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Dive into the research topics where Hidekatsu Yanai is active.

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Featured researches published by Hidekatsu Yanai.


Clinical Chemistry | 2003

Effects of Midstream Collection and the Menstrual Cycle on Urine Particles and Dipstick Urinalysis among Healthy Females

Mie Morimoto; Hidekatsu Yanai; Kenichi Shukuya; Kunihiko Kobayashi; Kazuhiko Matsuno

For urinalysis, midstream collection is recommended (1)(2)(3). Health-associated reference limits for leukocyte and erythrocyte counts in female urine are important for detecting hematuria, pyuria, and urinary tract infection (3). To understand the effects of urinary collection and the menstrual cycle on urinalysis, we examined first-stream and midstream urine samples from healthy female students with use of an automated dipstick reader and the fully automated urine cell analyzer, UF-100. Specimens were obtained from 64 healthy female students (age range, 18–20 years) at the College of Medical Technology. All were asymptomatic and had no extant urologic disease. They were instructed to collect only first and midstream urine samples in sterile containers at the same time and not to wipe or spread the labia. The volume of the first urine was measured, and the specimen was analyzed within 2 h. The students provided written, informed consent to participate in the study as well as information about their menstrual cycles. Specimens were classified into four groups according to the number of days after menstruation as follows: menstrual (1–7 days after menstruation; n = 15), follicular (8–15 days after menstruation; n = 21), ovulatory (16–19 days after menstruation; n = 6), and luteal (20–31 days after menstruation; n = 22). Particles in the urine were analyzed by use of a fully automated urine cell analyzer, UF-100 (Sysmex Corporation). We used the manufacturer-defined review …


Atherosclerosis | 2010

Administration of natural astaxanthin increases serum HDL-cholesterol and adiponectin in subjects with mild hyperlipidemia.

Hiroshi Yoshida; Hidekatsu Yanai; Kumie Ito; Yoshiharu Tomono; Takashi Koikeda; Hiroki Tsukahara; Norio Tada

BACKGROUND Astaxanthin has been reported to improve dyslipidemia and metabolic syndrome in animals, but such effects in humans are not well known. METHODS Placebo-controlled astaxanthin administration at doses of 0, 6, 12, 18 mg/day for 12 weeks was randomly allocated to 61 non-obese subjects with fasting serum triglyceride of 120-200mg/dl and without diabetes and hypertension, aged 25-60 years. RESULTS In before and after tests, body mass index (BMI) and LDL-cholesterol were unaffected at all doses, however, triglyceride decreased, while HDL-cholesterol increased significantly. Multiple comparison tests showed that 12 and 18 mg/day doses significantly reduced triglyceride, and 6 and 12 mg doses significantly increased HDL-cholesterol. Serum adiponectin was increased by astaxanthin (12 and 18 mg/day), and changes of adiponectin correlated positively with HDL-cholesterol changes independent of age and BMI. CONCLUSIONS This first-ever randomized, placebo-controlled human study suggests that astaxanthin consumption ameliorates triglyceride and HDL-cholesterol in correlation with increased adiponectin in humans.


Nutrition Journal | 2008

The underlying mechanisms for development of hypertension in the metabolic syndrome

Hidekatsu Yanai; Yoshiharu Tomono; Kumie Ito; Nobuyuki Furutani; Hiroshi Yoshida; Norio Tada

High blood pressure is an important constituent of the metabolic syndrome. However, the underlying mechanisms for development of hypertension in the metabolic syndrome are very complicated and remain still obscure. Visceral/central obesity, insulin resistance, sympathetic overactivity, oxidative stress, endothelial dysfunction, activated renin-angiotensin system, increased inflammatory mediators, and obstructive sleep apnea have been suggested to be possible factors to develop hypertension in the metabolic syndrome. Here, we will discuss how these factors influence on development of hypertension in the metabolic syndrome.


Atherosclerosis | 2000

β2-glycoprotein I deficiency: prevalence, genetic background and effects on plasma lipoprotein metabolism and hemostasis

Shinsuke Yasuda; Akito Tsutsumi; Hidekatsu Yanai; Yoshinori Miyoshi; Rie Takeuchi; Tetsuya Horita; Tatsuya Atsumi; Kenji Ichikawa; Eiji Matsuura; Takao Koike

Abstract β 2 -glycoprotein I (β 2 -GPI=apolipoprotein H) is an important autoantigen in patients with the antiphospholipid syndrome. It also plays a role in lipoprotein metabolism, such as anti-atherogenic property, triglyceride removal, and enhancement of lipoprotein lipase. Serum β 2 -GPI concentration of 812 apparently healthy Japanese individuals was measured by sandwich EIA. Two families with complete β 2 -GPI deficiency were identified. In one family, all affected had increased serum LDL-cholesterol levels or smaller particle sizes of LDL, while the other had no apparent abnormality in lipid metabolism. Individuals investigated had no history of thrombosis or overt abnormalities in hemostatic tests. A thymine corresponding to position 379 of the β 2 -GPI cDNA was deleted in every β 2 -GPI deficient individual. The incidence of this heterozygous deficiency determined by RFLP was 6.3% in Japanese and none in Caucasians. Heterozygotes had significantly lower concentrations of serum β 2 -GPI than did those without the mutation, yet no significantly different lipid profiles, such as total cholesterol, triglyceride, HDL-cholesterol, LDL-cholesterol, apoA-I, apoB and Lp(a), were observed. A low concentration of β 2 -GPI seemed not to be associated with apparent abnormality in lipoprotein metabolism.beta(2)-glycoprotein I (beta(2)-GPI=apolipoprotein H) is an important autoantigen in patients with the antiphospholipid syndrome. It also plays a role in lipoprotein metabolism, such as anti-atherogenic property, triglyceride removal, and enhancement of lipoprotein lipase. Serum beta(2)-GPI concentration of 812 apparently healthy Japanese individuals was measured by sandwich EIA. Two families with complete beta(2)-GPI deficiency were identified. In one family, all affected had increased serum LDL-cholesterol levels or smaller particle sizes of LDL, while the other had no apparent abnormality in lipid metabolism. Individuals investigated had no history of thrombosis or overt abnormalities in hemostatic tests. A thymine corresponding to position 379 of the beta(2)-GPI cDNA was deleted in every beta(2)-GPI deficient individual. The incidence of this heterozygous deficiency determined by RFLP was 6. 3% in Japanese and none in Caucasians. Heterozygotes had significantly lower concentrations of serum beta(2)-GPI than did those without the mutation, yet no significantly different lipid profiles, such as total cholesterol, triglyceride, HDL-cholesterol, LDL-cholesterol, apoA-I, apoB and Lp(a), were observed. A low concentration of beta(2)-GPI seemed not to be associated with apparent abnormality in lipoprotein metabolism.


Atherosclerosis | 2002

Unique character and metabolism of high density lipoprotein (HDL) in fetus

Hironori Nagasaka; Hideaki Kikuta; Harukuni Akita; Yukihiro Takahashi; Hidekatsu Yanai; Shu-Ping Hui; Hirotoshi Fuda; Hironobu Fujiwara; Kunihiko Kobayashi

Lipid and lipoprotein profiles, and enzymes for the lipid metabolism were compared between cord and adult blood. Consistent with previous reports, the major lipoprotein in cord blood was high-density lipoprotein (HDL), and that in adult blood was low-density lipoprotein (LDL). The level of apolipoprotein E (apo E) in cord blood was almost equivalent to that in adult blood, while other apolipoproteins and lipids were all lower than the adult level. In cord blood, apo E-rich HDL cholesterol represented more than 30% of total HDL cholesterol (around 11% in adult), and the concentration was about twice of that in adult blood. This apo E-rich HDL cholesterol was poorly esterified (E/T 56%) compared with that in adults (93%). The lecithin:cholesterol acyltransferase (LCAT) activity in cord blood was extremely low, while the activity and mass of cholesteryl ester transfer protein (CETP) were higher than those in adult blood. The apo E genotype did not show influences on total cholesterol, LDL cholesterol, total HDL cholesterol, and apo E rich HDL cholesterol levels in cord blood, as opposed to those in adult blood. The association of D442G mutation of the CETP gene with the increased HDL cholesterol in adult blood was not seen in cord blood. Rather, the mutation was associated with low total cholesterol and LDL cholesterol levels in cord blood. These results indicate that, in fetus, the character and metabolism of HDL, especially of apo E-rich HDL cholesterol, are distinct from those in adults.


Nutrition Journal | 2007

Diacylglycerol oil for the metabolic syndrome

Hidekatsu Yanai; Yoshiharu Tomono; Kumie Ito; Nobuyuki Furutani; Hiroshi Yoshida; Norio Tada

Excess adiposity has been shown to play a crucial role in the development of the metabolic syndrome. The elevated fasting and postprandial triglyceride-rich lipoprotein levels is the central lipid abnormality observed in the metabolic syndrome. Recent studies have indicated that diacylglycerol (DAG) is effective for fasting and postprandial hyperlipidemia and preventing excess adiposity by increasing postprandial energy expenditure. We will here discuss the mechanisms of DAG-mediated improvements in hyperlipidemia and in postprandial energy expenditure, and effects of DAG oil on lipid/glucose metabolism and on body fat. Further, the therapeutic application of DAG for the metabolic syndrome will be considered.


American Journal of Medical Genetics | 2000

Human CD36 deficiency is associated with elevation in low-density lipoprotein-cholesterol.

Hidekatsu Yanai; Hitoshi Chiba; Mie Morimoto; Keisuke Abe; Hironobu Fujiwara; Hirotoshi Fuda; Shu-Ping Hui; Yukihiro Takahashi; Harukuni Akita; G. A. Jamieson; Kunihiko Kobayashi; Kazuhiko Matsuno

To find out whether CD36 plays a role in the human lipoprotein metabolism, we studied lipoprotein profiles in subjects with CD36 deficiency. Apparently healthy Japanese volunteers (n = 790) were classified by flow cytometry into three groups of normal (platelet and monocyte CD36+, n = 741, 93.8%), type-II deficiency (platelet CD36- and monocyte CD36+, n = 45, 5.7%), and type-I deficiency (platelet and monocyte CD36-, n = 4, 0.5%). At least one of reported mutations in the CD36 gene was found in all four subjects with type-I deficiency and in 23 of the 45 subjects with type II. Among 779 subjects (731 normals, 44 type II, and four type I) with serum triglyceride levels of <400 mg/dL, serum total cholesterol and low-density lipoprotein (LDL) cholesterol were significantly elevated in type-II deficiency (P = 0.0095 and 0.0382 versus normal, respectively, Scheffes F-test), while differences were not significant in triglyceride and high-density lipoprotein-cholesterol. Similar tendency was observed in type-I deficiency, although the differences were not statistically significant because of small sample size. We conclude that CD36 deficiency elevates LDL cholesterol, indicating a contribution of CD36 to LDL metabolism.


Obesity | 2008

Effects of Diacylglycerol on Glucose, Lipid Metabolism, and Plasma Serotonin Levels in Lean Japanese

Hidekatsu Yanai; Hiroshi Yoshida; Yoshiharu Tomono; Yuji Hirowatari; Hideo Kurosawa; Akiyo Matsumoto; Norio Tada

Objective: Diacylglycerol (DAG)‐rich oil has been suggested to suppress postprandial hyperlipidemia and promote negative caloric balance by increasing energy expenditure (EE), due to small intestine physiochemical dynamics that differ from triacylglycerol (TAG). We studied the effect of DAG on postprandial glucose/insulin metabolism by loading of carbohydrate with oil. Further, to reveal the mechanism for increased EE by DAG, we measured plasma serotonin, which is mostly present in the small intestine and mediates peripheral sympathetic thermogenesis.


Journal of Clinical Medicine Research | 2012

Effects of 6-Month Sitagliptin Treatment on Glucose and Lipid Metabolism, Blood Pressure, Body Weight and Renal Function in Type 2 Diabetic Patients: A Chart-Based Analysis

Hidekatsu Yanai; Hiroki Adachi; Hidetaka Hamasaki; Yoshinori Masui; Reo Yoshikawa; Sumie Moriyama; Shuichi Mishima; Akahito Sako

Background Sitagliptin is one of the dipeptidyl peptidase-4 (DPP-4) inhibitors which prevent the inactivation of incretins, increasing the endogenous active incretin levels. Incretins stimulate insulin secretion from pancreatic β-cells and inhibit glucagon secretion from pancreatic α-cells, which is favorable for the treatment of diabetes. Sitagliptin is released on December, 2009, in Japan. We retrospectively studied effects of 6-month-treatment with sitagliptin on glucose and lipid metabolism, blood pressure, body weight and renal function in patients with type 2 diabetes by a chart-based analysis. Methods We retrospectively studied 220 type 2 diabetic patients who have taken sitagliptin for 6 months by a chart-based analysis. Subjects studied include patients treated with sitagliptin monotherapy, sitagliptin add-on therapy, and switching from glinide to sitagliptin. We selected patients who have both data before and after 6-month sitagliptin treatment and compared the data before the sitagliptin treatment with the data at 6 month after the sitagliptin treatment started. Body weight, blood pressure, plasma glucose, hemoglobin A1c (HbA1c), serum lipids, and estimated glomerular filtration rate in type 2 diabetic patients were measured almost at the same time points before and after 6-month-treatment with sitagliptin. Results Body weight was significantly reduced after 6-month sitagliptin treatment by 0.8 kg. HbA1c levels were also significantly decreased after the sitagliptin treatment by 0.6%. We found a significant and negative correlation between change in body weight and body mass index at baseline. We also observed a significant and negative correlation between change in HbA1c and HbA1c levels at baseline. The number of patients who showed the absence of urinary glucose was significantly increased after the sitagliptin treatment.


Journal of Clinical Medicine Research | 2015

Nutrition for Sarcopenia.

Hidekatsu Yanai

Aging-related sarcopenia means that muscle mass, strength, and physical performance tend to decline with age, and malnutrition is associated with sarcopenia. Therefore, nutritional interventions may make an important contribution to prevent the development of sarcopenia. Here I reviewed published articles about the effects of nutritional factors on sarcopenia in elderly people. A growing body of evidence suggests that metabolic factors associated with obesity and diabetes induce the progression of sarcopenia. However, the effectiveness and safety of caloric restriction for sarcopenia remained unclear. Protein intake and physical activity are the main anabolic stimuli for muscle protein synthesis. As optimal dietary protein intake, 1.0 - 1.2 g/kg (body weight)/day with an optimal repartition over each daily meal or 25 - 30 g of high quality protein per meal were recommended to prevent sarcopenia, which was supported by some observational studies. Protein supplementation using cheese and milk protein, essential amino acids, leucine, beta-hydroxy-beta-methylbutyrate and vitamin D has been investigated as a potential supplement to improve muscle quality in sarcopenic elderly people.

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Norio Tada

Jikei University School of Medicine

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Kumie Ito

Jikei University School of Medicine

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Mitsuhiko Noda

Saitama Medical University

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