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Recently, oral hypoglycemic agents with newer glucose lowering mechanisms have been on release. This is mostly to meet the diabetic patient’s need to avoid hypoglycemia, which is profoundly important for better long-term outcome of the treatment. In this study, we quantified the annual number of patients with type 2 diabetes who experienced hypoglycemia needing the third-party assistance who had random sample plasma glucose

Analysis of insulin and related glucoregulatory hormone secretion following high-molecular-weight insulin-like growth factor II (HMW-IGF-II)–releasing tumor excision has never been reported. In a man with chronic hypoglycemia—plasma glucose (PG), 2.1 mmol/L with undetectable serum insulin, less than 7.2 pmol/L on admission—the cause of the hypoglycemia was HMW-IGF-II in the serum secreted by an intrathoracic benign pleural solitary fibrous tumor (size: 15 × 17 × 12 cm). Removal of the tumor nullified serum HMW-IGF-II and hypoglycemia. Postoperative glucose metabolism was evaluated day 272 by 75 g oral glucose tolerance test (OGTT) and on days 5, 202, and 990 by fasted sampling. Glycated hemoglobin A1c (HbA1c) was 37 to 41 mmol/mol, fasting PG was 5.3 to 5.4 mmol/L, and 2-hour PG at 75 g OGTT was 6.9 mmol/L, indicating that he was at the prediabetes stage. Homeostasis Model Assessment 2 of Insulin Resistance and Homeostasis Model Assessment 2 of β-Cell levels were within the normal range but the Stumvoll first phase was lowered. Insulin sensitivity and secretion were compared to age-, sex-, and body mass index–matched controls with normal glucose metabolism. Long-term HMW-IGF-II exposure of pancreatic islet β cells caused the functional impairment, that is, suppressed glucose-stimulated insulin secretion (GSIS), leading to nondiabetic hyperglycemia. This fact suggests long-term HMW-IGF-II exposure of the islet β cell specifically dampens GSIS.

Context The role of hepatic steatosis (HS) in the initial stages of developing type 2 diabetes remains unclear. Objective We aimed to clarify the impact of HS indexed by Fatty Liver Index (FLI) and high-normal fasting plasma glucose (FPG) as risk factors for incident prediabetes in a nonobese cohort. Methods Data from 1125 participants with ADA-defined normal glucose metabolism (median age 52 years; BMI 23.1 kg/m2) were used for retrospective analysis. In the entire population, correlation between normal FPG and FLI was evaluated by multiple regression adjusted for age and sex. Follow-up data from 599 participants in whom 75-g OGTT was repeated 3.7 years later showed that 169 developed prediabetes. This was analyzed by the multivariate Cox proportional hazards model. Results In the entire population, FLI was positively correlated with FPG (P Conclusion Even among nonobese individuals, HS indexed by FLI and a high-normal FPG (≥ 5.3 mmol/L) are risk factors for prediabetes, independently from insulin.

The trajectory of glomerular filtration rate (GFR) in relation to glomerular hyperfiltration (GHF) has been unknown. It was evaluated retrospectively in 23,982 GHF-free health examinees who were followed for 2−10 yr (mean: 5.1 yr). GFR was estimated by the serum creatinine concentration, and GHF was defined as age- and sex-specific estimated GFR (eGFR) ≥ 95% of the Japanese general population. The temporal profile of eGFR was plotted in a GHF-centered way, which was fitted to a random coefficient linear mixed model. Of the 23,982 subjects, 797 and 23,185 subjects developed or did not develop GHF, respectively, so that they were termed as the GHF(+)and GHF(−)groups. At baseline, median eGFR was significantly elevated in the GHF(+)group compared with in the GHF(−)group: 94.1 versus 77.3 mL/min/1.73 m2( P < 0.001). Elevation of basal eGFR lasted for a mean (SD) of 3.3 (1.9) yr in the GHF(+)group; mean eGFR then rose to the GHF range, which was 108.5 mL/min/1.73 m2. The eGFR decline after the peak was steeper in the GHF(+)group than in the GHF(−)group: −0.984 versus −0.497 mL/min/1.73 m2/yr ( P < 0.001). Baseline eGFR, but no other variable, well predicted incident GHF, with an area under the receiver operating characteristic curve of 0.87 (95% confidence interval: 0.86–0.88). In conclusion, GHF occurs as a chronic, multiphasic phenomenon: initially with a sustained GFR elevation for years, followed by a GFR surge to the GHF range, which was accompanied by accelerated GFR declining.

Type 2 diabetes begins as conversion of normal glucose metabolism (NGM) to prediabetes, and 5-10% per year of people with prediabetes progress to diabetes. Therefore, understanding evolution of prediabetes is mandatory to know how type 2 diabetes starts. However, the process of conversion of NGM to prediabetes, which may be ethnicity-specific, has poorly been investigated. We analyzed 599 Japanese adults with NGM (fasting plasma glucose (FPG) Presentation: No date and time listed

A 59-year-old woman unaware of having diabetes was transferred due to coma. Upon discovery at home, her consciousness on the Glasgow Coma Scale was E1V2M4, BP 95/84 mmHg, body temperature 34.7°C. On arrival at ER, height was 1.63 m, weight 97 kg, plasma glucose (PG) 1,897 mg/dL, HbA1c 13.6%, osmolality 421 mosm/kg, arterial pH 7.185, lactate 6.34 mmol/L, β-hydroxybutyrate 7.93 mmol/L. With saline and regular insulin infusion, PG was lowered to 1,440 mg/dL at 2 hours and then to 250 mg/dL by Day 3, and consciousness normalized by Day 5. On admission, serum immunoreactive insulin (IRI) was undetectable (

Aims To compare impact of elevated HbA1c and fasting plasma glucose (FPG) on incident chronic kidney disease (CKD) in a non-diabetic cohort. Methods Data from diabetes- and CKD-free 25,109 health examinees were retrospectively analysed with a mean observation period of 5.3 years. Prediabetes was diagnosed by the ADA and WHO criteria, and CKD by estimated glomerular filtration rate (eGFR) Results For incident CKD (n = 2483), high HbA1c but not FPG was an independent risk: adjusted hazard ratio (AHR, 95%CI) for HbA1c 1% and FPG 1 mmol/L, 1.91 (1.70–2.16) and 0.85 (0.60–1.20), respectively. Prediabetes by the ADA and WHO criteria were both risk for CKD with AHR (95%CI), 1.21 (1.12–1.32) and 1.31 (1.16–1.48), respectively. Prediabetes diagnosed by ‘elevated HbA1c irrespective of FPG’, either by the ADA and the WHO definition, was a risk with AHR (95%CI), 1.48 (1.36–1.61) and 1.51 (1.31–1.74), respectively. In contrast, prediabetes diagnosed by ‘raised FPG irrespective of HbA1c’ was not a CKD risk. Conclusions Elevated HbA1c, but not FPG, identified CKD risk in non-diabetic individuals.

Objective We aimed to clarify the onset of diabetes. Design Data from 27,392 nondiabetic health examinees were retrospectively analyzed for a mean of 5.3 years. Trajectories of fasting plasma glucose (FPG), body mass index (BMI), and the single point insulin sensitivity (Si) estimator (SPISE), an index of Si, 10 years before diagnosis of prediabetes (PDM; n = 4781) or diabetes (n = 1061) were separately assessed by a mixed effects model. Diabetes and PDM were diagnosed by the American Diabetes Association definition on the basis of FPG and glycosylated hemoglobin A1c values. Results In individuals who developed diabetes, mean FPG and BMI were significantly higher (P < 0.01 each) and SPISE lower than those who did not at −10 years: FPG 101.5 mg/dL vs 94.5 mg/dL, BMI 24.0 kg/m2 vs 22.7 kg/m2, and SPISE 7.32 vs 8.34, P < 0.01 each. These measurements, in subjects who developed prediabetes, were slightly but definitely different from those who did not, already at −10 years: FPG 91.8 mg/dL vs 89.6 mg/dL, BMI 22.6 kg/m2 vs 22.1 kg/m2, and SPISE 8.44 vs 8.82, P < 0.01 each. In both cases, the differences were progressively greater toward year 0, the time of diabetes, or PDM diagnosis. Conclusions FPG was significantly elevated in those who developed diabetes at least 10 years before diagnosis of diabetes, and this was also the case in those who developed PDM. Glucose dysregulation precedes diagnosis of diabetes at least for 20 years., FPG already increased at 10 years before diagnosis of diabetes and also at 10 years before diagnosis of prediabetes. Diabetes may begin at least >20 years before its diagnosis.

A hypothesis that postchallenge hyperglycemia in subjects with low body weight (BW) may be due, in part, to small glucose volume (GV) was tested. We studied 11,411 nondiabetic subjects with a mean BW of 63.3 kg; 5,282 of them were followed for a mean of 5.3 yr. In another group of 1,537 nondiabetic subjects, insulin sensitivity, secretion, and a product of the two (index of whole body insulin action) were determined. Corrected 2 h-plasma glucose (2hPGcorr) during a 75-g oral glucose tolerance test in subjects with BW ≤ 59 kg was calculated as 2hPGcorr = δPG2h · ECW/[16.1 (males) or 15.3 (females)] + fasting PG (FPG), where δPG2h is plasma glucose increment in 2 h; ECW is extracellular water (surrogate of GV); FPG is fasting plasma glucose; and 16.1 and 15.3 are ECW of men and women, respectively, with BW = 59 kg. Multivariate analyses for BW with adjustment for age, sex, and percent body fat were undertaken. BW was, across its entire range, positively correlated with FPG ( P < 0.01). Whereas BW was correlated with 2hPG and δPG in a skewed J-shape, with inflections at around 60 kg ( P for nonlinearity < 0.01 for each). Nonetheless, in those with BW ≤ 59 kg, insulin sensitivity, secretion, and action were unattenuated, and incident diabetes was less compared with heavier counterparts. BW was linearly correlated with 2hPGcorr, i.e., the J-shape correlation was mitigated by the correction. In conclusion, postchallenge hyperglycemia in low BW subjects is in part due to small GV rather than impaired glucose metabolism.

Aim Risk profile for incident chronic kidney disease (CKD) in Japanese subjects has not been established. Our aim was to identify risk factors for CKD in Japanese. Methods Consecutive 171 536 health examinees (median age 49 years and estimated glomerular filtration rate (eGFR) 78.2 mL/min per 1.73 m2) without CKD were re-examined after a median period of 6.2 years. Results of Cox proportional hazards models in randomly assigned two thirds (Derivation cohort) were verified in the rest (Validation cohort). CKD was defined as eGFR

We encountered a 64‐year‐old man with hyperosmolar hyperglycemic syndrome, having a sudden‐onset homonymous right inferior quadrantanopia. This is the first documentation of such a phenomenon in hyperosmolar hyperglycemic syndrome. We believe this is a variant of hemianopia in patients with hyperglycemic hyperosmolar syndrome.

The quantitative impact of weight gain on prediabetic glucose dysregulation remains unknown; only one study quantitated the impact of weight loss. We quantified the impact of weight gain on the evolution and regression of prediabetes (PDM).In 4234 subjects without diabetes, using logistic regression analysis with a 4.8-year follow-up period, we analyzed the relationship between (1) δBMI (BMIMean (±s.d.) δBMI was 0.17 (±1.3) kg/mIn Japanese adults, an increase in the BMI by even 1 kg/m

Aims/Introduction ‘The Standard Diabetes Manual’ has been developed by clinical researchers from multiple major institutions in Japan, such as the National Center for Global Health and Medicine, as a comprehensive disease management program, including collaboration between primary care physicians (PCPs) and specialist services. The present study evaluated the efficacy of the manual as a quality improvement strategy in diabetes care by PCPs. Materials and Methods A total of 42 PCPs in eight domestic districts of the Japan Medical Association were allocated to either the intervention group or the control group in a cluster‐randomized design. The PCPs in both groups were provided with a copy of the Diabetes Treatment Guide published by the Japan Diabetes Society, and the PCPs in the intervention group additionally received a copy of the manual and a 30‐min relevant seminar at the inception of the intervention. The primary end‐point was the adherence to the following performances as quality indicators: evaluation of retinopathy, and urinary albumin excretion measurements and serum creatinine measurements, as recommended by the Japan Medical Association. Results A total of 416 patients were enrolled by 36 PCPs. During the 1‐year follow‐up period, the proportion of PCPs who adhered to recommendation‐concordant measurements of urinary albumin excretion was significantly higher in the intervention group than in the control group (adherence: 17.9% vs 5.3%, P = 0.016). The other parameters were not statistically different between the two groups. Conclusions Implementation of ‘The Standard Diabetes Manual’ potentially leads to an improved quality of diabetes management by PCPs.

A 43-yr-old hypertensive male was admitted due to hypokalemia (1.8 mEq/L) and renal dysfunction (eGFR, 20.0 mL/min/1.73 m2). His plasma aldosterone was 901.0 ng/dL, plasma renin activity 5.7 ng/mL/hr, and aldosterone/renin activity ratio 158. Angiotensin II (AII) was 0.7 pg/mL, ACTH

To clarify if prediabetes defined by the International Expert Committee (PrediabetesIEC) and/or the American Diabetes Society (PrediabetesADA) is a risk for incident glomerular hyperfiltration (GH). 24,524 health examinees without diabetes, chronic kidney disease (CKD), GH and antihypertensive treatment at baseline, and repeated examinations at least twice during a mean of 5.3 years were retrospectively analysed. Diabetes was defined as fasting plasma glucose (FPG) ≥ 7.0 mmol/L and/or HbA1c ≥ 47 mmol/mol, CKD by estimated glomerular filtration rate (eGFR)

Long-term glucose supplementation is required to prevent hypoglycemia after massive insulin overdosing. We fitted the blood insulin concentration-time profile to the model: I = A·exp(-a·t) + B·exp(-b·t), where I (μU/mL) is the serum/plasma insulin concentration, A (μU/mL) and B (μU/mL) are the peak insulin concentrations of each component, a (time-1) and b (time-1) are the time constants of each component, and t (h) is the time elapsed from the peak of blood insulin level. Additional components were considered as needed. Patient 1 had auto-injected 600 U NovoRapid® 30Mix, and Patient 2 had auto-injected 300 U Novolet®R (regular) and 1,800 U NovoLet®N (NPH). We used the disappearance of therapeutic doses of the respective insulin in healthy individuals as controls, and we obtained parameters by Excel solver. In Patient 1, the parameter values were A = 1490.04 and a = 0.15 for insulin aspart and B = 60.66 and b = 0.04 for protaminated aspart. In Patient 2, the values were A = 784.45 and a = 0.38 for regular insulin and B = 395.84 and b = 0.03 for NPH. Compared with controls, the half-lives (t1/2) for insulin aspart and protaminated aspart were 4 and 2 times longer, respectively, in Patient 1. In Patient 2, the t1/2 for regular and NPH insulin were 2 and 7 times longer than those in the controls, respectively. In conclusion, the t1/2 for insulin was elongated 2 to 7 times after massive overdosing, explaining why glucose supplementation is needed for long periods in these cases.

It has been unknown if attenuated insulin sensitivity (Si) in non-alcoholic fatty liver disease (NAFLD) is a cause or a result. We examined the impact of attenuated Si on NAFLD evolution. We observed 4856 NAFLD- and diabetes-free participants for a mean 2.9 years. Si was indexed by single point insulin sensitivity estimator (SPISE = [600 × HDL-c0.185]/[TG0.2 × BMI1.338]), correlating with 1/HOMA-IR in an independent cohort (n = 1537, Spearman rho = 0.519, P 10.06) as the reference, tertile 1 (

The biphasic response is a unique characteristic of glucose-stimulated insulin secretion by islet beta cells. Namely, upon exposure to a high concentration of glucose, insulin secretion increases sharply for approximately 5 min before it gradually wanes at the end of the first phase. The second phase is characterized by sustained insulin release that lasts for the entire duration of high extracellular glucose concentration. Recently, new insights into the mechanisms underlying this phenomenon have been gained due to molecular identification of beta cell glucoreceptors. It has been previously postulated that elevation in cytosolic calcium leading to the first phase of insulin secretion is solely due to membrane depolarization caused by the closure of ATP-sensitive potassium (KATP) channels. However, the rapid increase in intracellular calcium is also caused by glucoreceptor-down signaling. Therefore, the first phase of glucose-induced secretion, i.e., fusion of the beta granule and the plasma membrane, likely arises from both glucose-receptor binding and closure of KATP channels. The molecular nature of the so-called KATP-independent glucose action appears to be diverse and still remains elusive. The releasable pool of beta granules is replenished by this glucose action, leading to the second phase of insulin secretion; signals for this phase also involve the direct recognition of glucose molecules by specific receptors. In this chapter, we review data pertaining to the functions of glucoreceptors in relation to KATP-independent glucose action in beta cells.

Aims To test the hypothesis that 1-h plasma glucose in an oral glucose tolerance test is a better predictor of the development of diabetes than 2-h plasma glucose, independently of indices of insulin secretion or action in Japanese adults. Methods A historical cohort study was conducted in 1445 Japanese workers who did not have diabetes. The association between 1-h plasma glucose and the development of Type 2 diabetes was analysed. Results Overall, 95 of the study participants developed Type 2 diabetes during a mean follow-up of 4.5 years. The area under the receiver-operating characteristic curve for 1-h plasma glucose for future diabetes [0.88 (95% CI 0.84–0.91)] was greater than that for 2-h plasma glucose [0.79 (95% CI 0.74–0.84)], and for insulinogenic [0.73 (95% CI 0.68–0.78)] and disposition indices [0.79 (95% CI 0.74–0.84); P < 0.05]. Compared with the first quartile, the hazard ratio for future diabetes in the fourth quartile of 1-h plasma glucose was 42.5 [95% CI 5.7–315.2 (P < 0.05)] and the hazard ratio in the fourth quartile of 2-h plasma glucose was 4.4 [95% CI 1.8–10.8 (P < 0.05)], after adjustments for covariates including fasting plasma glucose. The significance of the elevated hazard ratio in the fourth quartile of 1-h plasma glucose was maintained after adjustments for 2-h plasma glucose, insulinogenic index or disposition index, whereas the elevation of the hazard ratio in the fourth quartile of 2-h plasma glucose was diminished and was no longer significant after adjustments for 1-h plasma glucose. Conclusions One-hour plasma glucose had a greater association with the future development of Type 2 diabetes than did 2-h plasma glucose, independently of oral glucose tolerance test-derived indices of insulin action in a Japanese population.

The impact of postchallenge glucose on the relationship between insulin sensitivity (SI) and secretion (β) is unknown. We analyzed data from 2,264 health examinees (male/female 1,524/740, median age 54 yrs) with normal glucose tolerance (NGT, n = 1,623), non-diabetic hyperglycemia (NDH, n = 555), or diabetes (DM, n = 86) using OGTT-derived indices of SI (insulin sensitivity index [ISI]-Matsuda, 1/HOMA-IR, and 1/fasting IRI) and β (δIRI0-30/δPG0-30, and Stumvoll 1st [Stumvoll-1] and 2nd [Stumvoll-2] phases). The combination of 1/HOMA-IR and Stumvoll-1 recapitulated the hyperbolic SI-β relationship with the slope of the fitted line -1.000 in NGT subjects, and therefore it was utilized in the following analysis of the SI-β correlation. In multiple regression analysis of the relationship between SI and β, an independent correlation was found for 1 h-plasma glucose (PG; PG60) but not for 2 h-PG. When the NGT subjects were grouped by PG60 quartile (Q), the fitted line was flat in Q1 but progressively steeper from Q2 to Q4, with a slope (95%CI) of -0.663 (-0.726~-0.605), -0.680 (-0.745~-0.622), -0.847 (-0.922~-0.779), and -1.259 (-1.370~-1.158) (P for trend < 0.05). The fitted line steepened further in the NDH and DM groups, with a slope of -1.545 and -1.915, respectively (P < 0.01 for the difference). The intercept of the fitted line for SI-β correlation was also progressively lower across the PG60 Q for NGT, NDH, and DM. In conclusion, using the 1/HOMA-IR-Stumvoll-1 pair for an analysis of the SI-β relationship, elevated PG60 was associated with steepening and downward shifting of the fitted line for the SI-β correlation. The finding suggests impaired beta cell function.

Objective To describe hypocalcaemia due to vitamin D deficiency in ‘hikikomori’ syndrome. Materials and methods A 37-year-old man with ‘hikikomori’ syndrome for a year was admitted with hypocalcaemia (serum ionic calcium 1.17 mmol/l). Serum 1,25(OH)2-vitamin D3 determined by liquid chromatography–tandem mass spectrometry was depressed at 12.1 pg/ml (29.0 pmol/l) and plasma intact PTH elevated at 324 ng/l. Administration of 1 μg/day 1α(OH)-vitamin D3 and 1 g/day calcium lactate for 1 week normalized calcium and PTH, and raised 1,25(OH)2-vitamin D3 to low normal levels. Conclusion This is the first report of hypocalcaemia due to vitamin D deficiency in a patient with ‘hikikomori’ syndrome. LEARNING POINTS A patient with psychiatric disorders can develop endocrine/metabolic abnormality. Hikikomori syndrome should be listed as a possible cause of hypocalcaemia in adults. Early diagnosis of hypocalcaemia in hikikomori syndrome prevents bone damage.

Although accelerated β-cell telomere shortening may be associated with diabetes that shows a dramatically increased incidence with aging, β-cell telomere length in diabetes has never been explored.The objective of the present study was to examine telomere length in the β-cells of patients with diabetes.We determined telomere length in β- and α-cells of pancreases obtained at autopsy from 47 patients with type 2 diabetes and 51 controls, all older than 60 years.The normalized telomere to centromere ratio (NTCR), an index of telomere length, was determined for β- (NTCRβ) and α- (NTCRα) cells by quantitative fluorescence in situ hybridization.The NTCRβ was reduced by 27% ± 25% and NTCRα by 15% ± 27% in the patients with diabetes relative to the controls (P.01 for both). Importantly, the degree of shortening was significantly (P.01) greater in β-cells than in α-cells. The histogram of NTCR distribution was significantly skewed to the left in the patients with diabetes relative to the controls for both β- and α-cells, indicating preferential depletion of longer-telomere islet cells. Glycated hemoglobin was negatively correlated with β-cell telomere length, and the telomeres were significantly shorter in patients who had used hypoglycemic agents than in those who had not.The telomeres of β-cells are shortened in patients with type 2 diabetes. There may be a vicious cycle involving β-cell telomere attrition and sustained hyperglycemia.

The population attributable fraction (PAF) of risk factors for the worsening of glucose metabolism in subjects with normal glucose tolerance (NGT) has not been calculated. Our aim was to obtain the PAF of increased body mass index (BMI) and attenuated beta-cell function (BCF) on worsening of glucose metabolism in subjects with NGT. We longitudinally analyzed 604 Japanese adults. The follow-up glucose tolerance status was determined 3.7 years later: 430 participants remained in the NGT category and 102 had progressed to impaired fasting glucose, 67 to impaired glucose tolerance, and 5 to diabetes mellitus. A product of ISIMatsuda and Stumvoll-1, i.e., oral disposition index (DIO), was used as a measure of BCF. The optimal cutoff baseline BMI and DIO values for the prediction of the worsening of glucose metabolism were 23.1 and 7.299 kg/m(2), respectively. Isolated increased BMI (iBMIHIGH), isolated low DI (iDIOLOW), and "BMIHIGH and DIOLOW (BMIHIGH/DIOLOW)" were all independently related to the worsening, and the PAF values (95 % CI) for worsening due to iBMIHIGH, iDIOLOW, and BMIHIGH/DIOLOW were 12.9 (3.2-18.4) %, 10.9 (5.0-13.9) %, and 31.4 (22.7-36.3) %, respectively. As much as 55 % of the worsening of glucose metabolism in the NGT subjects was attributable to increased BMI and/or attenuated BCF. The optimal cutoff for BMI was as low as 23.1 kg/m(2) in this population. We believe that these data should form the basis of future public health strategies for the prevention of diabetes in Japan.

Aim of the study was to clarify the relationship between metformin-induced vitamin B12 (B12) deficiency, hyperhomocysteinemia and vascular complications in patients with type 2 diabetes. Serum B12 concentrations, homocysteine plasma levels, the presence of retinopathy and history of macroangiopathy (stroke or coronary heart disease) were analyzed in patients without renal dysfunction (serum creatinine

To develop diabetes risk score (RS) based on the current definition of diabetes, we retrospectively analyzed consecutive 4,159 health examinees who were non-diabetic at baseline. Diabetes, diagnosed by fasting plasma glucose (FPG) ≥7.0 mmol/L, 2hPG ≥11.1 mmol/L and/or HbA1c ≥6.5% (48 mmol/mol), developed in 279 of them during the mean period of 4.9 years. A full RS (RSFull), a RS without 2hPG (RS-2hPG) and a non-invasive RS (RSNI) were created on the basis of multivariate Cox proportional model by weighted grading based on hazard ratio in half the persons assigned. The RSs were verified in the remaining half of the participants. Positive family history (FH), male sex, smoking and higher age, systolic blood pressure (SBP), FPG, 2hPG and HbA1c were independent predictors for RSFull. For RS-2hPG, 7 independent predictors, exclusive of 2hPG and smoking but inclusive of elevated triglycerides (TG) comparing to RSFull, were selected. FH, male sex, and higher age, SBP and HbA1c were independent predictors in RSNI. In the validation cohort, C-statistic (95%CI) of RSFull, RS-2hPG and RSNI were 0.80 (0.76-0.84), 0.75 (0.70-0.78) and 0.68 (0.63-0.72), respectively, which were significantly different from each other (P

Anjana et al. (1) analyzed the rate of worsening of glucose metabolism in subjects with normal glucose tolerance (NGT) and impaired fasting glucose (IFG)/impaired glucose tolerance (IGT), the rate of regression from abnormal glucose metabolism to NGT, and the risk factors for the worsening in an Asian Indian cohort. The study may be a valuable addition to the previously accumulated knowledge in the epidemiology of the diabetes evolution. However, we are afraid that the classification of glucose tolerance categories and terminology were confusing and misleading in their study. Namely, the current definition of prediabetes by the American Diabetes Association is …

Risk profile for incident chronic kidney disease (CKD) in Japanese subjects has not been established. Our aim was to identify risk factors for CKD in Japanese.Consecutive 171 536 health examinees (median age 49 years and estimated glomerular filtration rate (eGFR) 78.2 mL/min per 1.73 mIn the Derivation cohort, CKD developed in 1002 (5.8%) subjects. Seven variables such as lower eGFR, male gender, higher uric acid concentration, lower red cell count and higher age and systolic blood pressure were identified as significant risks for CKD, with lowered eGFR being an overwhelmingly strong risk: adjusted hazard ratio for those with the baseline eGFR70 mL/min per 1.73 mSeven risk factors for incident CKD were identified in Japanese health examinees. However, lowered baseline eGFR outweighed other risks to the degree that eGFR alone was suffice for CKD prediction.

Objective We undertook an investigation on the frequency and magnitude of elevated serum immunoglobulin G (IgG), and effects of treatment with L-thyroxine (T4) in patients with Hashimoto's thyroiditis. Methods Ninety-seven consecutive cases of Hashimoto's thyroiditis, 104 patients with simple goiter, and 75 normal subjects were analyzed retrospectively. Serum total T4, thyroid stimulating hormone (TSH), microsomal hemagglutination antibody (MHA) titer, and IgG were determined in all subjects. Results IgG was significantly elevated in patients with Hashimoto's thyroiditis as a group, and elevation above the upper limit of the normal range was found mostly in patients with hypothyroidism. There is a significant negative correlation between serum total T4 and IgG, and a significant positive correlation between TSH and IgG in patients with Hashimoto's thyroiditis. In addition, MHA titer was positively correlated with serum IgG. In a longitudinal analysis of hypothyroid patients with Hashimoto's thyroiditis, restoration of euthyroidism by L-T4 administration was associated with a consistent decrease in serum IgG. Conclusion Serum IgG concentration is increased in patients with Hashimoto's thyroiditis, particularly in hypothyroid patients, and treatment with L-T4 in such patients lowers IgG levels.

Since adult measles have been found，and outbreaks of measles have sometimes occurred in Japan in re-cent years，so twice vaccinations have been pointed out to be needed to take since 2006. Those who have no or once vaccination received for young generation should take twice of MR vaccine at age of 13 years old and at age of 17 old from 2008 to 2013. Unfortunately，ratio of MR vaccine taking is not so high，so out-breaks of Measles will be apprehensive to be occurring.

When I perform bone evaluation by supersonic wave measurement，I only evaluate the right foot without considering the subject’s laterality，or potential differences between right and left foot bone density. Puberty is the period during which bone density rises，and during which the influence of mechanical stress is considered great，and evaluation of the right foot has been considered sufficient to clarify this effect. From the viewpoint of general health and prevention of osteoporosis we must measure one’s bone density in puberty， raise the peak bone mass，and maintain it. The present experiment was performed to clarify what kind of influence laterality of foot and exercise habits had on the bone density of the right calcaneus. Exercise habits did not have much influence on the bone density rise if the right foot was non-dominant. However，a meaningful connection was recognized between exercise habits and bone density rise if the right foot was dominant. From these results，it was thought that the measurement of calcaneus bone density by a supersonic wave method in puberty is more effective if the dominant foot is used.

We reviewed what kind of factors became lifestyle-related diseases risk factors in girls at puberty. The purpose of this study was to gather data for the primary prevention of lifestyle-related diseases. Subjects were 57 basically healthy girls at the age of puberty，from seventh grade to twelfth grade. We measured body composition including bone density of the whole body using Dual Energy X-ray Absorptiometry. We used form PWV/ABI（Omron Colin Co.，Ltd.，Japan）for the measurement of Pulse Wave Velocity. It became clear that there was a danger of elevated baPWV values in girls whose percentage of body fat and soft tissue fat rate were low. On the other hand，it became clear that bone mineral density（BMD）was likely high in subjects whose percentage of body fat and soft tissue fat rate were high. It is thought that a higher-than-standard percent of body fat becomes an advantage for elevated bone density. From these results，it was concluded that lifestyle-related disease risk factors for girls at puberty with a high rate of body fat are low.

In the present study，we measured bone mineral density and related items for female collegiate track and field athletes，female collegiate rhythmic gymnasts，and female college students with no exercise habits in order to elucidate the effects of exercise on bone mineral density. The results showed that athletes competing in sprints，throwing events，and rhythmic gymnastics had a significantly higher overall bone mineral density compared to general students，but no significant differences were observed for athletes competing in middle and long distance events. However，for the bone mineral density of both legs，significant differences compared to general students were observed for athletes competing in middle and long distance events as well as sprints， throwing events， and rhythmic gymnastics. These findings indicate that parts other than the legs must also be included in the assessment of bone mineral density in young subjects.