference breast carcinoma samples. It is concluded that the present case of HBC was a solid variant of invasive lobular carcinoma exhibiting foamy to granular cytoplasmic change. Decreased expression of both E-cadherin and CD44 epithelial variant may be responsible for the loose cellular cohesiveness observed in HBC.

Aged↗
PubMed2005

Altered expression patterns of heterogeneous nuclear ribonucleoproteins A2 and B1 in the adrenal cortex.

Several proteins implicated in hormonogenesis of the adrenal cortex have alternatively spliced isoforms, which respond differently to adrenocorticotropic hormone (ACTH). Heterogeneous nuclear ribonucleoproteins A2 and B1 are among the abundant pre-mRNA-binding proteins involved in alternative splicing. We examined the expression of A2 and B1 in normal adrenal cortex and tumors. B1 was variably expressed in the zona fasciculata-reticularis, although A2 was diffusely expressed in the three zones. B1 was more abundant in compact cells than clear cells, and B1 expression was frequent in the zona reticularis, which consists mainly of compact cells. In three kinds of cortical adenomas autonomously producing hormones, B1 was generally overexpressed and there were no significant differences among them. In cortisol-producing tumors, non-tumor parts of the cortex, which were generally atrophic due to low ACTH, had less B1 protein than normal adrenals. These results suggested a correlation between B1 expression and the hormonal activity responding to ACTH. In vitro ACTH stimulation induced a biphasic expression of B1 in an H295R cortical carcinoma cell line, and it paralleled hormonogenesis. Conclusively, B1 expression varied in relation to the hormonal activity responding to the ACTH, and it may provide a key to elucidating the splicing mechanisms involved in hormonogenesis.

Adrenal Cortex↗
PubMed2005

Body mass index and lung cancer: a case-control study of subjects participating in a mass-screening program.

STUDY OBJECTIVES: An inverse relationship between body mass index (BMI) and the risk of lung cancer, suggesting that leanness is a risk factor for lung cancer, has been reported in previous studies. In order to evaluate the risk of lung cancer associated with lower levels of BMI in preclinical patients, we conducted a case-control study based on the results of community mass screening. DESIGN: The relationship between BMI (at the time of diagnosis, and at 1 to 5 years prior to diagnosis) and lung cancer was investigated in a case-control study of 363 lung cancer cases and 1,089 control subjects conducted between April 1993 and March 2003. Control subjects were selected from mass-screening subjects with no abnormalities on chest radiography and routine laboratory tests. RESULTS: In men, an inverse association between BMI and lung cancer was observed after adjustment for age and smoking (BMI < 20.8; range of the referent group, > or = 22.9 to < 25.0; odds ratio, 1.9; p = 0.0025; 95% confidence interval, 1.3 to 2.9). In women, however, no association was found between BMI and lung cancer (BMI < 20.8, p = 0.3868; and BMI </= 25.0, p = 0.4603, respectively). In addition, a negative association between BMI at 4 to 5 years prior to diagnosis and lung cancer was not observed in either gender (men, p = 0.2937 to 0.5783; women, p = 0.2042 to 0.9326). CONCLUSIONS: Our present study indicated the possibility that the previously reported association between leanness and the risk of lung cancer in women was not correct, and this apparent association might be influenced by other factors such as smoking and smoking-related respiratory diseases. A larger-scale cohort study combined with mass-screening project will confirm our results.

Aged↗
PubMed2005

Metastasis to appendix from lung adenocarcinoma.

We previously read with interest the case report by Filik et al. (International Journal of Gastrointestinal Cancer, 2003;34:55-58) on appendicular metastases from pancreatic adenocarcinoma. We would like to share our recent experience.A 64-yr-old man presented with a 2-d history of progressively increasing colicky abdominal pain and fever. His past medical history included a pneumonectomy of the left lung for locally advanced lung adenocarcinoma 9 mo previously. TNM stage of the original lung cancer was T2N2M0. On examination, his abdomen was slightly distended and he had an intermittent metallic bowel sound. Abdominal CT scan showed a low-density mass, 3 cm in diameter, in the right pelvic cavity. Endoscopic evaluation revealed no obstruction, but failed to identify mucosal abnormalities in the ileocecal region. Chest CT scan prior to surgery did not show any evidence of pulmonary recurrence or metastasis. He underwent a laparotomy, and tumor of the appendix, 3 x 3 cm in diameter, adhered to the surrounding tissue, but no perforation was seen. The mass was excised in combination with an ileocecal resection, followed by ileocolic anastomosis. Hisotologically, the neoplastic tumor cells infiltrated the submucosa, muscularis, and serosa, but mucosa of the appendix was intact, unremarkable, with no precursor lesion. The tumor was morphologically similar to the lung primary tumor. The patient had an uneventful postoperative course. He was examined at regular periodic follow-ups, but died from lung cancer 12 mo after the resection of the metastatic tumor to the appendix.

Abdominal Pain↗
PubMed2005

Adenovirus-mediated adiponectin expression augments skeletal muscle insulin sensitivity in male Wistar rats.

In this study, we investigated the chronic in vivo effect of adiponectin on insulin sensitivity and glucose metabolism by overexpressing the adiponectin protein in male Wistar rats using intravenous administration of an adenovirus (Adv-Adipo). Virally infected liver secreted adiponectin as high and low molecular weight complexes. After 7 days of physiological or supraphysiological hyperadiponectinemia, the animals displayed enhanced insulin sensitivity during the glucose tolerance and insulin tolerance tests. Glucose clamp studies performed at submaximal and maximal insulin infusion rates (4 and 25 mU x kg(-1) x min(-1), respectively) also demonstrated increased insulin sensitivity in Adv-Adipo animals, with the insulin-stimulated glucose disposal rate being increased by 20-67%. In contrast, insulin's effect on the suppression of hepatic glucose output and plasma free fatty acid levels was not enhanced in Adv-Adipo rats compared with controls, suggesting that high levels of adiponectin expression in the liver may lead to a local desensitization. Consistent with the clamp data, the activation of AMP-activated protein kinase was significantly enhanced in skeletal muscle (by 50%) but not in liver. One interesting finding was that in male Wistar rats, both AdipoR1 and AdipoR2 expression levels were higher in skeletal muscle than in liver, as it is the case in humans. These results indicate that chronic adiponectin treatment enhances insulin sensitivity and could serve as a therapy for human insulin resistance.

Adenoviridae↗
PubMed2004

GRK2 is an endogenous protein inhibitor of the insulin signaling pathway for glucose transport stimulation.

G protein-coupled receptor kinases (GRKs) represent a class of proteins that classically phosphorylate agonist-activated G protein-coupled receptors, leading to uncoupling of the receptor from further G protein activation. Recently, we have reported that the heterotrimeric G protein alpha-subunit, Galphaq/11, can mediate insulin-stimulated glucose transport. GRK2 contains a regulator of G protein signaling (RGS) domain with specificity for Galphaq/11. Therefore, we postulated that GRK2 could be an inhibitor of the insulin signaling cascade leading to glucose transport in 3T3-L1 adipocytes. In this study, we demonstrate that microinjection of anti-GRK2 antibody or siRNA against GRK2 increased insulin-stimulated insulin-responsive glucose transporter 4 (GLUT4) translocation, while adenovirus-mediated overexpression of wild-type or kinase-deficient GRK2 inhibited insulin-stimulated GLUT4 translocation as well as 2-deoxyglucose uptake. Importantly, a mutant GRK2 lacking the RGS domain was without effect. Taken together, these results indicate that through its RGS domain endogenous GRK2 functions as a negative regulator of insulin-stimulated glucose transport by interfering with Galphaq/11 signaling to GLUT4 translocation. Furthermore, inhibitors of GRK2 can lead to enhanced insulin sensitivity.

3T3-L1 Cells↗
PubMed2004

PGC-1 promotes insulin resistance in liver through PPAR-alpha-dependent induction of TRB-3.

Insulin resistance is a major hallmark in the development of type 2 diabetes, which is characterized by an impaired ability of insulin to inhibit glucose output from the liver and to promote glucose uptake in muscle. The nuclear hormone receptor coactivator PGC-1 (peroxisome proliferator-activated (PPAR)-gamma coactivator-1) has been implicated in the onset of type 2 diabetes. Hepatic PGC-1 expression is elevated in mouse models of this disease, where it promotes constitutive activation of gluconeogenesis and fatty acid oxidation through its association with the nuclear hormone receptors HNF-4 and PPAR-alpha, respectively. Here we show that PGC-1-deficient mice, generated by adenoviral delivery of PGC-1 RNA interference (RNAi) to the liver, experience fasting hypoglycemia. Hepatic insulin sensitivity was enhanced in PGC-1-deficient mice, reflecting in part the reduced expression of the mammalian tribbles homolog TRB-3, a fasting-inducible inhibitor of the serine-threonine kinase Akt/PKB (ref. 6). We show here that, in the liver, TRB-3 is a target for PPAR-alpha. Knockdown of hepatic TRB-3 expression improved glucose tolerance, whereas hepatic overexpression of TRB-3 reversed the insulin-sensitive phenotype of PGC-1-deficient mice. These results indicate a link between nuclear hormone receptor and insulin signaling pathways, and suggest a potential role for TRB-3 inhibitors in the treatment of type 2 diabetes.

Animals↗
PubMed2004

Left atrial thrombus in a patient with lung cancer.

We describe a rare case of a 64-year-old man with left atrial thrombus and stage IB adenocarcinoma of the lung. The patient was successfully treated with simultaneous cardiac operation and lobectomy for lung cancer.

Adenocarcinoma↗
PubMed2004

beta-arrestin-1 competitively inhibits insulin-induced ubiquitination and degradation of insulin receptor substrate 1.

beta-arrestin-1 is an adaptor protein that mediates agonist-dependent internalization and desensitization of G-protein-coupled receptors (GPCRs) and also participates in the process of heterologous desensitization between receptor tyrosine kinases and GPCR signaling. In the present study, we determined whether beta-arrestin-1 is involved in insulin-induced insulin receptor substrate 1 (IRS-1) degradation. Overexpression of wild-type (WT) beta-arrestin-1 attenuated insulin-induced degradation of IRS-1, leading to increased insulin signaling downstream of IRS-1. When endogenous beta-arrestin-1 was knocked down by transfection of beta-arrestin-1 small interfering RNA, insulin-induced IRS-1 degradation was enhanced. Insulin stimulated the association of IRS-1 and Mdm2, an E3 ubiquitin ligase, and this association was inhibited to overexpression of WT beta-arrestin-1, which led by decreased ubiquitin content of IRS-1, suggesting that both beta-arrestin-1 and IRS-1 competitively bind to Mdm2. In summary, we have found the following: (i) beta-arrestin-1 can alter insulin signaling by inhibiting insulin-induced proteasomal degradation of IRS-1; (ii) beta-arrestin-1 decreases the rate of ubiquitination of IRS-1 by competitively binding to endogenous Mdm2, an E3 ligase that can ubiquitinate IRS-1; (iii) dephosphorylation of S412 on beta-arrestin and the amino terminus of beta-arrestin-1 are required for this effect of beta-arrestin on IRS-1 degradation; and (iv) inhibition of beta-arrestin-1 leads to enhanced IRS-1 degradation and accentuated cellular insulin resistance.

Acetylcysteine↗
PubMed2004

Adenovirus-mediated chronic "hyper-resistinemia" leads to in vivo insulin resistance in normal rats.

We investigated the chronic in vivo effect of resistin on insulin sensitivity and glucose metabolism by overexpressing resistin protein in male Wistar rats using intravenous administration of an adenovirus encoding mouse resistin. After 7 days of elevated resistin levels at a supraphysiological concentration, the animals displayed glucose intolerance and hyperinsulinemia during glucose tolerance tests, and insulin tolerance tests demonstrated an impaired glucose-lowering effect of insulin. The glucose clamp studies were performed at submaximal (4 mU/kg/min) and maximal (25 mU/kg/min) insulin infusion rates and demonstrated the presence of insulin resistance induced by elevated resistin levels. Indeed, the insulin-stimulated glucose infusion rate was decreased by 12-31%; suppression of hepatic glucose output was attenuated by 28-55%; and insulin suppression of circulating FFA levels was inhibited by 7%. Insulin receptor substrate-1 and -2 phosphorylation and Akt activation were impaired in muscle and adipose tissue. Interestingly, activation of AMP-activated protein kinase in skeletal muscle, liver, and adipose tissue was also significantly downregulated. Together, these results indicate that chronic "hyper-resistinemia" leads to whole-body insulin resistance involving impaired insulin signaling in skeletal muscle, liver, and adipose tissue, resulting in glucose intolerance, hyperinsulinemia, and hypertriglyceridemia. Thus elevated resistin levels in normal rats fed a regular chow diet produce many of the features of human syndrome X.

AMP-Activated Protein Kinases↗