New horizons for the study of saffron (Crocus sativus L.) and its active ingredients in the management of neurological and psychiatric disorders: A systematic review of clinical evidence and mechanisms.

Saffron (Crocus sativus), as an herbal medicine, has been extensively investigated for treating neurological and psychiatric disorders. This systematic review aimed to assess the overall effects of saffron on cognition, depression, anxiety, sleep disorders, attention-deficit/hyperactivity disorder (ADHD), and obsessive-compulsive disorder (OCD). Relevant randomized controlled trials (RCTs) were identified by searching PubMed/Medline, Web of Science, and Clinical Trials databases up to June 2023 according to search terms and inclusion criteria. The participants were either healthy or suffering from some diseases, including neurological and psychiatric disorders, and consumed saffron or its extracts as an intervention. The risk of bias was assessed according to the Cochrane guidelines, and the PRISMA statement was followed. The meta-analysis was performed using RevMan and STATA software. A random-effects or fixed-effects model was used to calculate the pooled effect sizes. Forty-six RCTs were enrolled, and the duration of these trials ranged from 4 to 48 weeks with saffron or its extracts, both alone or in combination with conventional drugs. Saffron was more effective than placebo in improving cognition, depression with an overall effect size of -4.26 (95% CI: -5.76, -2.77), anxiety of -3.75 (95% CI: -5.83, -1.67), and sleep disorders of -1.91 (95% CI: -2.88, -0.93). Saffron was non-inferior to conventional drugs for treating cognitive disorders, depression, anxiety, ADHD, and OCD, and it exhibited good tolerance with few side effects. Saffron may exert protective roles for neurological and psychiatric disorders and represents a relatively favorable and safe treatment.

Apple Polyphenol Extract Ameliorates Atherosclerosis and Associated Cognitive Impairment through Alleviating Neuroinflammation by Weakening TLR4 Signaling and NLRP3 Inflammasome in High-Fat/Cholesterol Diet-Fed LDLR-/- Male Mice.

Although studies have supported the beneficial effects of the ingredients of apple polyphenol extract (APE), a polyphenol mixture being extracted from whole fresh apples, on neurodegenerative diseases, the role of APE in atherosclerosis-related cognitive impairment remains unclear. To clarify the role of APE in regulating cognitive dysfunction in mice with atherosclerosis and the underlying mechanisms, high-fat/cholesterol diet-fed male LDLR-/- mice were gavaged with 125 or 500 mg/(kg·bw·d) APE solution or sterile double-distilled water for consecutive 8 weeks, and age-matched C57BL/6 male mice were employed as normal control. APE intervention increased the serum concentration of high-density apolipoprotein cholesterol, improved atherosclerosis, and ameliorated cognitive function of mice by inhibiting the phosphorylation of tau protein, supporting with significantly reduced platform latency and obviously increased swimming distance in the target quadrant according to the Morris water maze test. APE intervention alleviated neuroinflammation by attenuating the activation of microglia and astrocytes and inhibiting TLR4 signaling with reduced protein expression of NF-κB, MyD88, TRIF, and IKKß. Meanwhile, APE intervention inactivated NLRP3 inflammasome with downregulated protein expression of caspase-1, IL-18, and IL-1ß. Additionally, APE intervention improved the damaged brain barrier structure by upregulating the protein expression of ZO-1 and occludin. Therefore, our research supplemented new data, supporting the potential of APE as an effective dietary bioactive ingredient to improve atherosclerosis and associated cognitive impairment.

Effect of low-glycemic index diet advice on pregnant outcomes in women with elevated risk of gestational diabetes mellitus: A meta-analysis of randomized controlled trails.

BACKGROUND AND AIMS: The beneficial effect of low-glycemic index (GI) diet on gestational diabetes mellitus (GDM) has been suggested in many observational studies; however, results from intervention trials remain inconsistent. This study aims to estimate the effect of interventions with low-GI dietary advice on pregnant outcomes in women with elevated risk of GDM. DESIGN: PubMed, Web of Science, Embase, and Cochrane Library databases were searched for randomized clinical trials (RCTs) through March 2022. Studies reporting the effect of low-GI diet advice intervention on maternal and fetal outcomes in pregnant women with increased risks of GDM were included. Random or fixed effects model was used to calculate combined treatment effects. Publication bias was assessed via Begg's and Egger's tests and funnel plot inspection. RESULTS: Nine RCTs recruiting 3416 participants were included. Low-GI diet advice did not modulate the risk of GDM. Compared with control diets, low-GI diet advice significantly reduced gestational weight gain (GWG) (weighted mean differences, WMD = -0.93 kg, 95% CI: -1.31, -0.55; p < 0.001; n = 7) and the risk of premature birth (RR = 0.55, 95% CI: 0.35, 0.88; p = 0.012; n = 5). In subgroup analyses, the effect of low-GI diet interventions on premature birth was significant only in women with BMI higher than 30 kg/m2 (RR = 0.28, 95% CI: 0.10, 0.77, p = 0.014; n = 3); the significant effect on GWG was not altered by stratification of BMI and the type of GDM risk factors. No significant changes in other maternal and newborn outcomes were found. CONCLUSIONS: Low-GI diet advice interventions during pregnancy decreased GWG and the risk of premature birth in women with elevated GDM risk; however, the interventions did not significantly prevent GDM development in these women.

Effects of betaine supplementation on inflammatory markers: a systematic review and meta-analysis of randomised controlled trials.

Several studies have suggested that betaine is closely related to inflammatory biomarkers that contribute to the development of metabolic diseases, but the effect remains controversial. This meta-analysis aimed to assess the effects of betaine supplementation on inflammatory markers based on randomised controlled trials (RCTs). PubMed, Web of Science and ResearchGate databases were searched up to March 2023. A total of 6 RCTs with 7 intervention trials involving 277 participants were included. Betaine supplementation led to a slight reduction in levels of circulating IL-1ß of 0.65 pg/mL (95% CI, -1.23 to -0.06) with high heterogeneity (I2 = 95%). Betaine produced a small but nonsignificant reduction in levels of circulating CRP (0.33 mg/L; 95% CI, -1.79 to 1.14), IL-6 (0.47 pg/mL; 95% CI, -1.13 to 0.18) and TNF-α (0.25 pg/mL; 95% CI, -0.98 to 0.48). The present meta-analysis does not provide sufficient evidence to conclude that betaine supplementation improved the inflammation state.

A meta-analysis and systematic review of randomized clinical trials on the effect of coffee consumption on heart rate.

CONTEXT: Resting heart rate (HR) is increasingly recognized as an indicator of disease and overall morbidity and mortality. Whether chronic coffee consumption affects resting HR is an important consideration for individual consumers as well as from a public health perspective. OBJECTIVE: A meta-analysis of randomized controlled trials (RCTs) was conducted to examine the effectiveness of coffee consumption on resting HR. DATA SOURCES: Original RCTs assessing the effect of coffee consumption on resting HR and published prior to March 2023 were identified by searching online databases, including PubMed, Web of Science, and Cochrane Library databases. DATA EXTRACTION AND ANALYSIS: Data searches and extraction and risk-of-bias assessments were performed according to the Cochrane guidelines, and the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines for systematic reviews were followed. Data on study characteristics, type, and amount of coffee and net change and measurement resting HR were extracted. A random-effects or a fixed-effects model was used to estimate the pooled effect sizes. Homogeneity was determined with the Cochran Q test, and publication bias was assessed through Begg's test, Egger's test, and funnel plots. RESULTS: A total of 6 RCTs with 11 intervention trials or arms involving 485 individuals were included. The participants were generally healthy, although some had hypertension, hypercholesterolemia, or were overweight. The trial duration ranged from 2 weeks to 24 weeks. The overall pooled analysis showed that coffee consumption resulted in a negligible increase in resting HR of 0.40 beats per minute (95% CI: -0.78 to 1.57; P = 0.506), which was statistically insignificant. Subgroup analysis of all specified categories was consistent with the overall analysis. No heterogeneity was observed among included trials (I2 = 0.0%, P = 0.756). CONCLUSION: The results of the present meta-analysis study demonstrate that daily coffee consumption of 3 to 6 cups for a period of 2 to 24 weeks has no statistically significant effect on resting HR.

Concentrations and homologue patterns of SCCPs and MCCPs in the serum of the general population of adults in Hangzhou, China.

Due to their ubiquitous presence in the environment and humans, chlorinated paraffins (CPs) are a major environmental and public health concern. CPs are known to persist, bioaccumulate and potentially threaten human health, but reports on their internal exposure in the adult general population are still scarce. In this study, serum samples collected from adults living in Hangzhou, China, were quantified for SCCPs and MCCPs using GC-NCI-MS methods. A total of 150 samples were collected and subjected to analysis. ∑SCCPs were detected in 98% of the samples with a median concentration of 721 ng/g lw. MCCPs were found in all serum samples with a median concentration of 2210 ng/g lw, indicating that MCCPs were the dominant homologous group. For SCCPs and MCCPs, ∑C10 and ∑C14 were found to be the dominant carbon chain length homologues. Our results showed that age, BMI and lifestyle were not found to be significantly associated with internal exposure to CPs for the samples in this study. Based on PCA analysis, an age-specific distribution of CP homologues was observed. This suggests that internal exposure to CPs in the general population is related to exposure scenarios and history. The results of this study may contribute to a better understanding of the internal exposure to CPs in the general population and may provide a direction for the investigation of the source of exposure to CPs in the environment and daily life.

Effect of Probiotics Supplementation on Heart Rate: A Systematic Review and Meta-Analysis of Randomized Clinical Trials.

Background and Aims: Probiotics consumption lowers the risk of cardiovascular disease, but whether it affects heart rate (HR) remains controversial. Therefore, our study aimed to assess the chronotropic effects of probiotics on heartbeat via a meta-analysis of randomized clinical trials. Methods: Relevant studies were identified by searching PubMed, Cochrane library, and Clinical Trials databases up to October 2021. Either a fixed-effects or a random-effects model was used to calculate the pooled effect sizes and 95% confidence intervals (CIs). Results: This meta-analysis included 13 studies involving 16 interventional trial arms and 931 participants according to inclusion criteria. The overall pooled estimate showed that probiotics supplementation had a slight, but no significant reduction of 0.28 bpm (95% CI: -1.17, 0.60) on HR. Relatively high heterogeneity was observed among included trials (I 2 = 80.8%, P heterogeneity < 0.001). Subgroup analysis displayed that probiotics supplementation significantly reduced HR by 2.94 bpm (95% CI: -5.06, -0.82) among participants with baseline HR ≥ 75 bpm, by 1.17 bpm (95% CI: -2.34, -0.00) with probiotics dose ≥1 × 1010 CFU/day, and by 1.43 bpm (95% CI: -2.69, -0.17) with multiple-strain intervention. Meta-regression analysis showed that baseline HR was a major potential effect modifier of probiotics supplementation on lowering HR. Conclusion: Hitherto, the overall evidence in the literature was insufficient to support the notion that probiotics supplementation has a class effect on HR reduction. However, in subgroup analysis, probiotics reduced HR significantly in those who had higher baseline HR, received a higher dose or multiple strains of probiotics.

Oat fiber supplementation alleviates intestinal inflammation and ameliorates intestinal mucosal barrier via acting on gut microbiota-derived metabolites in LDLR-/- mice.

OBJECTIVE: Gut microbiota-derived metabolites are involved in intestinal inflammation, which can affect the development of atherosclerotic plaques. Previous studies have shown that oat fiber can delay the progression of atherosclerosis via improving lipid metabolism. The aim of this study was to evaluate how oat fiber acted on gut microbiota-derived metabolites, inhibited intestinal inflammation, and protected the intestinal mucosal barrier. METHODS: Male low-density lipoprotein receptor knock-out (LDLR-/-) mice were fed a high-fat/cholesterol diet with or without oat fiber for 14 wk. Histopathology of the aorta was detected by Oil Red O staining, and the small intestine mucosal pathology was measured through hematoxylin and eosin staining. Non-targeted metabolomics of feces was performed using liquid chromatography-mass spectrometry. Western blot method was used to assess the relative levels of the proteins involved in the toll-like receptor (TLR)4 signal pathway and intestinal mucosal barrier in interest tissues. RESULTS: Pathologically, oat fiber reversed the increment of the atherosclerotic lesion and ameliorated intestinal mucosal barrier in LDLR-/- mice. Oat fiber regulated the levels of gut microbiota-derived metabolites along with a decrease in isobutyrylcarnitine, valerylcarnitine, 1-methylguanosine, and 2-methylguanosine, and an increase in l-tyrosine and niacinamide. Notably, oat fiber blocked the TLR4 signal pathway and decreased the expression of nuclear factor-κB p65 in both the aorta and gut tissues. Also, oat fiber raised the expression of tight junction proteins including ZO-1 and occludin. CONCLUSION: Taken together, the present study revealed that oat fiber feeding effectively attenuated the development of atherosclerosis, at least partly via affecting gut microbiota-derived metabolites, inhibiting the intestinal inflammatory response, and maintaining the integrity of the intestinal mucosal barrier.

Crocin alleviates cognitive impairment associated with atherosclerosis via improving neuroinflammation in LDLR-/- mice fed a high-fat/cholesterol diet.

Crocin has been extensively investigated in treating neurodegenerative diseases. However, its effect on cognitive impairment associated with atherosclerosis remains unknown. The present study aimed to explore the potential mechanism of crocin on cognitive impairment in a mouse model of atherosclerosis. LDLR-/- mice fed a high-fat/cholesterol diet were administered variable-dose crocin for 56 days through gavage. Biochemical tests showed that serum triglycerides and circulating lipopolysaccharide decreased in mice treated with crocin. Behavioral tests indicated that crocin alleviated cognitive impairment by reducing latency to the platform and increasing the swimming distance in the target quadrant. This mechanism might be associated with crocin inhibiting Aß deposition by decreasing Aß1-42 and tau phosphorylation. Crocin improved neuroinflammation by inhibiting the increase in reactive microglia and astrocytes, weakening NLRP3 inflammasome activation accompanied by a reduction in Caspase-1 and IL-1ß, and blocking TLR4 signaling accompanied by a decrease in NF-kB p65 and MyD88. In addition, crocin raised the protein expression of ZO-1 and occludin. These findings provide experimental support that crocin attenuates cognitive impairment associated with atherosclerosis by repressing neuroinflammation, which is attributed to its suppression on the activation of microglia and astrocytes, and the production of inflammatory cytokines via targeting the NLRP3 inflammasome and TLR4 signaling.

Oat Fiber Modulates Hepatic Circadian Clock via Promoting Gut Microbiota-Derived Short Chain Fatty Acids.

The biological alteration of circadian rhythm was found to be related to the development of metabolic disorders. Our previous studies reported that impaired lipid metabolism caused by a high-fat diet was improved by oat fiber, but did not attempt to answer whether the improvement is mechanistically linked to circadian rhythm. By focusing on circadian alteration, the present study aimed to elucidate the effect of gut microbiota-derived short chain fatty acids (SCFAs) on circadian rhythm in a high-fat diet experimental paradigm with and without dietary oat fiber feeding. The results showed that oat fiber prevented the production of obesity and dyslipidemia caused by a high-fat diet in C57BL/6 mice. From a circadian perspective specifically, a high-fat diet disrupted the hepatic circadian protein expressions of the liver clock genes, which were in parallel with the altered oscillation of serum triglycerides, low-density lipoprotein cholesterol, fasting insulin, and the homeostasis model assessment-insulin resistance index. Oat fiber, by contrast, reversed these disrupted diurnal oscillations. Most interestingly, what a high-fat diet induced and what oat fiber prevented were dictated in a close oscillation pattern resembling that of SCFA production facilitated by the intestinal microbiome. Given the results from the present study and from others that demonstrated the role played by SCFAs in regulating circadian rhythm, we conclude that the beneficial effects of oat fiber are likely mediated by complex processes involving multiple mechanisms including a signal transduction pathway of gut microbiota-derived SCFAs to hepatic circadian protein expression to lipid and other metabolic oscillations. The latter warrants more investigation to further determine whether the circadian rhythm pathway has any major and causal significance for the outcome measures in the prevention and treatment of metabolic disorders in humans.

Effects of Oat Fiber Intervention on Cognitive Behavior in LDLR-/- Mice Modeling Atherosclerosis by Targeting the Microbiome-Gut-Brain Axis.

It is known that cardiovascular disease can result in cognitive impairment. However, whether oat fiber improves cognitive behavior through a cardiovascular-related mechanism remains unclear. The present work was aimed to elucidate the potential of oat fiber on cognitive behavior by targeting the neuroinflammation signal and microbiome-gut-brain axis in a mouse model of atherosclerosis. Male low-density lipoprotein receptor knock-out (LDLR-/-) mice were treated with a high fat/cholesterol diet without or with 0.8% oat fiber for 14 weeks. Behavioral tests indicated that LDLR-/- mice exhibited a significant cognitive impairment; however, oat fiber can improve cognitive behavior by reducing latency to the platform and increasing the number of crossing and swimming distance in the target quadrant. Oat fiber can inhibit Aß plaque processing in both the cortex and hippocampus via decreasing the relative protein expression of GFAP and IBα1. Notably, oat fiber inhibited the nod-like receptor family pyrin domain-containing 3 inflammasome activation and blocked the toll-like receptor 4 signal pathway in both the cortex and hippocampus, accompanied by a reduction of circulating serum lipopolysaccharide. In addition, oat fiber raised the expressions of short-chain fatty acid (SCFA) receptors and tight junction proteins (zonula occludens-1 and occludin) and improved intestinal microbiota diversity via increasing the contents of gut metabolites SCFAs. In summary, the present study provided experimental evidence that dietary oat fiber retarded the progression of cognitive impairment in a mouse model of atherosclerosis. Mechanistically, the neuroprotective potential was related to oat fiber and its metabolites SCFAs on the diversity and abundance of gut microbiota that produced anti-inflammatory metabolites, leading to repressed neuroinflammation and reduced gut permeability through the microbiome-gut-brain axis.

[Effects of wheat bran fiber on lipid metabolism in ApoE~(-/-) mice].

OBJECTIVE: To explore the effect and mechanism of wheat bran fiber on lipid metabolism in ApoE~(-/-)mice fed a high fat diet. METHODS: Twenty 7-week-old male ApoE~(-/-)mice were randomly divided into two groups and fed either a high fat diet as AS model group or a high fat diet adding 0. 8% wheat bran fiber as W-fiber group. And five C57 BL/6 mice with the same genetic background were used as control group. After 18 weeks feeding, HE staining were performed for atherosclerotic lesions from transverse section of the aorta and hepatic histological examination. Liver homogenate total cholesterol(TC), triglyceride(TG)and free fatty acids(FFAs)were analyzed. Western blot was used to determine the protein expressions involved in hepatic lipid metabolism, including sterol regulatory element binding protein 1(SREBP-1), fatty acid synthase(FAS), acetyl-coA carboxylase(ACC), sterol regulatory element binding protein 2(SREBP-2), low-density lipoproteins receptor(LDLR) and scavenger receptor B1(SR-B1). RESULTS: At the end of the experiment, compared with control group, atherosclerotic plaque of the aorta and hepatic steatosis was obvious in the mice of AS model group, and wheat bran fiber alleviated the area of atheromatous plaque and hepatic lipid accumulation. Compared with AS model group, wheat bran fiber decreased liver homogenate TC level((60. 56±13. 49) µmol/g vs. (51. 10±5. 94) µmol/g)(P<0. 05), reduced protein expression of SREBP-1, FAS and ACC(P<0. 05), increased protein expression of SREBP-2SR-B1(P<0. 05). CONCLUSION: Taken together, wheat bran fiber can delay the occurance of AS by regulating the related protein expressions involved in lipid metabolism and improving hepatic lipid metabolism.

Cereal fiber improves blood cholesterol profiles and modulates intestinal cholesterol metabolism in C57BL/6 mice fed a high-fat, high-cholesterol diet.

BACKGROUND: Dietary intake of cereal fiber has been reported to benefit lipid metabolism through multiple mechanisms. The present study aimed to discover the potential mechanisms by which cereal fiber could modify the intestinal cholesterol metabolism. DESIGN: Male C57BL/6 mice were fed a reference chow (RC) diet; high-fat, high-cholesterol (HFC) diet; HFC plus oat fiber diet; or HFC plus wheat bran fiber diet for 24 weeks. Serum lipids were measured by enzymatic methods. Western blot was used to determine the protein expressions involved in intestinal cholesterol metabolism. RESULTS: Our results showed that HFC-induced elevations of serum triglycerides, total cholesterol, and low-density lipoprotein cholesterol were normalized in both groups that received cereal fiber. At the protein level, compared with the HFC diet group, the two cereal fibers, especially the oat fiber, significantly increased the protein expression of peroxisome proliferator-activated receptor alpha, liver X receptor alpha, sterol regulatory element-binding protein (SREBP) 2, low-density lipoprotein receptor, adenosine triphosphate (ATP)-binding cassette A1, and ATP-binding cassette G1, while decreasing the protein expression of Niemann-Pick C1-like protein 1, SREBP-1, fatty acid synthase, and acetyl-coenzyme A carboxylase, which were involved in intestinal cholesterol metabolism. CONCLUSION: Taken together, increased intake of cereal fiber improved blood cholesterol profiles and increased the intestinal cholesterol efflux and cholesterol clearance in C57BL/6 mice fed a HFC diet. Oat fiber had a stronger effect than wheat bran fiber on cholesterol metabolism by modulating the PPARα, LXRα, and SREBP signaling pathways.

Cereal Fiber Ameliorates High-Fat/Cholesterol-Diet-Induced Atherosclerosis by Modulating the NLRP3 Inflammasome Pathway in ApoE-/- Mice.

Cereal fiber is associated with decreasing the risk of cardiovascular diseases. However, whether cereal fiber modulates inflammatory response and improves atherosclerosis remains unclear. This study evaluated the anti-atherosclerotic effect of cereal fibers from oat or wheat bran and explored the potential anti-inflammatory mechanisms. Male ApoE-/- mice were given a high-fat/cholesterol (HFC) diet or a HFC diet supplemented with 0.8% oat fiber or wheat bran fiber. After 18 weeks of the feeding period, serum lipids and inflammatory cytokines were measured. The relative protein levels of the nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome pathway and nuclear factor κB (NF-κB) were determined by the western blot method in aorta tissues. Pathologically, oat fiber and wheat fiber significantly reduced atherosclerotic plaques by 43.3 and 27.1%, respectively. Biochemically, cereal fiber markedly decreased the protein levels of myeloid differentiation factor 88 (MyD88) and toll-like receptor 4 (TLR4) in aortic tissues. The expression of NF-κB was similarly inhibited by both cereal fibers. In comparison to wheat bran fiber, oat fiber had greater effects in reducing the plague size and inhibiting TLR4/MyD88/NF-κB pathways. Such differences might come from modulation of the NLRP3 inflammasome pathway because the expressions of the cleavage of caspase-1 and interleukin (IL)-1ß were inhibited only by oat fiber. The present study demonstrates that cereal fibers can attenuate inflammatory response and atherosclerosis in ApoE-/- mice. Such effects are pronounced with oat fiber and likely mediated by specific inhibition of oat fiber on the NLRP3 inflammasome pathway.

Effects of low-glycemic-index diets in pregnancy on maternal and newborn outcomes in pregnant women: a meta-analysis of randomized controlled trials.

PURPOSE: Maternal diet with a high glycemic index (GI) is associated with fetal overgrowth and higher infant body adiposity. Effects of low-GI diet on maternal and newborn outcomes have been assessed in both healthy pregnancy and gestational diabetes mellitus, but the results remain inconclusive. This meta-analysis aimed to examine the effects of low-GI diets on maternal and newborn outcomes. METHODS: PubMed, Clinical Trials, and Cochrane Library databases were searched for relevant randomized trials up to January 2016. Random- or fixed-effects models were used to calculate combined treatment effects. RESULTS: A total of 11 trials involving 1985 women were eligible for analysis. This meta-analysis assessed 7 maternal and 11 newborn outcomes. Of these, gestational weight gain (GWG), fasting blood glucose (FBG), newborn birth weight, ponderal index (PI), proportion of macrosomia, and large for gestational age (LGA) were investigated in more than 8 trials. Compared with control diets, low-GI diets significantly reduced FBG (weight mean differences (WMD) = -0.18 mmol/L, 95 % CI: -0.33, -0.02), 2-h postprandial glucose level (WMD = -0.33 mmol/L, 95 % CI: -0.54, -0.12), and the proportion of LGA (RR = 0.52, 95 % CI: 0.31, 0.89). A lower GWG (WMD = -0.69 kg, 95 % CI: -1.74, 0.36) and birth weight (WMD = -0.10 kg, 95 % CI: -0.23, 0.03) were also observed without significant differences. Heterogeneity was observed in the GWG, FBG, and birth weight analyses. Low-GI diets did not affect other maternal and newborn outcomes. In subgroup and sensitivity analyses, the intervention effects of low GI on GWG and FBG varied. CONCLUSIONS: Low-GI diets may have beneficial effects on maternal outcomes for those at risk of developing high glucose levels, without causing adverse effects on newborn outcomes. However, results should be interpreted with caution because of the evidence of heterogeneity and limited number of studies.

Vitamin D Combined with Resveratrol Prevents Cognitive Decline in SAMP8 Mice.

BACKGROUND: Vitamin D (VD) and resveratrol (RSV) are two nutritional molecules that have reported neuroprotective effects, and findings from cellular models suggest that resveratrol could potentiate vitamin D's effects. The senescence-accelerated mouse-prone 8 (SAMP8) is a useful model of Alzheimer's disease (AD)-related memory impairment. OBJECTIVE: We aimed to explore how the combination of vitamin D with resveratrol would affect memory impairments shown by SAMP8 mice, as well as the potential mechanisms. METHOD: SAMP8 mice and their control senescence-accelerated mouse resistant 1 (SAMR1) mice (10 weeks old) were divided into 5 groups, i.e. SAMR1 group, SAMP8 group, SAMP8 mice supplemented with VD group, SAMP8 mice supplemented with RSV group and SAMP8 mice supplemented with both VD and RSV group. At the end of the intervention, Morris water maze (MWM) test was used to assess cognitive function. Hippocampus and parietal cortex were dissected for further analysis. RESULTS: The combination of VD and RSV significantly increased time spent in target quadrant and the number of crossing via MWM test. In hippocampus, the combined intervention significantly reduced soluble Aß42 level and BACE1 protein expression. In cortex, the combined treatment significantly reduced phosphorylation of tau at serine404 and p-p53, as well as enhanced p-CREB protein expression. The combination also significantly reduced GFAP and p-NFκB p65 in both hippocampus and cortex. CONCLUSION: The combined intervention might exert greater neuroprotective effects in SAMP8 mice, this might be associated with the fact that the combined intervention could positively affect amyloidogenic pathways, neuroinflammation, tau phosphorylation and probably apoptosis markers.

Lipolysis and thermogenesis in adipose tissues as new potential mechanisms for metabolic benefits of dietary fiber.

OBJECTIVE: Dietary fiber consumption is associated with reduced risk for the development of noncommunicable diseases. The aim of the present study was to evaluate the effects of cereal dietary fiber on the levels of proteins involved in lipolysis and thermogenesis in white adipose tissue (WAT) and brown adipose tissue (BAT) of C57 BL/6 J mice fed a high-fat diet (HFD). METHODS: Male C57BL/6 J mice were fed normal chow diet (Chow), HFD, HFD plus oat fiber (H-oat), or HFD plus wheat bran fiber (H-wheat) for 24 wk. Body weight and food intake were recorded weekly. Serum adiponectin was assayed by an enzyme-linked immunosorbent assay kit. Western blotting was used to assess the protein expressions of adipose triacylglycerol lipase (ATGL), cAMP protein kinase catalytic subunit (cAMP), protein kinase A (PKA), perilipin A, hormone-sensitive lipase (HSL), uncoupling protein 1 (UCP1), fibroblast growth factor 21 (FGF-21), ß3-adrenergic receptor (ß3AR), and proliferator-activated receptor gamma coactivator-1 α (PGC-1 α) in the WAT and BAT. RESULTS: At the end of the feeding period, body and adipose tissues weight in both H-oat and H-wheat groups were lower than in the HFD group. Mice in the H-oat and H-wheat groups showed an increasing trend in serum adiponectin level. Compared with the HFD group, cereal dietary fiber increased protein expressions involved in the lipolysis and browning process. Compared with the H-wheat group, H-oat was more effective in protein expressions of PKA, PGC-1 α, and UCP1 of the WAT samples. Compared with the H-oat group, H-wheat was more effective in protein expressions of PKA, ATGL, UCP1, ß3AR, and FGF-21 of the BAT samples. CONCLUSIONS: Taken together, our results suggested that cereal dietary fiber enhanced adipocyte lipolysis by the cAMP-PKA-HSL pathway and promoted WAT browning by activation of UCP1, and consequently reduced visceral fat mass in response to HFD feeding.

Chronic leucine supplementation improves lipid metabolism in C57BL/6J mice fed with a high-fat/cholesterol diet.

BACKGROUND: Leucine supplementation has been reported to improve lipid metabolism. However, lipid metabolism in adipose tissues and liver has not been extensively studied for leucine supplementation in mice fed with a high-fat/cholesterol diet (HFCD). DESIGN: C57BL/6J mice were fed a chow diet, HFCD, HFCD supplemented with 1.5% leucine (HFCD+1.5% Leu group) or 3% leucine (HFCD+3% Leu group) for 24 weeks. The body weight, peritoneal adipose weight, total cholesterol (TC), triglyceride in serum and liver, and serum adipokines were analyzed. In addition, expression levels of proteins associated with hepatic lipogenesis, adipocyte lipolysis, and white adipose tissue (WAT) browning were determined. RESULTS: Mice in the HFCD group developed obesity and deteriorated lipid metabolism. Compared with HFCD, leucine supplementation lowered weight gain and TC levels in circulation and the liver without changing energy intake. The decrease in body fat was supported by histological examination in the WAT and liver. Furthermore, serum levels of proinflammatory adipokines, such as leptin, IL-6, and tumor necrosis factor-alpha, were significantly decreased by supplemented leucine. At the protein level, leucine potently decreased the hepatic lipogenic enzymes (fatty acid synthase and acetyl-coenzyme A carboxylase) and corresponding upstream proteins. In epididymal WAT, the reduced expression levels of two major lipases by HFCD, namely phosphorylated hormone-sensitive lipase and adipose triglyceride lipase, were reversed when leucine was supplemented. Uncoupling protein 1, ß3 adrenergic receptors, peroxisome proliferator-activated receptor g coactivator-1α, and fibroblast growth factor 21 were involved in the thermogenic program and WAT browning. Leucine additionally upregulated their protein expression in both WAT and interscapular brown adipose tissue. CONCLUSION: This study demonstrated that chronic leucine supplementation reduced the body weight and improved the lipid profile of mice fed with a HFCD. This beneficial effect was ascribed to hepatic lipogenesis, adipocyte lipolysis, and WAT browning.

Depot-specific effects of treadmill running and rutin on white adipose tissue function in diet-induced obese mice

White adipose tissue (WAT) is a critical organ involved in regulating metabolic homeostasis under obese condition. Strategies that could positively affect WAT function would hold promise for fighting against obesity and its complications. The aim of the present study is to explore the effects of treadmill exercise training and rutin intervention on adipose tissue function from diet-induced obese (DIO) mice and whether fat depot-specific effects existed. In epididymal adipose tissue, high-fat diet (HFD) resulted in reduction in adiponectin mRNA expression, peroxisome proliferator-activated receptors (PPAR)-γ and DsbA-L protein expression, elevation in endoplasmic reticulum (ER) stress markers including 78 kDa glucose-regulated protein (GRP-78), C/EBP homologous protein (CHOP) and p-c-Jun N-terminal kinase (JNK). Isoproterenol-stimulated lipolysis and insulin stimulated Akt phosphorylation ex vivo were blunted from HFD group. The combination of rutin with exercise (HRE) completely restored GRP78 and p-JNK protein expression to normal levels, as well as blunted signaling ex vivo. In inguinal adipose tissue, HFD led to increased adiponectin mRNA expression, PPAR-γ, GRP78, and p-JNK protein expression, and reduction in DsbA-L. HRE is effective for restoring p-JNK, PPAR-γ, and DsbA-L. In conclusion, depot-specific effects may exist in regard to the effects of rutin and exercise on key molecules involved in regulating adipose tissue function (i.e., ER stress markers, PPAR-γ and DsbA-L, adiponectin expression, and secretion, ex vivo catecholamine stimulated lipolysis and insulin stimulated Akt phosphorylation) from DIO mice (AU)

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Effects of 8-Week Hatha Yoga Training on Metabolic and Inflammatory Markers in Healthy, Female Chinese Subjects: A Randomized Clinical Trial.

We aimed to determine the effects of an 8 wk Hatha yoga training on blood glucose, insulin, lipid profiles, endothelial microparticles (EMPs), and inflammatory status in healthy, lean, and female Chinese subjects. A total of 30 healthy, female Chinese subjects were recruited and randomized into control or yoga practice group. The yoga practice included 8 wks of yoga practice (2 times/wk) for a total of 16 times. Fasting blood samples were collected before and after yoga training. Plasma was isolated for the measurement of lipid profiles, glucose, insulin, EMPs, and inflammatory cytokines. Whole blood was cultured ex vivo and stimulated with lipopolysaccharide (LPS) and Pam3Cys-SK4. Peripheral blood mononuclear cells (PBMCs) were isolated for the measurement of TLR2 and TLR4 protein expression. Yoga practice significantly reduced plasma cholesterol, LDL-cholesterol, insulin levels, and CD31+/CD42b- EMPs. Cultured whole blood from the yoga group has reduced proinflammatory cytokines secretion both at unstimulated condition and when stimulated with Pam3Cys-SK4; this might be associated with reduced TLR2 protein expression in PBMCs after yoga training. Hatha yoga practice in healthy Chinese female subjects could improve hallmarks related to MetS; thus it can be considered as an ancillary intervention in the primary MetS prevention for the healthy population. This trial is registered with ChiCTR-IOR-14005747.