Decreased risk of renal cell carcinoma in patients with type 2 diabetes treated with sodium glucose cotransporter-2 inhibitors.

Patients with type 2 diabetes (T2D) are at a higher risk of developing renal cell carcinoma (RCC) than the general population. In vitro and in vivo investigations of the effects of sodium glucose cotransporter-2 inhibitors (SGLT2I) have shown a significantly reduced risk of RCC. However, the impact of these drugs on the incidence of RCC in the human population is unclear. This study aimed to examine the association between SGLT2I use and RCC risk in patients with T2D. We undertook a nationwide retrospective cohort study using the Health and Welfare Data Science Center database (2016-2020). The primary outcome was the risk of incident RCC by estimating hazard ratios (HRs) and 95% confidence intervals (CIs). Multiple Cox regression modeling was applied to analyze the association between SGLT2I use and RCC risk in patients with T2D. In a cohort of 241,772 patients with T2D who were using SGLT2Is and 483,544 participants who were not, 220 and 609 RCC cases, respectively, were recorded. The mean follow-up period of the study subjects was 2 years. There was a decreased risk of RCC for SGLT2I users after adjusting for the index year, sex, age, comorbidities, and concurrent medication (adjusted HR 0.68; 95% CI, 0.58-0.81). The sensitivity test for the propensity score 1:1-matched analyses showed similar results (adjusted HR 0.67; 95% CI, 0.55-0.81). The subgroup analysis revealed consistent results for sex, age (<70 years), and comorbidity with chronic kidney disease. The present study indicates that SGLT2I therapy significantly decreases RCC risk in patients with T2D. This finding was also consistent among the sensitivity test and subgroup analysis for those with or without chronic kidney disease/hypertension.

The effect of commuting time on burnout: the mediation effect of musculoskeletal pain.

OBJECTIVES: This study explores the relationship among commuting, musculoskeletal (MS) pain, and burnout. METHODS: An observational and cross-sectional study was conducted at a medical university-affiliated hospital in Taichung, Taiwan in 2021. The two questionnaire was used and they included the Copenhagen Burnout Inventory (CBI) and the Nordic Musculoskeletal Questionnaire (NMQ). All participants were invited to complete the cross-sectional survey. A multiple linear regression was assessed correlations between commuting, MS pain, and burnout. RESULTS: After excluding those with missing data, 1,615 healthcare workers were deemed valid as research participants. In multiple linear regression, commuting time longer than 50 min was associated with personal burnout (PB) in the presence of adjusted confounders; however, long commuting time was not associated with work-related burnout (WB). Furthermore, the choice of commuting method did not affect PB or WB. Notably, both neck and shoulder pain (NBSP) and ankle pain (BAP) increase the risk of PB and WB. The mediation analysis demonstrated that NBSP is a mediating factor, increasing the level of PB and WB for commuting times longer than 50 min. CONCLUSIONS: Healthcare workers who commute for more than 50 min should be considered part of a high-risk group for burnout and musculoskeletal pain. They should also be provided with resources and programs focused on burnout prevention and MS pain relief.

The association between SGLT2 inhibitors and new-onset acute coronary syndrome in the elderly: a population-based longitudinal cohort study.

BACKGROUND: Several observational cohorts and meta-analytical studies on humans have shown that users of sodium-glucose cotransporter-2 inhibitors (SGLT2is) have a lower risk for new-onset acute coronary syndrome (ACS) than nonusers. However, some studies, including randomized clinical trials, reported the opposite results. This study aimed to investigate the impacts of a SGLT2i on new-onset ACS in a population. METHODS: We conducted a retrospective population-based cohort study involving 56,356 subjects who received SGLT2i therapy and 112,712 patients who did not receive SGLT2i therapy between May 1, 2016 and December 31, 2019. The outcome was the risk of new-onset ACS. Multivariable Cox proportional hazards models were used to calculate hazard ratios (HRs) and 95% confidence intervals for associations between SGLT2i use and ACS risk. RESULTS: A total of 670 and 1408 ACS events occurred in SGLT2i users and nonusers, respectively, during a follow-up of 3.7 years. SGLT2i use was associated with a nonsignificantly lower risk of ACS (adjusted HR 0.95, 95%confidence intervals (CI 0.87-1.04, P = 0.3218). We confirmed the robustness of these results through a propensity score 1:1 matching analysis. The results of the subgroup analysis of the subtype of the SGLT2i treatments were consistent with the main findings. An increased risk for the incidence of ACS in male and older (> 70 years) patients were also found. CONCLUSIONS: In this population-based cohort study, we found that SGLT2i use is associated with a nonsignificantly decreased risk of ACS. No difference in the SGLT2i subtype was observed in subgroup analyses. However, the results of this study indicated an increased risk for the incidence of ACS in male and older (> 70 years) patients.

Risk of New-onset Stroke in Patients with Type 2 Diabetes with Chronic Kidney Disease on Sodium-glucose Co-transporter-2 Inhibitor Users.

Clinical studies have investigated the effects of using sodium-glucose co-transporter-2 (SGLT2) inhibitors on the development of new-onset stroke (NOS) in patients with type 2 diabetes (T2D) and chronic kidney disease (CKD), but the findings are inconsistent. This study aimed to examine the association between the use of SGLT2 inhibitors and NOS risk in patients with T2D and CKD. We conducted a nationwide retrospective cohort study using data from the Taiwan Health Insurance Review and Assessment Service database for the years 2004 to 2019. The primary outcome was the risk of incident stroke, which was estimated using hazard ratios (HRs) and 95% confidence intervals (CIs). We used multiple Cox regression modeling to analyze the association between SGLT2 inhibitor use and the risk of stroke in patients with T2D and CKD. In a cohort of 113,710 patients with T2D and CKD who were using SGLT2 inhibitors and 227,420 patients with T2D and CKD who were not using SGLT2 inhibitors, after applying a 1:2 sex- and age-matching strategy, 2,842 and 7,169 NOS events were recorded, respectively. The event rate per 10,000 person-months was 10.60 (95% CI 10.21 to 11.03) for SGLT2 inhibitor users and 13.71 (13.39-14.03) for non-SGLT2 inhibitor users. After adjusting for the index year, sex, age, comorbidities, and concurrent medication, there was a decreased risk of NOS for SGLT2 inhibitor users (adjusted HR 0.80; 95% CI 0.77-0.84) compared with non-SGLT2 inhibitor users. The sensitivity test for the propensity score 1:1-matched analyses showed similar results (adjusted HR 0.80; 95% CI 0.76-0.84). The type of SGLT2 inhibitor subgroup analysis for incident stroke showed consistent results. We concluded that the use of SGLT2 inhibitors in patients with T2D and CKD was associated with significantly low rates of NOS. The significantly low rates of NOS in patients with T2D and CKD were greater among females and less than 50 years patients.

Risk of New-Onset Dementia in Patients with Chronic Kidney Disease on Statin Users: A Population-Based Cohort Study.

Patients with chronic kidney disease (CKD) are at a higher risk for developing dementia than the general population. Clinical studies have investigated the effects of statin use on new-onset dementia (NOD) in patients with CKD; however, the findings are inconsistent. This study examines the association between the use of statins and NOD in patients with CKD. We conducted a nationwide retrospective cohort study using the Taiwan Health Insurance Review and Assessment Service database (2003-2016). The primary outcome assessed the risk of incident dementia by estimating the hazard ratios and 95% confidence intervals. Therefore, multiple Cox regression models were conducted to analyse the association between statin use and NOD in patients with CKD. There were 24,090 participants with statin use and 28,049 participants without statin use in patients with new-diagnosed CKD; the NOD event was 1390 and 1608, respectively. There was a trend of reduction association between statin users and NOD events after adjusted sex, age, comorbidities, and concurrent medication (adjusted HR 0.93, 95% CI 0.87 to 1.00) in the 14 years of the follow-up. Sensitivity test for the propensity score 1:1 matched analyses showed similar results (adjusted HR 0.91, 95% CI 0.81 to 1.02). The subgroup analysis also identified the use of statins as having a trend against developing NOD in patients with hypertension. In conclusion, statin therapy may effectively reduce the risk of NOD in patients with CKD. More studies are needed to credibly evaluate the effects of statin therapy on the prevention of NOD in patients with CKD.

Acarbose Protects Glucolipotoxicity-Induced Diabetic Nephropathy by Inhibiting Ras Expression in High-Fat Diet-Fed db/db Mice.

Diabetic nephropathy (DN) exacerbates renal tissue damage and is a major cause of end-stage renal disease. Reactive oxygen species play a vital role in hyperglycemia-induced renal injury. This study examined whether the oral hypoglycemic drug acarbose (Ab) could attenuate the progression of DN in type 2 diabetes mellitus mice. In this study, 50 mg/kg body weight of Ab was administered to high-fat diet (HFD)-fed db/db mice. Their body weight was recorded every week, and the serum glucose concentration was monitored every 2 weeks. Following their euthanasia, the kidneys of mice were analyzed through hematoxylin and eosin, periodic acid Schiff, Masson's trichrome, and immunohistochemistry (IHC) staining. The results revealed that Ab stabilized the plasma glucose and indirectly improved the insulin sensitivity and renal functional biomarkers in diabetic mice. In addition, diabetes-induced glomerular hypertrophy, the saccharide accumulation, and formation of collagen fiber were reduced in diabetic mice receiving Ab. Although the dosages of Ab cannot decrease the blood sugar in db/db mice, our results indicate that Ab alleviates glucolipotoxicity-induced DN by inhibiting kidney fibrosis-related proteins through the Ras/ERK pathway.

Mulberry Leaf (Morus alba L.) Extracts and Its Chlorogenic Acid Isomer Component Improve Glucolipotoxicity-Induced Hepatic Lipid Accumulation via Downregulating miR-34a and Decreased Inflammation.

Mulberry leaf (Morus alba L.) is used as a traditional medicine and potential health food to treat various metabolic diseases, such as hypertension, diabetes, and hyperlipidemia. However, we sought the mechanisms by which functional components of mulberry leaves mediate diabetic steatohepatitis. We applied an in vitro model of HepG2 cells induced by glucolipotoxicity and evaluated the effects of MLE and its major components nCGA, Crp, and CGA. The results showed that MLE and nCGA reduced liver fat accumulation by inhibiting SREBP-1/FASN, SREBP-2/HMG-CoAR, and activating PPARα/CPT-1. Additionally, MLE and nCGA decreased inflammatory responses associated with NF-κB, TNF-α, and IL-6 to alleviate steatohepatitis. Furthermore, we showed that MLE and nCGA exerted anti-glucolipotoxicity effects by downregulating miR-34a, thus activating SIRT1/AMPK signaling, and subsequently suppressing hepatic lipid accumulation.

Mulberry Leaf and Neochlorogenic Acid Alleviates Glucolipotoxicity-Induced Oxidative Stress and Inhibits Proliferation/Migration via Downregulating Ras and FAK Signaling Pathway in Vascular Smooth Muscle Cell.

Mulberry leaf (Morus alba L.) has been used as a health food and in traditional medicine to treat several metabolic diseases, including diabetes, hypertension, and hyperlipidemia. However, the mechanism by which mulberry leaf and its functional components mediate atherosclerosis remains unclear. This study aimed to determine the effect of mulberry leaf extract (MLE) and its major component, neochlorogenic acid (nCGA), on the proliferation and migration of rat aortic vascular smooth muscle cells (VSMCs, A7r5 cell line) under diabetic cultured conditions (oleic acid and high glucose, OH). Our findings showed that MLE and nCGA significantly inhibited cell proliferation and migration in A7r5 cells as determined by a scratch wound assay and a Transwell assay. Furthermore, we observed MLE and nCGA inhibited cell proliferation and migration, such as reducing the phosphoinositide 3-kinases (PI3K)/protein kinase B (Akt), focal adhesion kinase (FAK), and small GTPase proteins using Western blot analysis. In conclusion, we confirmed the anti-atherosclerotic effects of MLE and nCGA in reducing vascular smooth muscle cell (VSMC) migration and proliferation under diabetic cultured conditions via inhibition of FAK/small GTPase proteins, PI3K/Akt, and Ras-related signaling.

Methylmercury Induces Mitochondria- and Endoplasmic Reticulum Stress-Dependent Pancreatic ß-Cell Apoptosis via an Oxidative Stress-Mediated JNK Signaling Pathway.

Methylmercury (MeHg), a long-lasting organic pollutant, is known to induce cytotoxic effects in mammalian cells. Epidemiological studies have suggested that environmental exposure to MeHg is linked to the development of diabetes mellitus (DM). The exact molecular mechanism of MeHg-induced pancreatic ß-cell cytotoxicity is still unclear. Here, we found that MeHg (1-4 µM) significantly decreased insulin secretion and cell viability in pancreatic ß-cell-derived RIN-m5F cells. A concomitant elevation of mitochondrial-dependent apoptotic events was observed, including decreased mitochondrial membrane potential and increased proapoptotic (Bax, Bak, p53)/antiapoptotic (Bcl-2) mRNA ratio, cytochrome c release, annexin V-Cy3 binding, caspase-3 activity, and caspase-3/-7/-9 activation. Exposure of RIN-m5F cells to MeHg (2 µM) also induced protein expression of endoplasmic reticulum (ER) stress-related signaling molecules, including C/EBP homologous protein (CHOP), X-box binding protein (XBP-1), and caspase-12. Pretreatment with 4-phenylbutyric acid (4-PBA; an ER stress inhibitor) and specific siRNAs for CHOP and XBP-1 significantly inhibited their expression and caspase-3/-12 activation in MeHg-exposed RIN-mF cells. MeHg could also evoke c-Jun N-terminal kinase (JNK) activation and reactive oxygen species (ROS) generation. Antioxidant N-acetylcysteine (NAC; 1mM) or 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid (trolox; 100 µM) markedly prevented MeH-induced ROS generation and decreased cell viability in RIN-m5F cells. Furthermore, pretreatment of cells with SP600125 (JNK inhibitor; 10 µM) or NAC (1 mM) or transfection with JNK-specific siRNA obviously attenuated the MeHg-induced JNK phosphorylation, CHOP and XBP-1 protein expression, apoptotic events, and insulin secretion dysfunction. NAC significantly inhibited MeHg-activated JNK signaling, but SP600125 could not effectively reduce MeHg-induced ROS generation. Collectively, these findings demonstrate that the induction of ROS-activated JNK signaling is a crucial mechanism underlying MeHg-induced mitochondria- and ER stress-dependent apoptosis, ultimately leading to ß-cell death.

The Effects of Frequent Coffee Drinking on Female-Dominated Healthcare Workers Experiencing Musculoskeletal Pain and a Lack of Sleep.

Previous research has demonstrated that chronic diseases can occur due to musculoskeletal (MS) pain and poor sleep. It is also worth noting that the caffeine in coffee can reduce overall sleep duration, efficiency, and quality. Thus, the present study examines the effects of frequent coffee drinking (two cups per day) on individuals experiencing MS pain and a lack of sleep during the COVID-19 period. This observational and cross-sectional study recruited 1615 individuals who completed the self-reported (Nordic musculoskeletal) questionnaire. Long-term, frequent coffee drinking and a sleep duration of less than 6 h per day were significantly associated with neck and shoulder pain among healthy individuals. The mediation model demonstrated that the shorter sleep duration and drinking multiple cups of coffee per day had a two-way relationship that worsened such pain over the long term. Specifically, individuals who experienced such pain frequently drank multiple cups of coffee per day, which, in turn, shortened their sleep durations. In summary, long-term coffee drinking creates a vicious cycle between MS pain and sleep duration. Therefore, the amount of coffee should be fewer than two cups per day for individuals who sleep less than 6 h per day or suffer from MS pain, especially neck and shoulder pain.

Case Report: A Rare Manifestation of Pulmonary Arterial Hypertension in Ankylosing Spondylitis.

Ankylosing spondylitis (AS) is an inflammatory disease that involves the axial skeleton and can present with extra-articular manifestations. However, there are scarce reports describing the link between AS and pulmonary arterial hypertension (PAH). Herein, we report on a 58-year-old man with a history of AS for 32 years who developed PAH as confirmed by echocardiography and right cardiac catheterization. To our knowledge, this is the first case of AS associated with PAH 32 years after the AS diagnosis with a detailed clinical description. We are recommended that physicians should be aware of this rare comorbidity in AS patients. Early echocardiographic screening is necessary for symptomatic patients.

Mulberry leaves extract ameliorates alcohol-induced liver damages through reduction of acetaldehyde toxicity and inhibition of apoptosis caused by oxidative stress signals.

Mulberry leaves (Morus alba L.), which are traditional Chinese herbs, exert several biological functions, such as antioxidant, anti-inflammation, antidiabetic, and antitumor. Alcohol intake increases inflammation and oxidative stress, and this increase causes liver injury and leads to liver steatosis, cirrhosis, and hepatocellular carcinoma, which are major health problems worldwide. Previous report indicated that mulberry leaf extract (MLE) exited hepatoprotection effects against chronic alcohol-induced liver damages. In this present study, we investigated the effects of MLE on acute alcohol and liver injury induced by its metabolized compound called acetaldehyde (ACE) by using in vivo and in vitro models. Administration of MLE reversed acute alcohol-induced liver damages, increased acetaldehyde (ACE) level, and decreased aldehyde dehydrogenase activity in a dose-dependent manner. Acute alcohol exposure-induced leukocyte infiltration and pro-inflammation factors, including cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6), were blocked by MLE in proportion to MLE concentration. MLE prevented alcohol-induced liver apoptosis via enhanced caveolin-1 expression and attenuated EGFR/STAT3/iNOS pathway using immunohistochemical analysis. ACE induced proteins, such as iNOS, COX-2, TNF-α, and IL-6, and inhibited superoxide dismutase expression, whereas co-treated with MLE reversed these proteins expression. MLE also recovered alcohol-induced apoptosis in cultured Hep G2 cells. Overall, our findings indicated that MLE ameliorated acute alcohol-induced liver damages by reducing ACE toxicity and inhibiting apoptosis caused by oxidative stress signals. Our results implied that MLE might be a potential agent for treating alcohol liver disease.

Acarbose attenuates migration/proliferation via targeting microRNA-143 in vascular smooth muscle cells under diabetic conditions.

Acarbose (an α-glucosidase inhibitor) has been demonstrated to reduce the progression of atherosclerosis without affecting serum levels of glucose in rabbits fed a high cholesterol diet. The main focus of recent atherosclerosis studies has been microRNA targets. However, the mechanism by which acarbose targets miRNA-mediated atherosclerosis remains unclear. This study aimed to evaluate the effect of acarbose on microRNA-related regulation of rat aortic vascular smooth cell line (A7r5 cell) migration and proliferation induced by diabetic conditions. We reported that acabose exhibit significantly inhibits proliferative and cell migration abilities in A7r5 cells. The expression of protein and levels of mRNA were measured by Western blot analysis and real-time PCR. Acarbose inhibited the phosphorylation of focal adhesion kinase (FAK) and phosphoinositide 3-kinases (PI3K)/protein kinase B (Akt), Ras signals, small GTPase proteins expression to attenuate cell migration and proliferation. Furthermore, acarbose upregulated the expression of miR-143, and transfected miR-143 mimic and its inhibitor to explore its mechanism. In conclusion, acarbose reduces VSMC migration and proliferation via upregulating miR-143 to inhibit Ras-related signaling, and potentially prevention of atherosclerosis.

Mulberry Polyphenol Extract Inhibits FAK/Src/PI3K Complex and Related Signaling To Regulate the Migration in A7r5 Cells.

Atherosclerosis is characterized by the buildup of plaque inside arteries. Our recent studies demonstrated that polyphenolic natural products can reduce oxidative stress, inflammation, angiogenesis, hyperlipidemia, and hyperglycemia. A previous study also showed that mulberry water extract (MWE) can inhibit atherosclerosis and contains considerable amounts of polyphenols. Therefore, in the present study, we investigated whether mulberry polyphenol extract (MPE) containing high levels of polyphenolic compounds could affect vascular smooth muscle cell (VSMC; A7r5 cell) motility. We found that MPE inhibited expression of FAK, Src, PI3K, Akt, c-Raf, and suppressed FAK/Src/PI3K interaction. Further investigations showed that MPE reduced expression of small GTPases (RhoA, Cdc42, and Rac1) to affect F-actin cytoskeleton rearrangement, down-regulated expression of MMP2 and vascular endothelial growth factor (VEGF) mRNA through NFκB signaling, and thereby inhibited A7r5 cell migration. Taken together, these findings highlight MPE inhibited migration in VSMC through FAK/Src/PI3K signaling pathway.

Molybdenum induces pancreatic ß-cell dysfunction and apoptosis via interdependent of JNK and AMPK activation-regulated mitochondria-dependent and ER stress-triggered pathways.

Molybdenum (Mo), a well-known toxic environmental and industrial pollutant, causes adverse health effects and diseases in humans and has received attention as a potential risk factor for DM. However, the roles of Mo in the mechanisms of the toxicological effects in pancreatic ß-cells are mostly unclear. In this study, the results revealed dysfunction of insulin secretion and apoptosis in the pancreatic ß-cell-derived RIN-m5F cells and the isolated mouse islets in response to Mo. These effects were accompanied by a mitochondria-dependent apoptotic signals including a decreased in the MMP, an increase in cytochrome c release, and the activation of caspase cascades and PARP. In addition, ER stress was triggered as indicated by several key molecules of the UPR. Furthermore, exposure to Mo induced the activation of ERK1/2, JNK, AMPKα, and GSK3-α/ß. Pretreatment with specific pharmacological inhibitors (in RIN-m5F cells and isolated mouse islets) of JNK (SP600125) and AMPK (Compound C) or transfection with si-RNAs (in RIN-m5F cells) specific to JNK and AMPKα effectively prevented the Mo-induced apoptosis and related signals, but inhibitors of ERK1/2 and GSK3-α/ß (PD98059 and LiCl, respectively) did not reverse the Mo-induced effects. Additionally, both the inhibitors and specific si-RNAs could suppress the Mo-induced phosphorylation of JNK and AMPKα each other. Taken together, these results suggest that Mo exerts its cytotoxicity on pancreatic ß-cells by inducing dysfunction and apoptosis via interdependent JNK and AMPK activation downstream-regulated mitochondrial-dependent and ER stress-triggered apoptosis pathways.

Association of Sitagliptin with cardiovascular outcome in diabetic patients: a nationwide cohort study.

AIMS: Although dipeptidyl peptidase-4 (DPP-4) inhibitor improves glycemic control, the actual cardiovascular outcomes remain unclear. The objective of this cohort study was to thus evaluate the cardiovascular outcome in diabetic patients who received DPP-4 inhibitors (Sitagliptin). METHODS: A total of 104,756 new diabetic patients were identified from the Taiwan National Health Insurance Research Database during the period from March 1, 2003 to December 31, 2011. Patients who received Sitagliptin therapy were included as exposures, and up to four age- and sex-matched controls were selected by risk-set sampling. Outcomes such as major adverse cardiovascular diseases (CVD) and deaths were assessed. Logistic regression models were applied to estimate the hazard ratios and 95 % CIs between DPP-4 inhibitor use and cardiovascular outcome. RESULTS: Over a mean of 14 months, the rates of total CVD per 1000 person-months were significantly lower in Sitagliptin users (3.41 vs. 5.17, p < 0.001), whereas other different CVDs (hazard ratio [HR] 0.59; 95 % confidence interval [CI] 0.48-0.72 for coronary heart disease; HR 0.75; 95 % CI 0.59-0.96 for ischemic stroke; HR 0.86; 95 % CI 0.45-1.65 for peripheral artery occlusive disease) and all-cause mortality (HR 0.56; 95 % CI 0.41-0.74]) were also fewer after adjustment for covariates. CONCLUSIONS: The results showed a favorable outcome of Sitagliptin as a class on lowering CVD incidence in patients with type 2 diabetes.

Association of Serum Uric Acid with Cardiovascular Disease in Taiwanese Patients with Primary Hypertension.

BACKGROUND: Hyperuricemia is closely linked to hypertension and may be a marker of susceptibility or an intermediate step in the development of metabolic syndrome. However, recently, there have been conflicting conclusions regarding the independent role of uric acid as a risk factor of cardiovascular disease (CVD). The specific role of serum uric acid (SUA) in relation to CVD remains controversial, and there are limited reports utilizing Asian data available on this issue. Therefore, this study investigated the association between SUA and cardiovascular disease in Taiwanese patients with essential hypertension. METHODS: There were 3472 participants from 55-80 years of age (1763 males, 1709 females) from 38 sites across Taiwan in this hospital-based cross-sectional study, covering the period November 2005 to December 2006. The CVD included diagnosed angina pectoris, myocardial infarction, congestive heart failure, and stroke. RESULTS: Hyperuricemia is positively associated with CVD in both sexes when a unified cut-off SUA level of 7 mg/dl was used. However, the odds ratios (ORs) for all CVD were greater in magnitude in hypertensive women than in men when there was co-morbidity of diabetes. The ORs of all CVD in the diabetes subgroup were statistically significantly (p = 0.01 for women, p = 0.07 for men). By multivariate analysis, hyperuricemia did not confer an increased risk of CVD. CONCLUSIONS: Hyperuricemia may be associated with increased risk of CVD, but is not an independent risk factor of CVD in essential hypertensive Taiwanese patients. KEY WORDS: Cardiovascular disease; Hypertension; Hyperuricemia; Uric acid.

Weight reduction effect of Puerh tea in male patients with metabolic syndrome.

Puerh tea has been proposed to promote weight loss and favorably modify glucose, insulin and blood lipids. This study tested the effect of daily Puerh tea consumption for 3 months on weight and body mass index (BMI), and select metabolic parameters. The effect of daily Puerh tea intake on weight, BMI and changes in glucose, HbA1c and lipids was evaluated in patients with metabolic syndrome. The patients (N = 70) were randomized into two groups: those taking Puerh tea extract capsule (333 mg Puerh tea extract) three times a day and those taking a placebo tea for 3 months. There was a decrease in body weight of 1.3 kg in the Puerh tea group (p = 0.077) versus 0.23 kg in the placebo arm (p = 0.186). There was also a slight decrease in BMI 0.47 kg/m(2) in the Puerh tea group (p = 0.076) versus 0.09 kg/m(2) in the placebo arm (p = 0.185), suggesting a trend of weight change, but without statistical significance. Subgroup analysis of the male patients demonstrated statistically significant improvements in body weight reduction (p = 0.004) and BMI (p = 0.004). However, the change in other metabolic parameters (cholesterol or triglyceride) or HbA1c was not statistically significant. Intake of Puerh tea for 3 months was associated with a slight reduction in body weight and BMI, especially in the male patients. Therefore, daily Puerh tea consumption may be an alternative choice to modify body weight.

A randomized, double-blind, placebo-controlled study to evaluate the efficacy and tolerability of Fufang Danshen (Salvia miltiorrhiza) as add-on antihypertensive therapy in Taiwanese patients with uncontrolled hypertension.

Hypertension generally requires the use of a combination therapy to achieve the satisfactory control of blood pressure. A traditional Chinese herb, Danshen (Salvia miltiorrhiza), has been shown to have cardioprotective effects in animals and humans. The study investigated the add-on effect of Fufang Danshen extract capsule in Taiwanese hypertensive patients with uncontrolled blood pressure. This was a double-blind, placebo-controlled, randomized, single-center study clinical trial. Fifty-five patients with uncontrolled mild to moderate hypertension were enrolled under current conventional antihypertensive treatment, randomized equally to receive a Fufang Danshen capsule (formula mixture) 1000 mg twice-daily or a placebo capsule for 12 weeks. Primary endpoints were the control rate and the response rate. By ITT analysis at week 12, the control rates were 25.5% in the Fufang Danshen group and 7.3% in the control group (p = 0.016). The response rates were 45.6% in the Fufang Danshen group and 38.2% in the placebo group (p = 0.946). A significant reduction of systolic blood pressure at week 12 was noted in the Fufang Danshen group compared with the placebo group (13.8 vs 4.2 mmHg, p = 0.005). A decrease of pulse rate was also noted in the Fufang Danshen group (- 3.2 vs +2.7/min, p = 0.027). Adverse events were not statistically different between the two groups. It was concluded that Fufang Danshen (Salvia miltiorrhiza) extract reduced systolic blood pressure and pulse rate, and was well tolerated in patients with hypertension.