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There has been an increased interest in determining calcium magnesium, sodium, and potassium's distinct effects on hypertension over the past decade, yet they simultaneously regulate blood pressure. We aimed at examining the association of dietary calcium, magnesium, sodium, and potassium independently and jointly with hypertension using National Health and Nutrition Examination Survey data from 2007 to 2014.
The associations were examined on a large cross-sectional study involving 16684 US adults aged>20 years, using multivariate analyses with logistical models.
Sodium and calcium quartiles assessed alone were not associated with hypertension. Potassium was negatively associated with hypertension in the highest quartile, 0.64 (95% confidence interval [CI], 0.48-0.87). When jointly assessed using the high and low cut-off points, low sodium and corresponding high calcium, magnesium, and potassium intake somewhat reduced the odds of hypertension 0.39 (95% CI, 0.20-0.76). The sodium-to-potassium ratio wium intake. In comparison, men would somewhat be protected from developing hypertension with calcium intake meeting the dietary goals and magnesium exceeding the nutritional goals.
Our results suggest that the studied minerals' association on hypertension is stronger when jointly assessed, mostly after gender stratification. As compared to men, women increased their risk of hypertension even with a low sodium intake. Women would also reasonably reduce their risk of developing hypertension by increasing calcium and magnesium intake. In comparison, men would somewhat be protected from developing hypertension with calcium intake meeting the dietary goals and magnesium exceeding the nutritional goals.
The extract from
exhibited diverse therapeutic potentials. We aimed to evaluate the efficacy and safety of
leaf extract for improving metabolic parameters in human.
A 12-week, double blind, placebo-controlled and randomized trial included a total of 74 adults, and they were assigned to the placebo group (n = 38) or 700 mg/day of
group (n = 36). The efficacy endpoints were changes in glycemic, lipid, obesity, and blood pressure (BP) parameters, in addition to the prevalence of metabolic syndrome (MetS) and the numbers of MetS components. Safety was assessed by monitoring adverse events (AEs).
After 12 weeks of treatment, the hemoglobin A1c (HbA1c) level significantly decreased in the
group compared to that of the placebo group (difference -0.13 ± 0.20% vs. 0.00 ± 0.28%,
= 0.031; % of change -2.27 ± 3.63% vs. 0.10 ± 5.10%,
= 0.025). The homeostatic model assessment for insulin resistance level also decreased significantly from its baseline in the
group. The systolic BP of
group decreased significantly than that of placebo group (difference -3.9 ± 9.8 mmHg vs. 3.3 ± 11.7 mmHg,
= 0.005; % of change -2.8 ± 7.7% vs. 3.3 ± 10.2%,
= 0.005). However, the lipid parameters and body composition including body weight did not differ between the groups. The prevalence of MetS (36.8% vs. 13.9%,
= 0.022) and the incidence of MetS (10.5% vs. 13.9%,
= 0.027) at 12 weeks was significantly lower in the
group than it was in the placebo group. No serious AEs occurred in either group.
Supplementation with
extracts over a 12-week period improved metabolic parameters such as HbA1c and BP and reduced the prevalence of MetS.
Clinical Research Information Service Identifier KCT0004672.
Clinical Research Information Service Identifier KCT0004672.
(Kitam.) Honda (AY) has remarkable bioactivities, such as antioxidant, anti-inflammation, and anti-cancer activities. On the other hand, the effects of AY against obesity-induced insulin resistance have not been reported. Therefore, this study examined the potential of AY against obesity-associated insulin resistance in high-fat diet (HFD)-fed mice.
An obesity model was established by feeding C57BL/6J mice a 60% HFD for 16 weeks. The C57BL6/When ethyl acetate fraction from AY (EFAY) at doses of 100 and 200 mg/kg/day was administered orally to mice fed a HFD for the last 4 weeks. Normal and control groups were administered water orally. The body weight and fasting blood glucose were measured every week. Dietary intake was measured every other day. After dissection, blood and tissues were collected from the mice.
The administration of EFAY reduced body and organ weights significantly compared to HFD-fed control mice. The EFAY-administered groups also improved the serum lipid profile by decreasing the triglyceride, total cholesterol, and low-density lipoprotein compared to the control group. In addition, EFAY ameliorated the insulin resistance-related metabolic dysfunctions, including the fasting blood glucose and serum insulin level, compared to the HFD-fed control mice. The EFAY inhibited lipid synthesis and insulin resistance by down-regulation of hepatic fatty acid synthase and up-regulation of the AMP-activated protein kinase pathway. EFAY also reduced lipid peroxidation in the liver, indicating that EFAY protected hepatic injury induced by obesity.
These results suggest that EFAY improved obesity-associated insulin resistance by regulating the lipid and glucose metabolism, suggesting that AY could be used as a functional food to prevent obesity and insulin resistance.
These results suggest that EFAY improved obesity-associated insulin resistance by regulating the lipid and glucose metabolism, suggesting that AY could be used as a functional food to prevent obesity and insulin resistance.
Ginseng extract (GSE) and taurine (TR) are widely used antifatigue resources in functional foods. However, the mechanism underlying the antifatigue effects of GSE and TR are still unclear. Hence, we investigated whether GSE and TR have synergistic effects against fatigue in mice.
L6 cells were treated with different concentrations of TR and GSE, and cell viability was determined using 2-(4-iodophenyl)-3-(4-nitrophenyl)-5-(2,4-disulfophenyl)-2
-tetrazolium. Oxidative stress was analyzed by immunocytochemistry using MitoTracker™ Red FM and an anti-8-oxoguanine antibody. Respiratory gas analysis was performed to investigate metabolism. Expression of an activated protein kinase was analyzed using immunohistochemistry. Gene expression of cluster of differentiation 36 and pyruvate dehydrogenase lipoamide kinase isozyme 4 was measured using reverse transcription-polymerase chain reaction. Mice were orally administered TR, GSE, or their combination for 30 days, and then fatigue-related parameters, including lactate, blood urea nitrogen, and glycogen, were measured after forced swimming.
TR and GSE reduced oxidative stress levels in hydrogen peroxide-stimulated L6 cells and enhanced the oxygen uptake and lipid metabolism in mice after acute exercise. After oral administration of TR or GSE for 30 days, the fatigue-related parameters did not change in mice. However, the mice administered GSE (400 mg/kg/day) alone for 30 days could swim longer than those from the other groups. Further, no synergistic effect was observed after the swimming exercise in mice treated with the TR and GSE combination for 30 days.
Taken together, our data suggest that TR and GSE may exert antifatigue effects in mice after acute exercise by enhancing oxygen uptake and lipid oxidation.
Taken together, our data suggest that TR and GSE may exert antifatigue effects in mice after acute exercise by enhancing oxygen uptake and lipid oxidation.
Peroxisome proliferator-activated receptor-gamma co-activator-1α (PGC-1α) has a central role in regulating muscle differentiation and mitochondrial metabolism. PGC-1α stimulates muscle growth and muscle fiber remodeling, concomitantly regulating lactate and lipid metabolism and promoting oxidative metabolism.
(Thumb.) has been widely employed as a traditional herbal medicine and possesses antioxidant, anti-obesity, anti-inflammatory, hypolipemic, hypoglycemic, and anticancer properties. We investigated whether
extract (GPE) and its active compound, gypenoside L (GL), affect muscle differentiation and mitochondrial metabolism via activation of the PGC-1α pathway in murine C2C12 myoblast cells.
C2C12 cells were treated with GPE and GL, and quantitative reverse transcription polymerase chain reaction and western blot were used to analyze the mRNA and protein expression levels. Myh1 was determined using immunocytochemistry. Mitochondrial reactive oxygen species generation was measured using the 2'7'-dicexercise performance by promoting myotube differentiation and mitochondrial metabolism through the upregulation of PGC-1α in C2C12 skeletal muscle.
Bitter taste receptors are taste signaling pathway mediators, and are also expressed and function in extra-gustatory organs. Skin aging affects the quality of life and may lead to medical issues. Apoptosis inhibitor The purpose of this study was to better understand the anti-skin aging effects of bitter taste receptors in D-galactose (D-gal)-induced aged human keratinocytes, HaCaT cells.
Expressions of bitter taste receptors in HaCaT cells and mouse skin tissues were examined by polymerase chain reaction assay. Bitter taste receptor was overexpressed in HaCaT cells, and D-gal was treated to induce aging. We examined the effects of bitter taste receptors on aging by using β-galactosidase assay, wound healing assay, and Western blot assay.
TAS2R16 and TAS2R10 were expressed in HaCaT cells and were upregulated by D-gal treatment. TAS2R16 exerted protective effects against skin aging by regulating p53 and p21, antioxidant enzymes, the SIRT1/mechanistic target of rapamycin pathway, cell migration, and epithelial-mesenchymal transition markers. TAS2R10 was further examined to confirm a role of TAS2R16 in cellular senescence and wound healing in D-gal-induced aged HaCaT cells.
Our results suggest a novel potential preventive role of these receptors on skin aging by regulating cellular senescence and wound healing in human keratinocyte, HaCaT.
Our results suggest a novel potential preventive role of these receptors on skin aging by regulating cellular senescence and wound healing in human keratinocyte, HaCaT.The present letter to the editor is in response to the research "Outcomes of curative liver resection for hepatocellular carcinoma in patients with cirrhosis" by Elshaarawy et al in World J Gastroenterol 2021; 13(5) 424-439. The preoperative assessment of the liver reserve function in hepatocellular carcinoma (HCC) patients with cirrhosis is crucial, and there is no universal consensus on how to assess it. Based on a retrospective study, Elshaarawy et al investigated the impact of various classical clinical indicators on liver failure and the prognosis after hepatectomy in HCC patients with cirrhosis. We recommend that we should strive to explore new appraisal indicators, such as the indocyanine green retention rate at 15 min.The following letter to the editor highlights the review titled "Liquid biopsy in cholangiocarcinoma Current status and future perspective" in World J Gastrointest Oncol 2021; 13 332-350. It is necessary to realize individualized therapy to improve the clinical prognosis of patients with cholangiocarcinoma.
Inflammatory bowel disease (IBD) patients with post-inflammatory polyps (PIPs) may carry an increased risk of colorectal neoplasia (CRN) including dysplasia and cancer. Current guidelines recommend active colonoscopy follow-up for these patients. However, the evidence for guidelines is still poor. In addition, some recent high-quality reports present a different view, which challenges the current guidelines. We hypothesize that IBD patients with PIPs are at increased risk of CRN.
To evaluate the risk of CRN in IBD patients with and without PIPs.
A systematic search of PubMed, Embase, Cochrane Library, and Web of Science was performed to identify studies that compared the risk of CRN in IBD patients with and without PIPs. In addition, we screened the reference lists and citation indices of the included studies. Quality assessment was performed using the Newcastle-Ottawa Scale. Pooled odds ratio (OR) was calculated using the random-effects model to explore the final pooled effect size of the included studies and determine whether PIPs increase the risk of CRN.
My Website: https://www.selleckchem.com/products/gossypol.html
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