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San-e Ishikawa

Publications and source records attributed to San-e Ishikawa.

7 recordsLinked to original sources
PubMed2004

Decrease in serum C-reactive protein levels by troglitazone is associated with pretreatment insulin resistance, but independent of its effect on glycemia, in type 2 diabetic subjects.

Insulin-sensitizing thiazolidinediones (TZDs) decrease inflammatory markers such as high-sensitive C-reactive protein (hsCRP) in sera in addition to their hypoglycemic effects. However, factors associated with the decrease in serum hsCRP concentrations are unclear. In the present study, an effect of troglitazone on serum hsCRP levels was investigated and compared with its effect on glycemia. A total of 34 subjects with type 2 diabetes (17 men and 17 women, aged 54+/-2 years and body mass index (BMI) 26.7+/-0.6 kg/m(2), mean+/-S.E.) were studied. Nineteen out of the 34 subjects was treated with troglitazone 400mg daily for 12 weeks. The remaining 15 subjects were treated with metformin 750 mg daily as a control group. Baseline hsCRP levels were comparable between the two groups, and those were positively associated with fasting insulin levels. After treatment, glycemic control assessed by HbA1c and fasting glucose levels improved in both groups, whereas insulin sensitivity index estimated by homeostasis model assessment (HOMA-R) decreased only in the troglitazone-treated group. Serum levels of hsCRP significantly decreased from 916+/-210 ng/ml to 569+/-123 ng/ml (P<0.05) in the troglitazone-treated group, whereas the levels remained unchanged in the metformin-treated group (from 1087+/-248 ng/ml to 1152+/-301 ng/ml). In the troglitazone-treated group, there was no difference in the absolute and percent change in serum hsCRP levels between responders, who displayed the decrease in HbA1c greater than 0.6% (n=12), and the remaining non-responders (n=7). The decrease in serum hsCRP concentrations was negatively related to baseline levels of serum hsCRP and insulin and HOMA-R. In conclusion, troglitazone, but not metformin, reduced serum hsCRP levels in type 2 diabetic patients. The decrease in serum hsCRP concentrations by troglitazone was associated with the pretreatment levels of hsCRP and insulin resistance, but independent of the changes in glycemia.

Blood Glucose↗
PubMed2003

Close association of severe hyponatremia with exaggerated release of arginine vasopressin in elderly subjects with secondary adrenal insufficiency.

OBJECTIVE: Hyponatremia occurs not infrequently in hypopituitarism. Arginine vasopressin (AVP)-induced impaired water excretion is found in patients with hypopituitarism and experimental models of glucocorticoid deficiency. DESIGN: The present study was undertaken to determine whether augmented release of AVP is involved in the development of hyponatremia in elderly subjects with secondary adrenal insufficiency. METHODS: Forty patients with ACTH-deficient, secondary adrenal insufficiency were examined. They were divided into three groups according to the age at which diagnosis was ascertained (group A <20 Years, group B 20-64 Years, and group C>or=65 Years). RESULTS: Hyponatremia was more manifest in the elderly group than in the other two groups, serum sodium (Na) levels being 124.7 mmol/l in the elderly group, a value significantly less than 141.5 and 133.5 mmol/l in groups A and B. Plasma AVP levels seemed likely to be high compared with the respective hypo-osmolality in plasma in the elderly group, as plasma AVP levels were 1.7 pmol/l despite a mean plasma osmolality of 259 mmol/kg. Such an alteration was less clear in group B and was not found in group A. Therefore, elevation of plasma AVP was apparent in the elderly patients. Hydrocortisone replacement promptly normalized serum Na levels from 125 to 142 mmol/l (P<0.01) and reduced plasma AVP levels from 1.7 to 0.9 pmol/l (P<0.05), which were comparable to the respective plasma osmolality in the elderly patients. CONCLUSION: These results indicate that non-suppressible release of AVP is crucially involved in the impaired water excretion and hyponatremia seen in elderly patients with secondary adrenal insufficiency compared with the younger patients, and that exaggerated release of AVP becomes manifest as the subjects grow older.

Adolescent↗
PubMed2002

Urinary excretion of aquaporin-2 water channel in diabetic ketoacidosis.

We studied the changes in plasma arginine vasopressin (AVP) and urinary excretion of aquaporin-2 (UAQP-2) water channel in 3 patients with diabetic ketoacidosis. They had marked hyperglycemia of 27.9 +/- 2.8 mmol/l (mean +/- SEM), and elevated hemoglobin A1c of 8.8 +/- 1.4%. Circulatory blood volume was decreased by approximately 25%, which was determined by the changes in hematocrit. Plasma AVP levels were elevated to 10.3 +/- 3.0 pmol/l and UAQP-2, 578 +/- 200 fmol/mg creatinine (normal, 153 +/- 28) at the hospitalization. When hyperglycemia was improved by the intravenous infusion of a small dose of insulin plus fluid administration, both plasma AVP and UAQP-2 promptly decreased to 1.2 +/- 0.2 pmol/l and 252 +/- 29 fmol/mg creatinine on day 7, respectively. These alterations were concomitant with the recovery of circulatory blood volume. In the present study, UAQP-2, in addition to plasma AVP, indicates circulatory blood volume depletion, and the changes in UAQP-2 estimates the AVP-dependent recovery of circulatory blood volume during the therapeutic period in the patients with diabetic ketoacidosis.

Adult↗
PubMed2002

Decrease in urinary excretion of aquaporin-2 associated with impaired urinary concentrating ability in diabetic nephropathy.

Aquaporin-2 (AQP-2) is known to be expressed in the renal collecting duct cells and participates in urinary concentration in response to arginine vasopressin (AVP). The present study was undertaken to determine whether progression of renal dysfunction affects urinary excretion of AQP-2 in diabetic nephropathy. The study was composed of 8 control subjects and 14 patients with type 2 diabetes classified into two groups according to serum creatinine level (cut-off point; 1.5 mg/dl). After an 8-hour water deprivation, both urinary osmolality (U(osm)) and urinary excretion of AQP-2 significantly decreased in the diabetic patients with chronic renal failure as compared to the control subjects (p < 0.0001, p < 0.05, respectively). After a water load (10 ml/kg), no differences were found in plasma osmolality (P(osm)), AVP levels and U(osm), whereas urinary excretion of AQP-2 significantly decreased in the patients with chronic renal failure as compared to the control subjects (p < 0.05). These results indicate that the decreased urinary excretion of AQP-2 in diabetic nephropathy is due to the impaired cellular signaling of AVP in collecting duct cells, which may be partly involved in the urinary concentrating defect in renal failure.

Aquaporin 2↗
PubMed2002

Contrast-enhanced endoscopic ultrasonography improves the preoperative localization of insulinomas.

We report a case in which endoscopic ultrasonography (EUS), intraductal ultrasonography (IDUS) and contrast-enhanced EUS using Levovist helped to localize insulinoma correctly. A 74-year-old woman complained of symptomatic fasting hypoglycemia with relatively high concentration of serum insulin level. Dynamic contrast-enhanced computed tomography revealed a small tumor of 8 mm diameter in the pancreatic head. Insulin secretion was strongly stimulated by calcium injection into the gastroduodenal artery. To clarify the precise localization, we performed EUS, IDUS and contrast-enhanced EUS. The tumor was enhanced clearly by Levovist, and the distance from the main pancreatic duct was more than 3 mm. Therefore, a preoperative decision could be made to use the enucleation method for resection of the tumor. The surgeon could enucleate the tumor in a brief operation according to the preoperative diagnosis, and serum glucose levels returned to normal range after the operation. Contrast-enhanced EUS using Levovist was shown to be a useful diagnostic method for precise localization of small insulinoma.

Aged↗
PubMed2002

[Nephrogenic diabetes insipidus associated with mutations of vasopressin V2 receptors and aquaporin-2].

Nephrogenic diabetes insipidus has two types of X-linked and autosomal recessive inheritance. The former is the mutations of arginine vasopressin (AVP) V2 receptors that have had 155 mutations in 239 families in the literature. The latter is the mutations of aquaporin-2(AQP-2) water channel, which have had 11 mutations. The functional analysis of V2 receptor mutations has resulted in two abnormalities. The mutated receptors retain in cytoplasma and can not fold into plasma membrane in most of AVP V2 receptor mutations. The other is that the mutated receptors, localized in plasma membrane, can not either bind to its ligand AVP or transduce its signal to the post-receptor pathway. Also, the mutated AQP-2 is functionally divided into two types of abnormality. In 10 out of 11 mutations, the mutated AQP-2 is located in endoplasmic reticulum or Golgi apparatus, and can not be translocated into apical plasma membrane. The mutated AQP-2 should functionally produce water permeability, if it could be routed into plasma membrane. Only one mutation of AQP-2 (T125M and G175R) can be folded in apical membrane, but it does not produce water permeability. Recently, the experimental trials have been begun for rescuing the mutated AVP V2 receptors or AQP-2.

Aquaporin 2↗