PubMed Health⌕ Search

Biomedical subjects

Matsuo Taniyama

Publications and source records attributed to Matsuo Taniyama.

15 recordsLinked to original sources
PubMed2003

Cellular localization of prolactin-releasing peptide receptors in the human pituitary.

The recently identified prolactin (PRL)-releasing peptide (PrRP) is the first hypothalamic peptide hormone found to operate as a ligand of an orphan receptor that specifically stimulates PRL production from the pituitary gland. However, its other biological functions remain unknown. Using immunohistochemistry, we examined the distribution of the PrRP receptor in various human tissues, as well as the precise localization of the PrRP receptor in the human normal pituitary. Among various tissues examined, PrRP receptor-immunopositive cells were detected only in the pituitary gland. A double immunohistochemical procedure was used to examine PrRP receptor-positive cells from ten normal human pituitary glands, and it was determined that numerous PrRP receptor-positive cells are also positive for adrenocorticotropic hormone (ACTH) but negative for PRL. Growth hormone-, beta-thyroid-stimulating hormone-, beta-follicle-stimulating hormone-, beta-luteinizing hormone- or alpha-subunit-positive cells did not test positive for the presence of PrRP receptors. Thus, we suggest that PrRP receptor and probably PrRP may play a regulatory role in ACTH secretion, rather than in the release of PRL from the human anterior pituitary. This is the first report to demonstrate colocalization of the PrRP receptor and ACTH by immunohistochemistry.

Animals↗
PubMed2003

Decrease in serum adiponectin level due to obesity and visceral fat accumulation in children.

OBJECTIVE: To determine whether serum adiponectin is decreased in obesity and is restored toward normal level after treatment in children. RESEARCH METHODS AND PROCEDURES: Subjects were 53 Japanese obese children, 33 boys and 20 girls (6 to 14 years old), and 30 age-matched nonobese controls for measuring adiponectin (16 boys and 14 girls). Blood was drawn after an overnight fast, and the obese children were subjected to anthropometric measurements including waist and hip circumferences and skinfold thicknesses. Paired samples were obtained from 21 obese children who underwent psychoeducational therapy. Visceral adipose tissue area was measured by computed tomography. Adiponectin was assayed by an enzyme-linked immunosorbent assay. RESULTS: The serum levels of alanine aminotransferase, uric acid, triglyceride, total cholesterol, low-density lipoprotein-cholesterol, total cholesterol/high-density lipoprotein-cholesterol, apo B, apo B/apo A(1), and insulin in obese children were higher than the reference values. Serum adiponectin level was lower in the obese children than in the controls (6.4 +/- 0.6 vs. 10.2 +/- 0.8 mg/L, means +/- SEM, p < 0.001). In 21 obese children whose percent overweight declined during therapy, the adiponectin level increased (p = 0.002). The adiponectin level was correlated inversely with visceral adipose tissue area in obese children (r = -0.531, p < 0.001). The inverse correlations of adiponectin with alanine aminotransferase, uric acid, and insulin were significant after being adjusted for percentage overweight, percentage body fat, or sex. DISCUSSION: Serum adiponectin level is decreased in obese children depending on the accumulation of visceral fat and is restored toward normal level by slimming.

Adiponectin↗
PubMed2002

SNP analysis of the inter-alpha-trypsin inhibitor family heavy chain-related protein (IHRP) gene by a fluorescence-adapted SSCP method.

BACKGROUND: Single-nucleotide polymorphisms (SNPs) are considered to be useful polymorphic markers for genetic studies of polygenic traits. Single-stranded conformational polymorphism (SSCP) analysis has been widely applied to detect SNPs, including point mutations in cancer and congenital diseases. In this study, we describe an application of the fluorescent labeling of PCR fragments using a fluorescent-adapted primer for SSCP analysis as a novel method. METHODS: Single-nucleotide polymorphisms (SNPs) of the inter-alpha-trypsin inhibitor family heavy chain-related protein (IHRP) gene were analyzed using a fluorescence-adapted SSCP method. The method was constructed from two procedures: 1) a fluorescent labeling reaction of PCR fragments using fluorescence-adapted primers in a single tube, and 2) electrophoresis on a non-denaturing polyacrylamide gel. RESULTS: This method was more economical and convenient than the single-stranded conformational polymorphism (SSCP) methods previously reported in the detection of the labeled fragments obtained. In this study, eight SNPs of the IHRP gene were detected by the fluorescence-adapted SSCP. One of the SNPs was a new SNP resulting in an amino acid substitution, while the other SNPs have already been reported in the public databases. Six SNPs of the IHRP were associated with two haplotypes. CONCLUSIONS: The fluorescence-adapted SSCP was useful for detecting and genotyping SNPs.

Journal Article↗
PubMed2002

Correlation of the adipocyte-derived protein adiponectin with insulin resistance index and serum high-density lipoprotein-cholesterol, independent of body mass index, in the Japanese population.

Adiponectin, which is secreted specifically by adipose tissue, has been shown to act as an anti-atherosclerotic protein by direct effects on endothelial cells. Clinical studies have shown that adiponectin levels are lower in individuals with obesity, diabetes and coronary artery disease. The present study investigated relationships between serum adiponectin levels and body mass index (BMI), blood pressure, insulin resistance index, lipid profile, uric acid and high-sensitivity C-reactive protein levels in a large number of Japanese subjects not taking any medication for metabolic disease and without severe illness (705 men and 262 women; age 30-65 years; BMI 22.5+/-2.9 kg/m(2)). The serum adiponectin concentration was measured by ELISA, without a protein-denaturing step. The insulin resistance index was assessed by homoeostasis model assessment (HOMA-IR). The serum concentration of adiponectin in women (13.5+/-7.9 microg/ml) was significantly higher than that in men (7.2+/-4.6 microg/ml). The serum adiponectin level was negatively correlated with BMI, systolic blood pressure, diastolic blood pressure, fasting plasma glucose, insulin, HOMA-IR, total cholesterol, triacylglycerols, low-density lipoprotein (LDL)-cholesterol and uric acid, and positively correlated with high-density lipoprotein (HDL)-cholesterol. The correlations between serum adiponectin level and insulin, HOMA-IR, triacylglycerols, HDL-cholesterol, LDL-cholesterol and uric acid were significant even after adjustment for age, sex and BMI. Stepwise multiple regression analysis revealed that HDL-cholesterol, sex, BMI and HOMA-IR were independently correlated with the serum adiponectin level (R(2)=0.377). These findings suggest that the serum adiponectin level is negatively correlated with HOMA-IR and positively correlated with HDL-cholesterol, independent of age, sex and BMI, in the Japanese population.

Adiponectin↗
PubMed2002

Effects of pioglitazone on metabolic parameters, body fat distribution, and serum adiponectin levels in Japanese male patients with type 2 diabetes.

The aim of this study was to evaluate the effects of pioglitazone on clinical and metabolic parameters, body fat distribution, and serum adiponectin, a recently discovered antiatherosclerotic hormone, in Japanese patients with type 2 diabetes. Ten male patients aged 40 to 66 (57.7 +/- 7.4) years, who were being treated with dietary therapy alone (n = 7) or with a stable dose of sulfonylurea (n = 3), were studied at baseline and after 3 months of pioglitazone treatment (30 mg/d). Body mass index (BMI), blood pressure, fasting plasma glucose (FPG), glycosylated hemoglobin (HbA1c), serum insulin, adiponectin, and lipid profile were measured. Also, visceral adipose tissue area (VAT) and subcutaneous adipose tissue area (SAT) at the umbilical level were determined by computed tomographic (CT) scanning. Mean blood pressure (109 +/- 14 to 101 +/- 10 mm Hg), FPG (8.6 +/- 1.4 to 7.0 +/- 1.0 mmol/L), serum insulin (54 +/- 11 to 30 +/- 8 pmol/L, P <.01 for all), and HbA1c (6.7 +/- 0.8 to 6.1% +/- 0.6%, P =.013) decreased significantly during 3 months of pioglitazone treatment. BMI (26.4 +/- 3.2 to 27.0 +/- 3.5 kg/m2), low-density lipoprotein (LDL) cholesterol (124 +/- 24 to 138 +/- 24 mg/dL) and SAT (155 +/- 69 to 179 +/- 81cm2, P <.05 for all) increased, while triglycerides and high-density lipoprotein (HDL) cholesterol did not change significantly after 3 months of pioglitazone treatment. Serum adiponectin level increased in all patients (4.8 +/- 1.7 to 14.4 +/- 2.1 microg/mL, P =.005). VAT tended to increase (165 +/- 38 to 180 +/- 46 cm2) and VAT/SAT ratio tended to decrease (1.2 +/- 0.3 to 1.1 +/- 0.3), but these differences did not reach statistical significance. These results suggest that pioglitazone exerts good glycemic and blood pressure control despite increased BMI and SAT in Japanese male patients with type 2 diabetes. It is also suggested that pioglitazone may have an antiatherosclerotic effect by increasing serum adiponectin level.

Adiponectin↗
PubMed2002

PPAR(gamma)2 gene Pro12Ala polymorphism may influence serum level of an adipocyte-derived protein, adiponectin, in the Japanese population.

Adiponectin is an adipocyte-derived protein, which possesses an anti-atherosclerotic action and improves insulin sensitivity. Peroxisome proliferator-activated receptor gamma (PPAR(gamma)) regulates the transcription of many adipocyte-specific genes. A Pro12Ala polymorphism has been detected in the PPAR(gamma)2 gene, and this substitution has been reported to reduce transactivation activity in vitro. We hypothesized that individuals possessing this Ala12 allele may have a lower serum adiponectin level, because of the observation that PPAR(gamma) agonists increase the plasma adiponectin level in humans. To test this hypothesis, we investigated the effects of the PPAR(gamma)2 Pro12Ala polymorphism on anthropometric and metabolic parameters, including serum adiponectin level, in 478 Japanese men and 117 women aged 30 to 65 years. There were no homozygous subjects for the Ala12 allele of the PPAR(gamma)2 gene in this study. Plasma adiponectin levels were significantly lower in subjects with the Ala12 allele in the Japanese population of both sexes, although body mass index (BMI), plasma glucose, serum lipids, and insulin resistance index were not significantly different between subjects with and without this polymorphism. It is suggested that the Pro12Ala polymorphism of the PPAR(gamma)2 gene may reduce serum adiponectin level in the Japanese population.

Adiponectin↗
PubMed2002

Genetic variation in the gene encoding adiponectin is associated with an increased risk of type 2 diabetes in the Japanese population.

An adipocyte-derived peptide, adiponectin (also known as GBP28), is decreased in subjects with type 2 diabetes. Recent genome-wide scans have mapped a diabetes susceptibility locus to chromosome 3q27, where the adiponectin gene (APM1) is located. Herein, we present evidence of an association between frequent single nucleotide polymorphisms at positions 45 and 276 in the adiponectin gene and type 2 diabetes (P = 0.003 and P = 0.002, respectively). Subjects with the G/G genotype at position 45 or the G/G genotype at position 276 had a significantly increased risk of type 2 diabetes (odds ratio 1.70 [95% CI 1.09-2.65] and 2.16 [1.22-3.95], respectively) compared with those having the T/T genotype at positions 45 and 276, respectively. In addition, the subjects with the G/G genotype at position 276 had a higher insulin resistance index than those with the T/T genotype (1.61 +/- 0.05 vs. 1.19 +/- 0.12, P = 0.001). The G allele at position 276 was linearly associated with lower plasma adiponectin levels (G/G: 10.4 +/- 0.85 microg/ml, G/T: 13.7 +/- 0.87 microg/ml, T/T: 16.6 +/- 2.24 microg/ml, P = 0.01) in subjects with higher BMIs. Based on these findings together with the observation that adiponectin improves insulin sensitivity in animal models, we conclude that the adiponectin gene may be a susceptibility gene for type 2 diabetes.

Adiponectin↗