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Makoto Daimon

Publications and source records attributed to Makoto Daimon.

At least 19 recordsLinked to original sources

Is the measurement of glycated hemoglobin A1c alone an efficient screening test for undiagnosed diabetes? Japan National Diabetes Survey.

The aim of the study was to assess the screening test properties of HbA1c for undiagnosed diabetes (DM) according to the 1999-WHO criteria and its relevance of the Japan National Diabetes Survey Cut-off points for possible and probable DM: HbA1c >or=5.6 and 6.1%. Screening properties of HbA1c predicting undiagnosed DM was examined and compared with that of fasting plasma glucose (FPG) in 1904 Funagata-town inhabitants aged 35-89 years old. The prevalence of previous DM, undiagnosed DM, and impaired glucose regulation (IGR) were 5.5, 6.0, and 18.6%, while the prevalence of probable and possible DM were 7.7 and 5.4%. The area under the receiver operating characteristic curve for undiagnosed DM was similar between HbA1c (0.856 [95% CI: 0.812-0.899]) and FPG (0.902 [0.869-0.936]). HbA1c of 5.6% gave a sensitivity of 56.5%, a specificity of 95.1%, positive and negative predictive values of 44.2 and 97.0%, and a proportion of people above the cut-off point of 8.2%. True positive tests were significantly higher with mean levels of BMI, fasting, and 2-h plasma glucose, and HbA1c, but lower with mean levels of high-density-lipoprotein cholesterol than in false negative tests. The measurement of HbA1c alone may be efficient to screen undiagnosed DM and the cut-off point of 5.6% might be proper with respect to screening tests properties for undiagnosed DM, and prediction of vascular complications in Japan.

Adult↗

The role of G-protein-coupled receptor kinase 5 in pathogenesis of sporadic Parkinson's disease.

Sporadic Parkinson's disease (sPD) is a common neurodegenerative disorder, characterized by selective degeneration of dopaminergic neurons in the substantia nigra. Although the pathogenesis of the disease remains undetermined, phosphorylation of alpha-synuclein and its oligomer formation seem to play a key role. However, the protein kinase(s) involved in the phosphorylation in the pathogenesis of sPD has not been identified. Here, we found that G-protein-coupled receptor kinase 5 (GRK5) accumulated in Lewy bodies and colocalized with alpha-synuclein in the pathological structures of the brains of sPD patients. In cotransfected cells, GRK5 phosphorylated Ser-129 of alpha-synuclein at the plasma membrane and induced translocation of phosphorylated alpha-synuclein to the perikaryal area. GRK5-catalyzed phosphorylation also promoted the formation of soluble oligomers and aggregates of alpha-synuclein. Genetic association study revealed haplotypic association of the GRK5 gene with susceptibility to sPD. The haplotype contained two functional single-nucleotide polymorphisms, m22.1 and m24, in introns of the GRK5 gene, which bound to YY1 (Yin Yang-1) and CREB-1 (cAMP response element-binding protein 1), respectively, and increased transcriptional activity of the reporter gene. The results suggest that phosphorylation of alpha-synuclein by GRK5 plays a crucial role in the pathogenesis of sPD.

Aged↗

Correlation between change in body weight rather than current body weight and change in serum adiponectin levels in a Japanese population -- the Funagata study.

Serum adiponectin levels are decreased in obese subjects. We examined the association of current body weight (BW) and its change with a change in serum adiponectin levels. Serum adiponectin levels at the baseline (from 1995 to 1997) and the 5-year follow-up (from 2000 to 2002) examinations were evaluated in 1003 (M/F, 425/578; age at the baseline examinations, 58.3 +/- 11.7/57.5 +/- 11.0 years) Japanese subjects from a cohort population (N = 2013) of the Funagata study. Correlations and associations of BW at the baseline examinations and changes in BW between the baseline and the follow-up examinations (deltaBW) with changes in the serum adiponectin levels in the study period (deltaAdiponectin) were examined. Stepwise regression analyses revealed a significant correlation of the deltaBW (r = -0.233 and -0.204 for men and women, respectively; r = -0.324 for the upper tertile group divided based on their body mass index in women) with the deltaAdiponectin. However, the BW at the baseline examinations was not significantly correlated in both sexes. Multiple logistic regression analyses revealed that subjects who reduced their BW by 2 kg or more were 2.56 (95% confidence interval, 1.21-5.42; P = .014) and 8.24 times (95% confidence interval, 3.59-18.9; P < .001) more likely to be in the upper tertile of the deltaAdiponectin than those who increased their BW by 2 kg or more in men and women, respectively, independent of their BW at the baseline examinations. In conclusion, we showed here that the deltaBW was strongly associated with the deltaAdiponectin in both sexes, whereas the BW at the baseline examinations was not associated with the deltaAdiponectin, at least in women.

Adiponectin↗

Cardiovascular risk factors and retinal microvascular signs in an adult Japanese population: the Funagata Study.

OBJECTIVE: To describe the prevalence of retinal vascular signs and their association with cardiovascular risk factors in a Japanese population. DESIGN: Population-based cross-sectional study. PARTICIPANTS: Adult persons aged 35 years or older from Funagata, Yamagata Prefecture, Japan (n = 1481). METHODS: The Funagata Study is a Japanese population-based study of persons aged 35 years or older, and included 1961 nondiabetic participants (53.3% of 3676 eligible subjects). A nonmydriatic retinal photograph was taken of 1 eye to assess retinal microvascular signs. Retinal arteriolar wall signs (focal arteriolar narrowing, arteriovenous nicking, enhanced arteriolar wall reflex) and retinopathy were assessed in 1481 participants without diabetes (40.3% of eligible persons) using a standardized protocol. Using a computer-assisted method, retinal vessel diameters were measured in 921 participants with gradable retinal image (25.1% of eligible persons). MAIN OUTCOME MEASURES: Prevalence of retinal microvascular signs and their association with cardiovascular risk factors. RESULTS: Moderate or severe focal arteriolar narrowing, arteriovenous nicking, enhanced arteriolar wall reflex, and retinopathy were found in 8.3%, 15.2%, 18.7%, and 9.0%, respectively, of the study population. Mean (+/-standard error) values for retinal arteriolar diameter were 178.6+/-21.0 mum, and mean values (+/-standard error) for venular diameter were 214.9+/-20.6 mum. Older persons were more likely to have retinal arteriolar wall signs, retinopathy, and narrower retinal vessel diameters. After adjusting for multiple factors, each 10-mmHg increase in mean arterial blood pressure was associated with a 20% to 40% increased likelihood of retinal arteriolar signs and a 2.8-mum reduction in arteriolar diameter. Retinopathy was associated with higher body mass index and both impaired glucose tolerance and impaired fasting glucose. CONCLUSIONS: In nondiabetic Japanese adults, retinal arteriolar wall signs were associated with older age and increased blood pressure, whereas retinopathy was associated with older age, higher body mass index, impaired glucose tolerance, and impaired fasting glucose. These findings are comparable with data from white populations.

Adult↗

Association of the ABCA1 gene polymorphisms with type 2 DM in a Japanese population.

To examine the association of the ATP-binding cassette transporter 1 (ABCA1) gene with type 2 diabetes (DM), we studied genetic polymorphisms of the ABCA1 gene including its linkage disequilibrium (LD) and haplotype analyses using a Japanese population. A sample set (DM:72, IGT:75, and NGT:227) was genotyped with 34 SNPs distributed from the promoter region to the last exon of the ABCA1 gene. LD between SNPs was assessed in pairwise manner. Among 13 LD blocks constructed, an LD block at the 5'-region showed a significant difference in the haplotype distribution between the study groups (NGT vs. IGT + DM: overall p = 0.0180; NGT vs. DM: 0.0001). Fisher's exact probability test (NGT vs. DM) showed a significant association of the haplotype 2 of the LD block (p = 0.0001), with an odds ratio (OR) of 2.53 (95%CI:1.62-4.12). Diplotype analysis also showed a significant association of the diplotypes with the haplotype 2 (OR:2.59, 95%CI:1.48-4.54, p = 0.0013).

ATP Binding Cassette Transporter 1↗

Insulin inhibits glucagon-induced glycogenolysis normally in perivenous hepatocytes of Wistar fatty rats.

Wistar fatty (WF) rats are obese, hyperinsulinemic and hyperglycemic, and thus a model of type 2 diabetes mellitus. Since we have found that insulin specifically inhibits glucagon-induced glycogenolysis in perivenous hepatocytes (PVH) from normal rats, we examined the inhibitory effect of insulin on glucagon-induced glycogenolysis in PVH of hyperinsulinemic WF rats. Basal glucose release was 64.0+/-4.1 nmol/mgprotein/30 min from PVH of lean littermates (WL rats) and 137.0+/-19.3 nmol/mgprotein/30 min from that of WF rats (p<0.01). These were proportional to the glycogen content in PVH of WL and WF rats (56.7+/-7.2 and 131.0+/-20.3 microg/mgprotein, p<0.01), and increased to 109.0+/-8.8 and 225.8+/-17.9nmol/mgprotein/30min, respectively, with 0.1 nmol/l glucagon. When 10 nmol/l insulin was coincubated, 0.1 nmol/l glucagon-induced increase in glucose release decreased to 93.3+/-10.9 nmol/mgprotein/30 min in PVH of WL rats (p<0.01) and to 181+/-20.7 nmol/mgprotein/30 min in PVH of WF rats (p<0.01). Thus, insulin antagonized glucagon-induced glycogenolysis in PVH similarly between WL and WF rats, to 56.7+/-13.3% and to 46.1+/-7.5%, respectively. Thus, the antagonizing effect of insulin on glucagon-induced increase in glycogenolysis was preserved in PVH of hyperinsulinemic and hyperglycemic WF rats.

Animals↗

Association of decrease in serum dehydroepiandrosterone sulfate levels with the progression to type 2 diabetes in men of a Japanese population: the Funagata Study.

Association of serum dehydroepiandrosterone sulfate (DHEAS) levels with insulin resistance and impairment of insulin secretion have been reported. We here examined the association of serum DHEAS levels with type 2 diabetes mellitus (DM) and the progression to DM. The serum DHEAS levels at baseline (from 1995 to 1997) were evaluated in 1709 individuals (998 women and 711 men) from a cohort population (n = 3706) of the Funagata Study. Glucose tolerance was evaluated at baseline as well as at 5-year follow-up examinations (n = 970, follow-up rate, 56.8%) according to the 1985 World Health Organization criteria. The statistical significance of the difference between any 2 groups was determined by the Student t test. Multiple logistic regression analysis determined the association of the traits with the progression to DM at the 5-year follow-up examinations. P < .05 was accepted as statistically significant. The serum DHEAS levels were significantly lower in DM than in normal glucose tolerance. However, this difference was not significant when adjusted for age. In men, the decrease in serum DHEAS levels by the 5-year follow-up examinations was significantly larger in the subjects who became diabetic than in the subjects who remained normal glucose tolerance, even when adjusted for age ( P = .0003). Multiple logistic regression analysis revealed a significant association of the decrease in serum DHEAS levels with the progression to DM, with an odds ratio (per 0.1 log ng/mL) of 1.410 (95% confidence interval [CI], 1.020-1.948, P = .038), independently from age, height, and 2-hour plasma glucose in men. A decrease in serum DHEAS levels seems to be associated with the progression to DM in Japanese men.

Aged↗

A human granin-like neuroendocrine peptide precursor (proSAAS) immunoreactivity in tau inclusions of Alzheimer's disease and parkinsonism-dementia complex on Guam.

The deposition of tau inclusions is one of the neuropathological hallmarks in neurodegenerative disorders with dementia. We have reported that the N-terminal fragment of a human granin-like neuroendocrine peptide precursor (N-proSAAS) is accumulated in Pick bodies. However, it is unknown whether N-proSAAS is widely accumulated in tau inclusions in other tauopathies. Here, we performed an immunohistochemical examination using antibodies against both the N- and C-terminal sequence of proSAAS in the brains of patients with Alzheimer's disease and parkinsonism-dementia complex on Guam. The antibody against N-proSAAS immunostained neurofibrillary tangles and neuritic plaques in both diseases, whereas the antibody against the C-terminal sequence of proSAAS did not. The results of the present study suggest that N-proSAAS or proSAAS-like molecules were trapped within the tau fibrils and accumulated in tau inclusions.

Aged↗

Progression of diabetic nephropathy enhances the plasma osteopontin level in type 2 diabetic patients.

Osteopontin (OPN) is thought to play multiple roles in the progression of atherosclerotic plaque including diabetic vascular complications. However, it still remains unclear whether the level of OPN in vivo is indeed clinically associated with the progression of diabetic complications. This study evaluated whether the levels of OPN in plasma and urine are correlated with the progression of diabetic complications, such as retinopathy, neuropathy, and nephropathy in patients with type 2 diabetes. In 229 patients with type 2 diabetes, OPN level in plasma and urine was evaluated by both the severity of diabetic complications, such as retinopathy, neuropathy, and nephropathy, and the clinical characteristics and the substantial laboratory findings. Plasma OPN level increased significantly with aging and the progression of diabetic nephropathy, especially at the stage of renal failure (p<0.05). However, the level was not related to the progression of retinopathy or neuropathy, or to laboratory findings, such as HbA1c or serum lipids. In contrast, urinary OPN level was not associated with diabetic complications in any of the subjects. There was no correlation between the plasma and urinary values of OPN. The results established that the plasma OPN was elevated in proportion to the progression of diabetic nephropathy, indicating that the plasma concentration may be a potential diagnostic predictor of diabetic end-stage renal disease.

Aged↗

[A family of acute intermittent porphyria].

A 62-year-old man who had twice received laparotomies for abdominal pain of unknown origin was admitted to our hospital with acute abdominal pain. His family history of acute intermittent porphyria (AIP) suggested that it arose from acute porphyria. We treated the patient with 5% glucose solution by i.v. drip infusion and his abdominal pain improved rapidly. Diagnosis of AIP was established by the demonstration of reduced erythrocyte porphobilinogen deaminase (PBGD) activity and a point mutation (CAG --> CGG) in a splicing site in intron 10/exon 11 in the PBGD gene by DNA analysis. For screening of AIP carriers in his family, we measured erythrocyte PBGD activity. Four of his seven children were successfully diagnosed as AIP carriers. This is the ninth AIP family report, in which a mutation in the PBGD gene was revealed by DNA analysis.

Abdominal Pain↗

An N-terminal fragment of ProSAAS (a granin-like neuroendocrine peptide precursor) is associated with tau inclusions in Pick's disease.

The deposition of aggregated tau in cytoplasmic inclusions is one of the common neuropathological features in various dementing neurodegenerative disorders. At present, it remains unclear whether tau inclusions exert neurotoxicity or they are simply the consequence of neurodegeneration. In our approach for the analysis of the composition of tau inclusions, we detected the intense binding of anti-diacylglycerol kinase-zeta (DGK-zeta) antibodies to Pick bodies (PBs), which represent tau inclusions in Pick's disease. The polyclonal antibodies were found to cross-react with a 21-kDa protein, but not with tau or ubiquitin, on Western blots of normal human brain extracts. Analysis of the 21-kDa protein by two-dimensional-gel electrophoresis and mass-spectrometry revealed that the protein is an N-terminal fragment of proSAAS (a human granin-like neuroendocrine peptide precursor). Our results suggest that sequestration of the N-terminal fragment of proSAAS in intracellular PBs may cause a functional disturbance of neurons in Pick's disease.

Amino Acid Sequence↗

Glucagon-like peptide-1 inhibits glucagon-induced glycogenolysis in perivenous hepatocytes specifically.

Hepatocytes form the hepatic acinus as a unit of microcirculation. Following the bloodstream, at least two different zones can be discerned: the periportal (PPH) and the perivenous (PVH) zones. Recently, we found that insulin inhibits glucagon-induced glycogenolysis in PVH specifically. We therefore investigated the region-specific functional effects of glucagon-like peptide-1 (GLP-1), which is known to have an insulin-like activity, on glucagon-induced glycogenolysis in isolated PPH and PVH prepared by the digitonin-collagenase method. GLP-1 inhibited 0.1 nM glucagon-induced increase in glucose release from the PVH of fed rats specifically (p < 0.01) and had an additive effect with insulin. Insulin binding did not differ between PPH and PVH of fed rats. GLP-1 did not displace [125I]-glucagon binding to the purified hepatic cell membrane. Thus, it is directly confirmed that GLP-1 has an insulin-like activity in the liver.

Animals↗

Large-scale search of SNPs for type 2 DM susceptibility genes in a Japanese population.

The etiology of type 2 diabetes (DM) is polygenic. We investigated here genes and polymorphisms that associate with DM in the Japanese population. Single-nucleotide polymorphisms (SNPs) of 398 derived from 120 candidate genes were examined for association with DM in a population-based case-control study. The study group consisted of 148 cases and 227 controls recruited from Funagata, Japan. No evident subpopulation structure was detected for the tested population. The association tests were conducted with standard allele positivity tables (chi(2) tests) between SNP genotype frequency and case-control status. The independent association of the SNPs from serum triglyceride levels and body mass index was examined by multiple logistic regression analysis. A value of P<0.01 was accepted as statistically significant. Six genes (met proto-oncogene, ATP-binding cassette transporter A1, fatty acid binding protein 2, LDL receptor defect C complementing, aldolase B, and sulfonylurea receptor) were shown to be associated with DM.

ATP-Binding Cassette Transporters↗