Dietary intake and physical activity in Japanese patients with type 2 diabetes: the Japan Diabetes Complication and its Prevention prospective study (JDCP study 8).

Medical nutrition therapy and exercise therapy are the cornerstones of treatment for patients with type 2 diabetes; however, there has not been a nationwide study on the actual dietary intake and physical activity status of patients since the 2000s. We aimed to clarify this in Japanese patients with type 2 diabetes using data from the Japan Diabetes Complication and its Prevention prospective (JDCP), a nationwide study launched in 2007. A total of 1992 patients with type 2 diabetes, aged 40-75 years, completed either the Brief-type, self-administered Diet History Questionnaire (1643 patients) or International Physical Activity Questionnaire (1834 patients), and their data were analyzed in this study. Mean daily energy intake for all participants was 1686.8 kcal/day, and the mean proportions of carbohydrate, protein, and fat comprising total energy intake were 60.2, 16.2, and 23.6%, respectively. The patients in this study had similar energy and nutrient intake status to patients in the 1996 Japan Diabetes Complications Study; however, Japanese patients still had higher carbohydrate and lower fat consumption than patients with diabetes in Western countries. The physical activity questionnaire reported that 31.0% of patients did not have exercise habits; this was particularly noticeable in female patients and patients under the age of 65. BMI increased from 22.7 to 24.1 kg/m2 in men and 23.2 to 24.8 kg/m2 in women from 1996 to 2007, respectively. Further research is required to investigate how dietary intake and physical activity associates with the risk of developing complications in type 2 diabetes patients.

Relationship between diet/exercise and pharmacotherapy to enhance the GLP-1 levels in type 2 diabetes.

The rapid rise in the prevalence of type 2 diabetes mellitus (T2DM) poses a huge healthcare burden across the world. Although there are several antihyperglycaemic agents (AHAs) available including addition of new drug classes to the treatment algorithm, more than 50% of patients with T2DM do not achieve glycaemic targets, suggesting an urgent need for treatment strategies focusing on prevention and progression of T2DM and its long-term complications. Lifestyle changes including implementation of healthy diet and physical activity are cornerstones for the management of T2DM. The positive effects of diet and exercise on incretin hormones such as glucagon-like peptide-1 (GLP-1) have been reported. We hypothesize an IDEP concept (Interaction between Diet/Exercise and Pharmacotherapy) aimed at modifying the diet and lifestyle, along with pharmacotherapy to enhance the GLP-1 levels, would result in good glycaemic control in patients with T2DM. Consuming protein-rich food, avoiding saturated fatty acids and making small changes in eating habits such as eating slowly with longer mastication time can have a positive impact on the GLP-1 secretion and insulin levels. Further the type of physical activity (aerobic/resistance training), intensity of exercise, duration, time and frequency of exercise have shown to improve GLP-1 levels. Apart from AHAs, a few antihypertensive drugs and lipid-lowering drugs have also shown to increase endogenous GLP-1 levels, however, due to quick degradation of GLP-1 by dipeptidyl peptidase-4 (DPP-4) enzyme, treatment with DPP-4 inhibitors would protect GLP-1 from degradation and prolong its activity. Thus, IDEP concept can be a promising treatment strategy, which positively influences the GLP-1 levels and provide additive benefits in terms of improving metabolic parameters in patients with T2DM and slowing the progression of T2DM and its associated complications.

The Addition of Xanthan Gum to Enteral Nutrition Suppresses Postprandial Glycemia in Humans.

The semi-solidified nutrition supplemented with soluble dietary fiber, xanthan gum (XG), inhibited postprandial glycemia in rats. The purpose of the present study is to examine whether XG exerts the same effects in humans. Subjects fasted for 12 h and then ingested the enteral nutrient, Meibalance with or without XG at 9 AM. Blood glucose levels were measured 0, 20, 40, 60, and 120 min after its ingestion. Postprandial blood glucose levels were lower in the XG group than in the control group. At 20 min, postprandial blood glucose levels were significantly lower in the XG group (84±5.3 mg/dL) than in the control group (107±7.8 mg/dL) (p<0.05). A significant difference was also observed in ΔAUC between the two groups. These results demonstrate that XG exerts inhibitory effects on glucose excursion in humans.

Lipopolysaccharide inhibits hepatic gluconeogenesis in rats: The role of immune cells.

AIMS/INTRODUCTION: Bacterial septicemia has diverse clinical symptoms including severe hypoglycemia. However, sepsis-induced hypoglycemia has not yet been examined in detail. The aim of the present study was to investigate the mechanisms underlying hypoglycemia in sepsis. MATERIALS AND METHODS: We induced endotoxin shock in rats using lipopolysaccharide (LPS). After an intraperitoneal injection of LPS, we measured gluconeogenesis using the pyruvate tolerance test. The effects of LPS on glucose metabolism were investigated in perfused livers and isolated hepatocytes. Furthermore, its effects on the production of inflammatory cytokines were examined in isolated splenocytes. The interaction between splenocytes and hepatocytes in response to LPS was investigated in vitro using a co-culture of splenocytes and hepatocytes. RESULTS: In the pyruvate tolerance test, the pretreatment with LPS decreased gluconeogenesis. The in vivo pretreatment of rats with LPS did not inhibit glucose production in perfused livers. The in vitro treatment of isolated hepatocytes with LPS did not decrease hepatic gluconeogenesis. Although LPS increased the production of inflammatory cytokines (tumor necrosis factor-α, interferon-γ, interleukin-1ß, interleukin-6 and interleukin-10) and nitric oxide in isolated splenocytes, only nitric oxide significantly inhibited gluconeogenesis in isolated hepatocytes. When splenocytes and hepatocytes were co-cultured in medium containing LPS, the messenger ribonucleic acid expression of glucose-6-phosphatase in hepatocytes was suppressed. CONCLUSIONS: LPS reduced hepatic gluconeogenesis, at least in part, by stimulating the production of nitric oxide in splenocytes. This effect could contribute to the mechanisms responsible for septicemia-induced hypoglycemia.

Okara ameliorates glucose tolerance in GK rats.

Okara, a food by-product from the production of tofu and soy milk, is rich in three beneficial components: insoluble dietary fiber, ß-conglycinin, and isoflavones. Although isoflavones and ß-conglycinin have recently been shown to improve glucose tolerance, the effects of okara have not yet been elucidated. Therefore, we herein investigated the effects of okara on glucose tolerance in Goto-Kakizaki (GK) rats, a representative animal model of Japanese type 2 diabetes. Male GK rats were fed a 10% lard diet with or without 5% dry okara powder for 2 weeks and an oral glucose tolerance test was performed. Rats were then fed each diet for another week and sacrificed. The expression of genes that are the master regulators of glucose metabolism in adipose tissue was subsequently examined. No significant differences were observed in body weight gain or food intake between the two groups of GK rats. In the oral glucose tolerance test, increases in plasma glucose levels were suppressed by the okara diet. The mRNA expression levels of PPARγ, adiponectin, and GLUT4, which up-regulate the effects of insulin, were increased in epididymal adipose tissue by the okara diet. These results suggest that okara provides a useful means for treating type 2 diabetes.

Hyperoxia reverses glucotoxicity-induced inhibition of insulin secretion in rat INS-1 ß cells.

Chronic hyperglycemia has deleterious effects on pancreatic ß-cell function, a process known as glucotoxicity. This study examined whether chronic high glucose (CHG) induces cellular hypoxia in rat INS-1 ß cells, and whether hyperoxia (35% O2) can reverse glucotoxicity-induced inhibition of insulin secretion. CHG (33.3 mm, 96 h) reduced insulin secretion, and down-regulated insulin and pancreatic duodenal homeobox factor 1 gene expression. CHG also increased intracellular pimonidazole-protein adducts, a marker for hypoxia. CHG also enhanced hypoxia-inducible factor 1α (HIF-1α) protein expression and its DNA-binding activity, which was accompanied by a decrease in mRNA expression of glucose transporter 2 (GLUT2), glucokinase and uncoupling protein-2 and an increase in mRNA expression of GLUT1 and pyruvate dehydrogenase kinase 1. Hyperoxia restored the decrease in insulin secretion and the gene expression except for GLUT2, and suppressed intracellular hypoxia and HIF-1α activation. These results suggest that glucotoxicity may cause ß-cell hypoxia. Hyperoxia might prevent glucotoxicity-induced ß-cell dysfunction and improve insulin secretion.

Enteral supplement enriched with glutamine, fiber, and oligosaccharide attenuates experimental colitis in mice.

OBJECTIVE: Ulcerative colitis is a chronic recurrent disease characterized by acute inflammation of the colonic mucosa. In Japan, a dietary supplementation product enriched with glutamine, dietary fiber, and oligosaccharide (GFO) is widely applied for enteral nutrition support. These three components have been suggested to improve intestinal health. In this study, we investigated whether GFO has suppressive effects on mucosal damage in ulcerative colitis in an experimental mouse model. METHODS: C57BL/6 mice received 2.5% dextran sulfate sodium in drinking water for 5 d to induce colitis. Then, they were given 0.25 mL of GFO or a 20% glucose solution twice daily for 10 d. Another set of mice receiving unaltered drinking water was used as the normal control group. RESULTS: The body weight loss and disease activity index were significantly lower in the GFO-treated mice compared with the glucose-treated mice (P < 0.05). The decrease in colon length induced by dextran sulfate sodium was significantly alleviated in GFO-treated mice compared with glucose-treated mice (P < 0.01). In addition, the histologic findings showed that intestinal inflammation was significantly attenuated in mice treated with GFO. Furthermore, treatment with GFO significantly inhibited the dextran sulfate sodium-induced increase in the mRNA expression of interleukin-1ß. CONCLUSION: These results suggest that GFO has potential therapeutic value as an adjunct therapy for ulcerative colitis.

Low birth weight as cardiometabolic risk in Japanese high school girls.

OBJECTIVE: To examine the relationships between birth weight and metabolic syndrome (MS) risk factors in healthy Japanese high school girls. METHODS: After obtaining informed consent, we carried out health surveys for the Food Educational Program (FEP) in 2007 and 2008 in 243 healthy Japanese high school girls aged 16.4 ± 1.4 years and examined anthropometric measurements, including abdominal circumference, systolic and diastolic blood pressures (SBP and DBP, respectively), triglycerides (TG), high-density lipoprotein cholesterol (HDL), insulin, and blood glucose to calculate insulin resistance after fasting for 3 hours after lunch. Birth weight was checked by maternity record book, and food customs were recorded using a questionnaire. We analyzed the prevalence of MS risk factors by Bonferroni test following 1-way analysis of variance and their relationships with birth weight by correlation analyses. RESULTS: According to criteria for MS risk factors in Japanese children and adults, the prevalence of obesity, high blood pressure, dyslipidemia, and high blood glucose was 7.4%, 9.1%, 7.0%, and 16.0%, respectively, and MS was detected in only 1 girl who had obesity and 2 more risks (high SBP and TG). Among 180 subjects who reported their birth weights, birth weights were significantly inversely related with SBP (p = 0.007), DBP (p = 0.033), TG (p = 0.009), insulin level (p = 0.047), insulin resistance ( p= 0.050), and number of metabolic risk factors (p = 0.022). Thirteen girls (7.2%) whose birth weights were lower than 2500 g had significantly higher SBP (p = 0.037), DBP (p = 0.032), TG (p = 0.011), insulin level (p=0.037), and insulin resistance (p = 0.043), than 31 girls (17.2%) with birth weights equal to or more than 3400 g. CONCLUSION: The association of low birth weight could be detected to be significant with such risks of MS as SBP, DBP, TG, insulin level, and insulin resistance even in healthy Japanese high school girls, indicating the importance of follow-up and FEP for children with low birth weight for the prevention of MS in the later life.

Effect of percutaneous electrical muscle stimulation on postprandial hyperglycemia in type 2 diabetes.

AIMS: The aim of this study was to examine whether percutaneous electrical muscle stimulation (EMS) attenuates postprandial hyperglycemia in type 2 diabetes. METHODS: Eleven patients with type 2 diabetes participated in two experimental sessions; one was a 30-min EMS 30 min after a breakfast (EMS trial) and the other was a complete rest after a breakfast (Control trial). In each trial, blood was sampled before and at 30, 60, 90, and 120 min after the meal. RESULTS: Postprandial glucose level was significantly attenuated in EMS trial at 60, 90, and 120 min after a meal (p<0.05). The C-peptide concentration was also significantly lowered in EMS trial (p<0.01). On the other hand, there was no significant increase in creatine phosphokinase (CPK) concentration in each trial. CONCLUSIONS: The present results provide first evidence indicating that EMS is a new exercise method for treating postprandial hyperglycemia in individuals with type 2 diabetes, especially who cannot perform adequate voluntary exercise because of excessive obesity, orthopedic diseases, or severe diabetic complications.

γ-Tocotrienol attenuates TNF-α-induced changes in secretion and gene expression of MCP-1, IL-6 and adiponectin in 3T3-L1 adipocytes.

Tocotrienols, members of the vitamin E family, have been shown to possess anti-inflammatory properties and display activity against a variety of chronic diseases, such as cancer, cardiovascular and neurological diseases. However, whether tocotrienols contribute to the prevention of inflammatory responses in adipose tissue remains to be elucidated. In this study, we examined the effects of γ-tocotrienol, the most common tocotrienol isomer, on tumor necrosis factor-α (TNF-α)-induced inflammatory responses by measuring the expression of the adipokines, monocyte chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6) and adiponectin in 3T3-L1 adipocytes. Exposure to TNF-α (10 ng/ml) for 24 h increased MCP-1 and IL-6 secretion, and decreased adiponectin secretion and peroxisome proliferator-activated receptor-γ (PPARγ) mRNA expression. γ-tocotrienol effectively improved the TNF-α-induced adverse changes in MCP-1, IL-6 and adiponectin secretion, and in MCP-1, IL-6, adiponectin and PPARγ mRNA expression. Furthermore, TNF-α-mediated IκB-α phosphorylation and nuclear factor-κB (NF-κB) activation were significantly suppressed by the γ-tocotrienol treatment. Our results suggest that γ-tocotrienol may improve obesity-related functional abnormalities in adipocytes by attenuating NF-κB activation and the expression of inflammatory adipokines.

High-fat diet-induced reduction of peroxisome proliferator-activated receptor-γ coactivator-1α messenger RNA levels and oxidative capacity in the soleus muscle of rats with metabolic syndrome.

Animal models of type 2 diabetes exhibit reduced peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) messenger RNA (mRNA) levels, which are associated with decreased oxidative capacity, in skeletal muscles. In contrast, animal models with metabolic syndrome show normal PGC-1α mRNA levels. We hypothesized that a high-fat diet decreases PGC-1α mRNA levels in skeletal muscles of rats with metabolic syndrome, reducing muscle oxidative capacity and accelerating metabolic syndrome or inducing type 2 diabetes. We examined mRNA levels and fiber profiles in the soleus muscles of rats with metabolic syndrome (SHR/NDmcr-cp [cp/cp]; CP) fed a high-fat diet. Five-week-old CP rats were assigned to a sedentary group (CP-N) that was fed a standard diet (15.1 kJ/g, 23.6% protein, 5.3% fat, and 54.4% carbohydrates) or a sedentary group (CP-H) that was fed a high-fat diet (21.6 kJ/g, 23.6% protein, 34.9% fat, and 25.9% carbohydrates) and were housed for 10 weeks. Body weight, energy intake, and systolic blood pressure were higher in the CP-H group than in the CP-N group. Nonfasting glucose, triglyceride, total cholesterol, and leptin levels were higher in the CP-H group than in the CP-N group. There was no difference in insulin levels between the CP-N and CP-H groups. Muscle PGC-1α mRNA levels and succinate dehydrogenase activity were lower in the CP-H group than in the CP-N group. We concluded that a high-fat diet reduces PGC-1α mRNA levels and oxidative capacity in skeletal muscles and accelerates metabolic syndrome.

Effects of cooking using multi-ply cookware on absorption of potassium and vitamins: a randomized double-blind placebo control study.

This 2-week interventional study involved a randomized allocation of subjects into three groups: Group A (daily ingestion of 350 g vegetables cooked without water using multi-ply [multilayer-structured] cookware), Group B (daily ingestion of 350 g vegetables; ordinary cookware) and Group C (routine living). Before and after intervention, each subject underwent health examination with 24-h urine sampling. Blood vitamin C significantly increased after intervention from the baseline in Group A (P < 0.01) and Group B (P < 0.05). ß-Carotene levels also increased significantly after intervention in Group A (P < 0.01) and Group B (P < 0.01). Oxidized low-density lipoprotein decreased significantly after intervention in Group A (P < 0.01). In Group A, 24-h urinary potassium excretion increased significantly (P < 0.01) and 24-h urinary sodium (Na)/K ratio improved significantly (P < 0.05) after intervention. In conclusion, a cooking method modification with multi-ply cookware improved absorption of nutrients from vegetables and enhanced effective utilization of the antioxidant potentials of vegetable nutrients.

The effects of running exercise on oxidative capacity and PGC-1α mRNA levels in the soleus muscle of rats with metabolic syndrome.

Skeletal muscles in animals with metabolic syndrome exhibit reduced oxidative capacity. We investigated the effects of running exercise on fiber characteristics, oxidative capacity, and mRNA levels in the soleus muscles of rats with metabolic syndrome [SHR/NDmcr-cp (cp/cp); CP]. We divided 5-week-old CP rats into non-exercise (CP) and exercise (CP-Ex) groups. Wistar-Kyoto rats (WKY) were used as the control group. CP-Ex rats were permitted voluntary exercise on running wheels for 10 weeks. Triglyceride levels were higher and adiponectin levels lower in the CP and CP-Ex groups than in the WKY group. However, triglyceride levels were lower and adiponectin levels higher in the CP-Ex group than in the CP group. The soleus muscles in CP-Ex rats contained only high-oxidative type I fibers, whereas those in WKY and CP rats contained type I, IIA, and IIC fibers. Muscle succinate dehydrogenase (SDH) activity was higher in the CP-Ex group than in the CP group; there was no difference in SDH activity between the WKY and CP-Ex groups. Muscle proliferator-activated receptor γ coactivator-1α (PGC-1α) mRNA levels were higher in the CP-Ex group than in the CP group; there was no difference in PGC-1α mRNA levels between the WKY and CP-Ex groups. In CP-Ex rats, longer running distance was associated with increased muscle SDH activity and PGC-1α mRNA levels. We concluded that running exercise restored decreased muscle oxidative capacity and PGC-1α mRNA levels and improved hypertriglyceridemia in rats with metabolic syndrome.

PGC-1α mRNA level and oxidative capacity of the plantaris muscle in rats with metabolic syndrome, hypertension, and type 2 diabetes.

We examined the fiber profiles and the mRNA levels of peroxisome proliferator-activated receptors (PPARα and PPARδ/ß) and of the PPARγ coactivator-1α (PGC-1α) in the plantaris muscles of 15-week-old control (WR), metabolic syndrome (CP), hypertensive (SHR), and type 2 diabetic (GK) rats. The deep regions in the muscles of SHR and GK rats exhibited lower percentages of high-oxidative type I and IIA fibers and higher percentages of low-oxidative type IIB fibers compared with WR and CP rats. The surface regions in the muscles of CP, SHR, and GK rats exhibited lower percentages of high-oxidative type IIA fibers and higher percentages of low-oxidative type IIB fibers compared with WR rats. The muscles of SHR and GK rats had lower oxidative enzyme activity compared with WR rats. The muscles of SHR rats had the lowest PPARδ/ß mRNA level. In addition, the muscles of SHR and GK rats had lower PGC-1α mRNA level compared with WR and CP rats. We concluded that the plantaris muscles of rats with hypertension and type 2 diabetes have lower oxidative capacity, which is associated with the decreased level of PGC-1α mRNA.

Pitavastatin reduces elevated IL-18 levels in Japanese subjects with hypercholesterolemia: sub-analysis of Kansai investigation of statin for hyperlipidemic intervention in metabolism and endocrinology (KISHIMEN).

AIM: Pitavastatin significantly improved lipid profiles and reduced serum high-sensitivity C-reactive protein (hs-CRP) levels in a multi-center and prospective study. The aim of this study was to explore the effect of pitavastatin on serum levels of another inflammatory biomarker, interleukin-18 (IL-18), in a sub-analysis of the previous multi-center prospective study. METHODS: The subjects were 83 patients derived from the KISHIMEN study. Pitavastatin (1-2 mg/day) was administered for 12 months. Serum total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), remnant-like particle cholesterol (RLP-C), triglycerides (TG), IL-18, and high sensitivity C-reactive protein (hs-CRP) levels were measured. RESULTS: TC, LDL-C, and RLP-C levels were significantly reduced by 18.3%, 30.1%, and 21.0% (mean values) at 12 months after pitavastatin administration. TG levels were decreased by 9.8% in subjects whose basal TG levels were above 150 mg/dL. HDL-C levels were significantly increased at 6 months (11.9%). Pitavastatin did not significantly alter IL-18 levels in overall subjects, but reduced IL-18 levels in the highest quartile by 24.5% (median value) at 12 months. Pitavastatin significantly reduced hs-CRP levels by 28.6% in overall subjects and by 62.4% in the highest quartile at 12 months. There was a significant correlation between IL-18 and hs-CRP at baseline after both values were transformed into logarithms (Pearson's correlation coefficient, r = 0.259, p = 0.0181); however, percent changes in these levels were not significantly correlated. CONCLUSION: Pitavastatin significantly improves lipid profiles, and reduces enhanced inflammation monitored by IL-18, as well as by hs-CRP, in hypercholesterolemic subjects.

Practical dietary calorie management, body weight control and energy expenditure of diabetic patients in short-term hospitalization.

AIM: We investigated how dietary management affected body weight (BW) reduction and energy expenditure in obese and normal-weight type 2 diabetic patients. METHODS: Type 2 diabetic patients who were hospitalized for diabetic control (93 men and 51 women) were checked for resting energy expenditure (REE). Subjects were divided into the two groups according to body mass index (BMI): obese (BMI > or = 25), and normal-weight (BMI <25). Following the recommendations by JDS, JAS and JASSO, ideal body weight was calculated as [IBW=height (m) x height (m) x 22 (kg/m(2))], and dietary calorie (kcal/day) was determined as 25 kcal/kg IBW. RESULTS: Dietary calorie intake during hospitalization was similar in both groups. REE was greater in obese than in normal-weight patients. The difference between the calorie intake and energy expenditure (Deltacalorie) was -222+/-26 kcal in obese patients and 69+/-27 kcal in normal-weight patients. Obese patients therefore had larger BW decreases than normal-weight patients (-171+/-12 vs. -92+/-11 g/day, p<0.005). In the obese group, a positive correlation was found between the change of BW and Deltacalorie. This correlation remained after adjusting for age, BMI, gender, and respiratory quotient. Serum lipid profiles were significantly improved in both groups. CONCLUSION: These diet instructions showed the appropriate calorie restriction depending on the BMI and induced reasonable BW reduction in both obese and normal-weight subjects. The dietary program recommended by JDS, JAS and JASSO is practically useful for BW control and for improving lipid metabolism in type 2 diabetic patients.

Hyperbaric oxygen exposure improves blood glucose level and muscle oxidative capacity in rats with type 2 diabetes.

BACKGROUND: The effects of exposure to hyperbaric oxygen on blood glucose level and muscle oxidative capacity in rats with type 2 diabetes were investigated. METHODS: Five-week-old male Goto-Kakizaki rats were divided into four groups: normobaric (NN; exposed to 21% oxygen at 760 mm Hg for 8 weeks), hyperbaric to normobaric (HN; exposed to 36% oxygen at 950 mm Hg for 4 weeks, followed by 21% oxygen at 760 mm Hg for 4 weeks), normobaric to hyperbaric (NH; exposed to 21% oxygen at 760 mm Hg for 4 weeks, followed by 36% oxygen at 950 mm Hg for 4 weeks), and hyperbaric (HH; exposed to 36% oxygen at 950 mm Hg for 8 weeks). RESULTS: Blood glucose levels were lower in the HN, NH, and HH groups than in the NN group. Up-regulated mRNA expression levels of peroxisome proliferator-activated receptor-gamma co-activator-1alpha were observed in the soleus muscles of the HN, NH, and HH groups and in the plantaris muscles of the HN and HH groups. The soleus muscles of the NN group contained only type I fibers, whereas those of the HN, NH, and HH groups contained type I, type IIA, and type IIC fibers. An increased percentage of type I fibers and a decreased percentage of type IIB fibers were observed in the plantaris muscles of the NH, HN, and HH groups. CONCLUSIONS: Exposure to hyperbaric oxygen reduces high blood glucose levels and improves oxidative capacities in the skeletal muscles of rats with diabetes, and these effects are maintained under normobaric conditions even after exposure to hyperbaric oxygen.

Association of estrogen receptor-alpha gene polymorphisms with cardiac autonomic nervous activity in healthy young Japanese males.

BACKGROUND: Estrogens exert beneficial effects on the cardiovascular system that are mediated by estrogen receptors. We examined the association between the estrogen receptor alpha gene (ESR1) PvuII and XbaI polymorphisms and cardiac autonomic nervous function in Japanese males. METHODS: We examined 252 young healthy males for association of ESR1 PvuII and XbaI polymorphisms and short-term heart rate variability (HRV) during supine rest and in a standing position. The very low frequency (VLF), low frequency (LF), and high frequency (HF) components of HRV were quantified by frequency domain analysis. RESULTS: Carriers of the ESR1 PvuII C allele had higher mean blood pressure (BP), while the XbaI GG genotype was significantly associated with higher diastolic and mean BP, but lower HR. In the haplotype analysis, carriers of the ESR1 haplotype 2 (PvuII C and XbaI A) allele had a higher systolic and mean BP, and lower HRV spectral powers (total power, VLF, LF, and HF components) in a supine rest compared with those of non-carriers. CONCLUSIONS: The ESR1 PvuII and XbaI haplotype is associated with BP variation and the reduction in cardiac autonomic nervous activity in young Japanese males, which may be precursors of future pathological episodes of cardiovascular diseases.

Skeletal muscle characteristics of rats with obesity, diabetes, hypertension, and hyperlipidemia.

AIM: Data on the skeletal muscle characteristics of patients and animals with lifestyle-related diseases are limited. We investigated mRNA expression levels and fiber profiles in the skeletal muscles of rats with obesity, diabetes, hypertension, and/or hyperlipidemia. METHODS: The mRNA expression levels of peroxisome proliferator-activated receptors (PPARalpha and PPARdelta/beta), PPARgamma coactivator-1alpha (PGC-1alpha), stearoyl-CoA desaturase-1 (SCD-1), carnitine palmi-toyl-transferase I (CPT I), medium-chain acyl-CoA dehydrogenase (MCAD), and mitochondrial transcriptional factor A (TFAM) in the soleus muscles were compared among 15-week-old control (WR), type 2 diabetic (GK), hypertensive (SHR), and hyperlipidemic (CP) rats. The fiber profiles in the soleus muscles of these rats were also determined. RESULTS: GK rats showed lower PPARdelta/beta, PGC-1alpha, and MCAD expression levels than WR rats. SHR rats showed higher PPARalpha and MCAD and lower PPARdelta/beta expression levels than WR rats. CP rats showed lower PPARdelta/beta and higher SCD-1 expression levels than WR rats. The muscles of WR, SHR, and CP rats had low-oxidative type I and high-oxidative type IIA and type IIC fibers, whereas the muscle of GK rats had only low-oxidative type I fibers. CONCLUSIONS: The skeletal muscles of rats with lifestyle-related diseases have unique mRNA expres-sion patterns and fiber profiles depending on the type of disease. For example, the lower PGC-1alpha and MCAD mRNA expression levels in the soleus muscles of type 2 diabetic rats are associated with the presence of only low-oxidative type I fibers in the muscle.