Vitamin Intake and Loss of Muscle Mass in Older People with Type 2 Diabetes: A Prospective Study of the KAMOGAWA-DM Cohort.

The aim of this prospective cohort study was to examine the relationships between the intakes of various vitamins and the loss of muscle mass in older people with type 2 diabetes (T2DM). The change in skeletal muscle mass index (SMI, kg/m2) (kg/m2/year) was defined as follows: (SMI at baseline (kg/m2) - SMI at follow-up (kg/m2))/follow-up period (year). The rate of SMI reduction (%) was calculated as follows (the change in SMI (kg/m2/year)/SMI at baseline (kg/m2)) × 100. The rate of SMI reduction ≥ 1.2% was considered as the loss of muscle mass. Among 197 people with T2DM, 47.2% of them experienced the loss of muscle mass at the 13.7 ± 5.2 month follow-up. Vitamin B1 (0.8 ± 0.3 vs. 0.8 ± 0.3 mg/day, p = 0.031), vitamin B12 (11.2 ± 8.3 vs. 13.4 ± 7.5 µg/day, p = 0.049), and vitamin D (16.5 ± 12.2 vs. 21.6 ± 13.0 µg/day, p = 0.004) intakes in people with the loss of muscle mass were significantly lower than those without. Vitamin D intake was related to the loss of muscle mass after adjusting for sex, age, exercise, alcohol, smoking, body mass index, SMI, glucagon-like peptide-1 agonist, sodium glucose cotransporter-2 inhibitor, insulin, HbA1c, creatinine, energy intake, and protein intake (adjusted odds ratio 0.93, 95% confidence interval: 0.88-0.97, p = 0.003). This study showed that vitamin D intake was related to the loss of muscle mass in older people with T2DM. Vitamin B12 intake tended to be related to the loss of muscle mass, although vitamin A, vitamin B2, vitamin B6, vitamin C, and vitamin E intake were not related.

Group 3 Innate Lymphoid Cells Protect Steatohepatitis From High-Fat Diet Induced Toxicity.

Background and Aims: Emerging evidence has revealed that innate lymphoid cells (ILCs) play a key role in regulating metabolic disorders. Here, we investigated the role of group 3 ILCs (ILC3s) in the modulation of Non-alcoholic fatty liver disease (NAFLD). Methods: RORγ gfp/gfp (RORgt KI/KI) and Rag2-/- mice with the administration of A213, RORgt antagonist, fed with a high-fat-diet (HFD) for 12 weeks, were used. We performed flow cytometry, real time PCR, and lipidomics analysis of serum and liver, and used RAW264.7 cells and murine primary hepatocytes in vitro. Results: HFD increased ILC3s and M1 macrophages in the liver, and RORgt KI/KI mice deficient in ILC3 showed significant fatty liver, liver fibrosis and significantly increased palmitic acid levels in serum and liver. In addition, administration of A213 to Rag2-/- mice caused significant fatty liver, liver fibrosis, and a significant increase in serum and liver palmitate concentrations, as in RORgt KI/KI mice. Addition of palmitc acid stimulated IL-23 production in cell experiments using RAW264.7. IL-22 produced by ILC3s inhibited the palmitate-induced apoptosis of primary hepatocytes. Conclusions: HFD stimulates IL-23 production by M1 macrophages, thus promoting ILC3 proliferation, whereas IL-22 secreted by ILC3s contributes to the upregulation of hepatic lipid metabolism and has anti-apoptosis activity.

Liver Stiffness Is Associated With Progression of Albuminuria in Adults With Type 2 Diabetes: Nonalcoholic Fatty Disease Cohort Study.

OBJECTIVES: Previous studies have shown the association between liver fibrosis and albuminuria. However, the effect of liver fibrosis on change in albuminuria is unclear. Thus, we investigated the effect of liver fibrosis on change in albuminuria in patients with type 2 diabetes. METHODS: In this retrospective cohort study, we assessed 105 patients with type 2 diabetes concomitant with nonalcoholic fatty disease. A change in urinary albumin excretion (UAE) was defined as follows: change in UAE=(logarithm [UAE+1] at follow-up examination minus logarithm [UAE+1] at baseline examination) / follow-up duration (1 year in this study). Elastography was performed to assess controlled attenuation parameter (dB/m) and liver stiffness measurement (LSM; kPa) values. RESULTS: Mean (standard deviation) data were as follows: age, 63.3 (12.1) years; body mass index, 25.4 (4.3) kg/m2; controlled attenuation parameter, 273.1 (53.0) dB/m; and LSM, 6.2 (3.4) kPa. Median UAE value (interquartile range) was 16 (6 to 43) mg/g creatinine. LSM was associated with changes in UAE (r=0.27, p=0.005). Multiple regression analysis demonstrated that LSM was associated with change in UAE (ß=0.28, p=0.015) after adjusting for sex, age, duration of diabetes, smoking status, exercise habits, glycated hemoglobin, body mass index, estimated glomerular filtration rate, systolic blood pressure, logarithm (UAE+1) at baseline examination, use of renin‒angiotensin system inhibitors, new use of sodium glucose cotransporter-2 inhibitors and glucagon-like peptide-1 and controlled attenuation parameter. CONCLUSIONS: Liver stiffness is an independent risk factor for the progression of albuminuria in patients with type 2 diabetes.

Immune modulating effects of additional supplementation of estradiol combined with testosterone in murine testosterone-deficient NAFLD model.

Nonalcoholic fatty liver disease (NAFLD) is associated with testosterone deficiency. However, NAFLD patients generally do not respond to treatment with testosterone alone. We investigated the innate immune mechanisms underlying the effects of treatment with testosterone alone, estrogen alone, or combined testosterone and estrogen on high-fat diet (HFD)-induced NAFLD due to testosterone deficiency. Orchiectomized (OCX) male Rag2-/- mice were used as a model of testosterone deficiency. To assess NAFLD severity, NAFLD activity score (NAS) is adopted. Moreover, immunological change was analyzed by multicolor flow cytometry. Treatment with both testosterone and estrogen significantly decreased body weight to that of the sham mice/normal diet (ND). NAS and liver fibrosis in OCX-HFD mice were significantly deteriorated, and treatment with testosterone and estrogen improved same as sham-ND mice. HFD increased the ratio of both type 2 and 3 innate lymphoid cells (ILC2s and ILC3s) to CD45-positive cells in the liver. Treatment with testosterone alone decreased the ratio of ILC2 to CD45 but not the ILC3-to-CD45 ratio. Addition of estrogen to the treatment reduced the ratios of ILC2-to-CD45 and ILC3-to-CD45 to the same level observed in sham-HFD mice. Moreover, OCX-HFD mice had a decreased proportion of M2 macrophages compared with sham-ND mice. Treatment with testosterone alone did not restore the proportion of M2 macrophages; however, combination treatment with both estrogen and testosterone increased that to the same level as that in sham-HFD mice. Treatment with both testosterone and estrogen improves liver fibrosis and decreases ILC3 and increases M2 macrophage abundance in the liver.NEW & NOTEWORTHY The progression of nonalcoholic fatty liver disease (NAFLD) is associated with testosterone deficiency. NAFLD patients generally do not respond to treatment with testosterone alone. In animal studies, treatment with testosterone and estrogen reduced the ratios of ILC2:CD45 and ILC3:CD45 and increased M2 macrophages in liver. Our study suggests, based on our immunological data, that a combination of estrogen and testosterone may be clinically relevant for the treatment of NAFLD in patients with male menopause.

A Pilot Study on the Effect of Anti-Thrombopoietin Antibody on Platelet Count in Patients with Type 2 Diabetes.

Thrombopoietin (THPO) is a circulatory cytokine that plays an important role in platelet production. The presence of anti-THPO antibody relates to thrombocytopenia and is rarely seen in hematopoietic and autoimmune diseases. To date, there had been no reports that focused on the anti-THPO antibody in patients with type 2 diabetes mellitus (T2DM). To evaluate prevalence of the anti-THPO antibody in patients with T2DM and the relationship between anti-THPO antibody and platelet count, a cross-sectional study was performed on 82 patients with T2DM. The anti-THPO antibody was measured by ELISA using preserved sera and detected in 13 patients. The average platelet count was significantly lower in patients with the anti-THPO antibody than in those without the anti-THPO antibody. Multivariate linear regression analyses showed a significant relationship between the anti-THPO antibody and platelet count, after adjusting for other variables. To our best knowledge, this was the first report on the effect of the anti-THPO antibody on platelet count in patients with T2DM. Further investigation is needed to validate the prevalence and pathological significance of the anti-THPO antibody in patients with T2DM.

miR-23b-3p acts as a counter-response against skeletal muscle atrophy.

To investigate the role of microRNA (miRNA) in muscle atrophy, we performed microarray analysis of miRNA expression in skeletal muscles of Sham, orchiectomized (ORX) mice, and ORX mice treated with androgen and identified that the expression of miR-23b-3p in ORX mice was significantly higher than that in Sham mice (P = 0.007); however, miR-23b-3p expression in ORX mice treated with androgen was lower (P = 0.001). We also investigated the mechanism by which overexpression or knockdown of miR-23b-3p influences the expression of myosin heavy chain, muscle protein synthesis, ATP activity, and glucose uptake in C2C12 myotube cells. Moreover, we examined the serum miR-23b-3p levels among male subjects with type 2 diabetes and whether the serum miR-23b-3p levels could be a biomarker for muscle atrophy. The overexpression of miR-23b-3p in C2C12 myotube cells significantly upregulated the expression of myosin heavy chain, protein synthesis, ATP activity, and glucose uptake. Reporter assays raised a possible direct post-transcriptional regulation involving miR-23b-3p and the 3'-UTR of PTEN mRNA. Among subjects with type 2 diabetes, serum miR-23b-3p levels in the subjects with decreased muscle mass were significantly higher compared to the levels in the subjects without. Our results indicate that miR-23b-3p downregulates the expression of PTEN in myotube cells and induces the growth of myosin heavy chain. In addition, the serum level of miR-23b-3p can be used as a diagnostic marker for muscle atrophy.

Preparation of Immunotolerant Space Under the Skin and Transplantation of Islets in the Space.

IMPACT STATEMENT: Although transplantation of islets of Langerhans has been accepted as a fundamental treatment for insulin-dependent diabetes mellitus (IDDM), several problems are still remaining in order that it becomes the standard medical treatment of IDDM patients. In this study, using diabetic rat models, a subcutaneous space surrounded with highly vascularized granulomatous tissue was formed by agarose-bFGF rod implantation. Allogeneic islets transplanted into the space could survive and release insulin for a long period under no immunosuppressive medication. In conjunction with sufficient supply of islets from iPS/ES cells, our method can make islet transplantation the standard medical treatment of IDDM patients.

Late-night-dinner is associated with poor glycemic control in people with type 2 diabetes: The KAMOGAWA-DM cohort study.

Skipping breakfast or irregular breakfast is associated with poor glycemic control. However, a relationship between the timing of dinner and glycemic control in people with type 2 diabetes remains indefinite. Therefore, we investigated the relationship between late-night-dinner and glycemic control in people with type 2 diabetes. We performed questionnaire survey for lifestyle factors in this cross-sectional study. We defined having dinner later than eight pm as late-night-dinner. We examined the differences in clinical and metabolic parameters between those who have late-night-dinner and those who do not have. We also examined the relationship between late-night-dinner and HbA1c, using multiple regression analysis. Ninety-five people (23.2%) had a late-night-dinner, among 409 people with type 2 diabetes. Metabolic parameters (mean (SD) or median (interquartile range)) of people with late-night-dinner were worse than those of without, including body mass index (BMI) (24.4 (4.0) vs. 23.2 (3.4) kg/m2, p = 0.006), triglycerides (1.5 (1.1-2.1) vs. 1.2 (0.8-1.7) mmol/L, p < 0.001), HDL-cholesterol (1.4 (0.4) vs. 1.6 (0.4) mmol/L, p = 0.004) and hemoglobin A1c (58.1 (13.3) vs. 55.2 (10.2) mmol/mol, (7.5 (1.2) vs. 7.2 (0.9) %), p = 0.023)). Late-night-dinner (standardized regression coefficient = 0.13, p = 0.028) was associated with hemoglobin A1c after adjusting for age, BMI, sex, duration of diabetes, smoking, exercise, alcohol, snacking after dinner, nighttime sleep duration, time from dinner to bedtime, skipping breakfast, and medication for diabetes. Late-night-dinner is independently associated with poor glycemic control in people with type 2 diabetes.

Long-term Functioning of Allogeneic Islets in Subcutaneous Tissue Pretreated With a Novel Cyclic Peptide Without Immunosuppressive Medication.

BACKGROUND: There exists a need for a minimally invasive method of islet transplantation without immunosuppressive drugs for the treatment of type 1 diabetes. METHODS: In diabetic August Copenhagen Irish rats, an agarose rod containing the cyclic oligopeptide SEK-1005 (agarose-SEK rod) was implanted at 2 dorsal subcutaneous sites. Then these rods were removed, and 1500 islets of Langerhans isolated from Fischer 344 rats were transplanted into each of the pockets. RESULTS: Ten days after implantation of agarose-SEK rods, vascularized pockets were present. Nonfasting blood glucose levels confirmed long-term survival of the allogeneic islet grafts, without immunosuppressive therapy, in 8 of 10 recipients. Flow cytometry and gene expression analyses were performed to investigate the mechanisms underlying graft acceptance. Agarose-SEK rod implantation led to the formation of granulomatous tissue containing regulatory T cells that suppressed immune reactions against the allogeneic islet grafts. CONCLUSIONS: These results indicate that the use of an agarose-SEK rod to prevascularize a subcutaneous site may be a useful method for achieving successful allogeneic islet transplantation without immunosuppression.

Protein Intake, Especially Vegetable Protein Intake, Is Associated with Higher Skeletal Muscle Mass in Elderly Patients with Type 2 Diabetes.

BACKGROUND/AIMS: Protein intake is important for maintaining muscle mass in general population. However, it remains to be elucidated the association between dietary protein intake and skeletal muscle mass in elderly patients with type 2 diabetes. METHODS: In this cross-sectional study of 168 elderly patients with type 2 diabetes, we investigated the relationship between skeletal muscle index (SMI) and protein intake. Bioimpedance analysis was used for measurement for skeletal muscle mass (kg) and SMI (%), which was defined as skeletal muscle mass (kg)/total body weight (kg) × 100. Habitual food and nutrient intake were estimated by a questionnaire. RESULTS: Protein intake was independently correlated with SMI after adjusting for age, hemoglobin A1c, C-peptide index, exercise, smoking, insulin treatment, total energy intake, and C-reactive protein (standardized regression coefficient = 0.664, P < 0.001 in men and standardized regression coefficient = 0.516, P = 0.005 in women). Additionally, the animal protein to vegetable protein ratio was negatively correlated with SMI after adjusting for covariates in men (standardized regression coefficient = -0.339, P = 0.005). CONCLUSIONS: We found that total protein intake, especially vegetable protein intake, was positively associated with skeletal muscle mass in elderly patients with type 2 diabetes.

Weight gain since age of 20 as risk of metabolic syndrome even in non-overweight individuals.

PURPOSE: Metabolic syndrome (MetS), regardless of the presence of obesity, is known as a risk of diabetes and cardiovascular disease. Weight gain after age 20 reported to be associated with these diseases. Impact of the difference between the body mass index (BMI) at examination and BMI at age 20 (ΔBMIexa-20y) on MetS, especially in non-overweight individuals, remains to be elucidated. METHODS: We analyzed the data of 24,363 individuals (14,301 men and 10,062 women) in this cross-sectional study. The diagnosis of MetS was diagnosed when three or more of the following criteria were present: hypertension, hyperglycemia, hypertriglyceridemia, low HDL-cholesterol level, and abdominal obesity. Logistic regression was performed to calculate odds ratios (ORs) and 95% confidence intervals (CIs) adjusting for age, alcohol, smoking, exercise, and BMI at examination. RESULTS: Compared to the lowest ΔBMIexa-20y tertile (ΔBMIexa-20y < 1.2 kg/m2 in men and ≤0 kg/m2 in women), the highest tertile (ΔBMIexa-20y ≥ 3.2 kg/m2 in men and ≥2.0 kg/m2 in women) was associated with the risk of the presence of MetS (multivariate OR = 1.80, 95%CI 1.53-2.11, p < 0.001 in men and OR = 3.27, 95%CI 2.22-4.96, p < 0.001 in women). This result was also applicable in non-overweight individuals (multivariate OR = 2.06, 95%CI 1.46-2.92, p < 0.001 in men and OR = 2.49, 95%CI 1.40-4.64, p < 0.001 in women). CONCLUSIONS: Our analyses showed that ΔBMIexa-20y is associated with the risk of the presence of MetS, even in non-overweight individuals. It is thus important to check weight changes from early adulthood, even in non-overweight individuals.

Impact of fatty liver disease and metabolic syndrome on incident type 2 diabetes; a population based cohort study.

Fatty liver disease and metabolic syndrome (MetS) are both shown to increase the risk of type 2 diabetes. The aim of this study was to investigate the combined effect of fatty liver and MetS on incident diabetes. In this cohort study of 17,810 participants, fatty liver was diagnosed by abdominal ultrasonography and MetS was defined by a joint interim statement. We divided the participants into four groups according to the presence of fatty liver and/or MetS. Type 2 diabetes was defined as HbA1c ≥6.5%, fasting plasma glucose ≥7.0 mmol/L or treatment for diabetes. During the follow up examination (median 5.1 years), 804 participants developed diabetes. Compared with non-MetS without fatty liver, hazard ratios (HR) for incident diabetes after adjusting for age, body mass index, smoking status, exercise habit, alcohol consumption, family history of diabetes logarithm of alanine aminotransferase and fasting plasma glucose, were as follow: 2.35 (95 % CI 1.91-2.89, p<0.001) in non-MetS with fatty liver, 1.70 (95% CI 1.30-2.20, p<0.001) in MetS without fatty liver, and 2.33 (95% CI 1.85-2.94, p<0.001) in MetS with fatty liver. In addition, adjusted HRs for incident diabetes compared with MetS without fatty liver were 1.39 (95% CI 1.07-1.80, p=0.012) in non-MetS with fatty liver and 1.38 (95% CI 1.07-1.79, p=0.013) in MetS with fatty liver. Fatty liver affects more on the risk of incident diabetes than MetS. To prevent the further risk of diabetes, we should pay more attention to fatty liver.

Nonoverweight nonalcoholic fatty liver disease and incident cardiovascular disease: A post hoc analysis of a cohort study.

Nonalcoholic fatty liver disease (NAFLD) is known as a risk of incident cardiovascular disease (CVD). About 20% of NAFLD occurs in nonobese individuals. However, it remains to be elucidated the association between nonoverweight with NAFLD and a risk of incident CVD. Therefore, we investigated the risk of nonoverweight with NAFLD for incident CVD.We performed a post-hoc analysis of the previous prospective cohort study, in which 1647 Japanese were enrolled. Abdominal ultrasonography was used to diagnose NAFLD. Overweight was defined as body mass index ≥23 kg/m, which is recommended by World Health Organization for Asian. We divided participants into 4 phenotypes by existence of NAFLD and/or overweight. The hazard risks of the 4 phenotypes for incident CVD were calculated by Cox hazard model after adjusting for age, sex, smoking status, exercise, hypertension, hyperglycemia, hypertriglyceridemia, and low high-density lipoprotein cholesterol at baseline examination.Incident proportions of CVD were 0.6% in nonoverweight without NAFLD, 8.8% in nonoverweight with NAFLD, 1.8% in overweight without NAFLD, and 3.3% in overweight with NAFLD. Compared with nonoverweight without NAFLD, the adjusted hazard ratios of incident CVD were 10.4 (95% confidence interval 2.61-44.0, P = .001) in nonoverweight with NAFLD, 1.96 (0.54-7.88, P = .31) in overweight without NAFLD, and 3.14 (0.84-13.2, P = .09) in overweight with NAFLD.Nonoverweight with NAFLD was associated with higher risk of incident CVD. We should pay attention to NAFLD, even in nonoverweight individuals, to prevent further CVD events.

Fatty liver as a risk factor for progression from metabolically healthy to metabolically abnormal in non-overweight individuals.

PURPOSE: Recent studies identified that metabolically abnormal non-obese phenotype is a risk factor for cardiovascular diseases. However, little is known about risk factor for progression from metabolically healthy non-overweight to metabolically abnormal phenotype. We hypothesized that fatty liver had a clinical impact on progression from metabolically healthy non-overweight to metabolically abnormal phenotype. METHODS: In this retrospective cohort study, 14,093 Japanese (7557 men and 6736 women), who received the health-checkup program from 2004 to 2012, were enrolled. Overweight and obesity were defined as body mass index 23.0-25.0 and ≥25.0 kg/m2. Four metabolic factors (impaired fasting glucose, hypertension, hypertriglyceridemia and low high density lipoprotein-cholesterol concentration) were used for definition of metabolically healthy (less than two factors) or metabolically abnormal (two or more). We divided the participants into three groups: metabolically healthy non-overweight (9755 individuals, men/women = 4290/5465), metabolically healthy overweight (2547 individuals, 1800/747) and metabolically healthy obesity (1791 individuals, 1267/524). Fatty liver was diagnosed by ultrasonography. RESULTS: Over the median follow-up period of 5.3 years, 873 metabolically healthy non-overweight, 512 metabolically healthy overweight and 536 metabolically healthy obesity individuals progressed to metabolically abnormal. The adjusted hazard risks of fatty liver on progression were 1.49 (95% confidence interval 1.20-1.83, p = 0.005) in metabolically healthy non-overweight, 1.37 (1.12-1.66, p = 0.002) in metabolically healthy overweight and 1.38 (1.15-1.66, p < 0.001) in metabolically healthy obesity, after adjusting for age, sex, alcohol, smoking, exercise, impaired fasting glucose, hypertension, hypertriglyceridemia, low high density lipoprotein-cholesterol concentration, and abdominal obesity. CONCLUSIONS: Fatty liver is an independent risk factor for progression from metabolically healthy status to metabolically abnormal phenotype, even in non-overweight individuals.

The relationship between hepatic steatosis and skeletal muscle mass index in men with type 2 diabetes.

Recent cross-sectional studies revealed that sarcopenia is associated with non-alcoholic fatty liver disease (NAFLD) in general population. However, it remains to be elucidated that the association between skeletal muscle mass index (SMI) and hepatic steatosis in patients with type 2 diabetes. In this cross-sectional study of 145 Japanese patients (79 men and 66 women) with type 2 diabetes, we examined the correlation of SMI with hepatic steatosis. Skeletal muscle mass was estimated from bioimpedance analysis measurements and SMI (%) was defined as skeletal muscle mass (kg)/total body weight (kg) × 100. Controlled attenuation parameter (CAP) evaluated with transient elastography, was used for assessment of hepatic steatosis. In addition, we also investigated the association between SMI and prevalence of NAFLD, which was defined as CAP over 237.8 dm-1, using logistic regression analysis. Fifty-eight (74%) men and thirty-nine (60%) women had NAFLD. Multiple regression analysis demonstrated that SMI was independently correlated with CAP (ß = -0.35, P = 0.007) in men after adjusting for age, body mass index, hemoglobin A1c, triglycerides/ HDL-C ratio, C-reactive protein and gamma-glutamyl transferase. On the other hand, SMI was not associated with CAP in women. Odds ratio per incremental 1% of SMI for prevalence of NAFLD was 0.80 (95% CI 0.64-0.97, P = 0.021) after adjusting for age, BMI, smoking statues, triglycerides/ HDL-C ratio, HbA1c, and gamma-glutamyl transferase in men. In conclusion, SMI was negatively associated with hepatic steatosis in men with type 2 diabetes.

Effect of Brazilian green propolis in patients with type 2 diabetes: A double-blind randomized placebo-controlled study.

Propolis contains a variety of chemical compounds, including polyphenols, flavonoids, phenolic aldehydes, amino acids and vitamins, and presents numerous biological and pharmacological properties. The aim of the present study was to evaluate the effect of propolis on blood examination data in patients with type 2 diabetes. In the double-blind, 8-week randomized controlled study, 80 patients with type 2 diabetes were enrolled. Patients were randomly assigned to receive Brazilian green propolis (226.8 mg/day for 8 weeks) (n=41) or the placebo (n=39). The primary endpoint was to detect changes in blood examination data associated with metabolic disorders in patients suffering from diabetes mellitus, including the homeostasis model assessment of insulin resistance (HOMA-IR), uric acid and estimated glomerular filtration rate (eGFR) from baseline to the end of this study. The value of HOMA-IR was not significantly changed by the 8-week administration of propolis or placebo from the baseline data. Values of blood uric acid and eGFR in patients taking the placebo became worse at 8 weeks compared to the baseline, whereas this did not occur in patients consuming Brazilian green propolis. However, HOMA-IR was not improved by propolis intake. A randomized, controlled 8-week trial suggests that Brazilian green propolis (226.8 mg/day) prevents patients with type 2 diabetes from developing worse blood uric acid and eGFR.

Is home blood pressure reporting in patients with type 2 diabetes reliable?

The aim of this study was to evaluate the reliability of self-reported home blood pressure (HBP) in patients with type 2 diabetes by comparing the self-reported values with HBP measurements stored in the memory of the blood pressure (BP) monitor. We also examined what factors affect the reliability of HBP measurements. A cross-sectional study was conducted in 280 patients with type 2 diabetes. Patients were requested to perform triplicate morning and evening measurements over a span of 2 weeks and to enter their HBP values into logbooks. Patients were not informed about the memory function of their BP monitoring devices. The concordance rate of HBP reporting was 78.6%. A total of 51.4% of patients (n=144) had >90% concordant data, and 15.7% of patients (n=44) had ⩽50% concordant data. In general, HBP values from the logbook were significantly lower and less variable than those from the stored memory (P<0.05). The most common type of incorrect data was selected data that were reported in the logbooks that were randomly selected from multiple readings by the HBP monitors (55.8%). The concordance rate of HBP reporting significantly correlated with hemoglobin A1c levels (ß=-0.156; P=0.0149) and with smoking status (current vs. never, ß=-0.165; P=0.0184). In conclusion, HBP measurements from the patients' logbooks were lower and less variable than those from the stored memory in the BP monitors of patients with type 2 diabetes, and the reliability of HBP reporting was affected by glycemic control and smoking status. Repeated instructions regarding HBP measurement to the patients or the use of stored BP measurements is recommended to ensure accurate HBP measurements in patients with type 2 diabetes.

Improvement of insulin resistance, blood pressure and interstitial pH in early developmental stage of insulin resistance in OLETF rats by intake of propolis extracts.

Propolis, a resinous mixture collected from plants by the Apis mellifera bee, contains high level nutrient factors including vitamins, polyphenols, and amino acids that would be expected to improve insulin sensitivity. Insulin resistance would secondarily cause elevation of blood pressure and increase the risk of cardiovascular diseases. The purpose of this study is to investigate the effect of propolis extracts on blood glucose levels and blood pressures in an early developmental stage of insulin resistance in Otsuka Long-Evans Tokushima Fatty (OLETF) rats. OLETF rats (10 weeks old) were divided into three different groups: normal diet, 0.1% propolis diet, and 0.5% propolis diet. After 8 weeks, blood glucose levels, blood pressures, plasma metabolic factors and hormones, and interstitial fluid pH were measured. Casual blood glucose levels were decreased associated with a reduction of plasma insulin levels in both propolis diet groups compared with normal diet group. Propolis decreased systolic blood pressure with no significant changes in plasma aldosterone levels. We also found that interstitial fluid pH in ascites, liver, and skeletal muscle was higher in rats fed propolis diet than rats fed normal diet. These data suggests that dietary propolis improves insulin sensitivity and blood pressures in the early stage of the process in development of insulin resistance, which may be mediated by suppression of metabolic acidosis.

Reconstruction of the right ventricular outflow tract after surgical removal of a cardiac hemangioma.

An asymptomatic 73-year-old man underwent resection of a cardiac tumor arising from the right ventricular outflow tract, and reconstruction of the right ventricular outflow tract using an expanded polytetrafluoroethylene sheet. Histological examination revealed a cavernous-capillary type cardiac hemangioma, which is a very rare cardiac tumor.

[Clinical evaluation of tonsillectomy with modified high-dose intravenous methylprednisolone therapy in patients with IgA nephropathy].

Immunoglobulin A nephropathy (IgAN) is now recognized as the most common form of primary glomerulonephritis worldwide and is the major cause of end-stage renal disease. As reported, the renal survival rate is 61% at 20 years and the renal prognosis of this disease is relatively poor on long-term observation, hence various protocols have been attempted to control this disease. At Iizuka Hospital, a prospective study of tonsillectomy with methylprednisolone pulse therapy was performed for the treatment of patients with IgA nephropathy from August 2002. We reviewed the clinical efficacy of our protocol. From August 2002 to July 2006, 31 patients whose IgA nephropathy was demonstrated by percutaneous renal biopsy were administered our regimen. In our study, 12 patients had an observation period of more than 24 months. Our protocol consisted of tonsillectomy with one course of methylprednisolone pulse therapy. Methylprednisolone at the daily dose of 1,000 mg for 3 consecutive days followed by oral steroid at the daily dose of 20 mg, was gradually tapered, and discontinued one year later. All of the patients were administered angiotensin-converting enzyme inhibitors or angiotensin receptor blockers with favorable control of hypertension. The mean observation period for the 12 patients with IgA nephropathy was 37.4 months. The mean age at renal biopsy was 34.8 +/- 12.2 years. The male-female ratio was 3:9. At the renal biopsy in our hospital, mean creatinine value was 0.95 +/- 0.38 mg/dL, mean creatinine clearance was 92.1 +/- 34.9 mL/min, and the mean urinary protein and urinary creatinine ratio was 3.52 +/- 4.36. After 24 months, mean creatinine value was 1.03 +/- 0.59 mg/dL, mean creatinine clearance was 91.2 +/- 42.3 mL/min, and the mean urinary protein and urinary creatinine ratio was 0.83 +/- 0.98. Urinary protein and urine occult blood became negative in 66.7% of patients, and the urinary remission rate was 58.3%. On our protocol, mean length of the hospital stay was 11.4 +/- 4.7 days. Our prospective study showed that tonsillectomy with one course of methylprednisolone pulse therapy in IgA nephropathy appears to be beneficial for urinary remission and contributes to a short hospital stay.