scholarly journals Dose-Responses Relationship in Glucose Lowering and Gut Dysbiosis to Saskatoon Berry Powder Supplementation in High Fat-High Sucrose Diet-Induced Insulin Resistant Mice

2021 ◽  
Vol 9 (8) ◽  
pp. 1553
Author(s):  
Ruozhi Zhao ◽  
Fei Huang ◽  
Garry X. Shen
Keyword(s):  
Inflammatory Markers ◽  
Plasminogen Activator Inhibitor ◽  
Model Assessment ◽  
High Fat ◽  
Plasminogen Activator Inhibitor 1 ◽  
Insulin Resistant ◽  
Gut Dysbiosis ◽  
Freeze Dried ◽  
Factor Α ◽  
High Sucrose

Administration of freeze-dried powder of Saskatoon berry (SB), a popular fruit enriched with antioxidants, reduced glucose level, inflammatory markers and gut microbiota disorder in high fat-high sucrose (HFHS) diet-induced insulin resistant mice. The present study examined the dose-response relationship in metabolic, inflammatory and gut microbiotic variables to SB power (SBp) supplementation in HFHS diet-fed mice. Male C57 BL/6J mice were fed with HFHS diet supplemented with 0, 1%, 2.5% or 5% SBp for 11 weeks. HFHS diet significantly increased the levels of fast plasma glucose (FPG), cholesterol, triglycerides, insulin, homeostatic model assessment of insulin resistance (HOMA-IR), tumor necrosis factor-α, monocyte chemotactic protein-1 and plasminogen activator inhibitor-1, but decreased fecal Bacteroidetes phylum bacteria and Muribaculaceae family bacteria compared to low fat diet. SBp dose-dependently reduced metabolic and inflammatory variables and gut dysbiosis in mice compared with mice receiving HFHS diet alone. Significant attenuation of HFHS diet-induced biochemical disorders were detected in mice receiving ≥1% SBp. The abundances of Muribaculaceae family bacteria negatively correlated with body weights, FPG, lipids, insulin, HOMA-IR and inflammatory markers in the mice. The results suggest that SBp supplementation dose-dependently attenuated HFHS diet-induced metabolic and inflammatory disorders, which was associated with the amelioration of gut dysbiosis in the mice.

scholarly journals Impact of Cyanidin-3-Glucoside on Gut Microbiota and Relationship with Metabolism and Inflammation in High Fat-High Sucrose Diet-Induced Insulin Resistant Mice

2020 ◽  
Vol 8 (8) ◽  
pp. 1238
Author(s):  
Fei Huang ◽  
Ruozhi Zhao ◽  
Min Xia ◽  
Garry X. Shen
Keyword(s):  
Insulin Resistance ◽  
Gut Microbiota ◽  
Relative Abundance ◽  
Inflammatory Markers ◽  
Gut Bacteria ◽  
Rrna Gene ◽  
High Fat ◽  
Insulin Resistant ◽  
Freeze Dried ◽  
High Sucrose

The present study assessed the effects of freeze-dried cyanidin-3-glucoside (C3G), an anthocyanin enriched in dark-red berries, compared to Saskatoon berry powder (SBp) on metabolism, inflammatory markers and gut microbiota in high fat-high sucrose (HFHS) diet-induced insulin-resistant mice. Male C57 BL/6J mice received control, HFHS, HFHS + SBp (8.0 g/kg/day) or HFHS + C3G (7.2 mg/kg/day, equivalent C3G in SBp) diet for 11 weeks. The HFHS diet significantly increased plasma levels of glucose, cholesterol, triglycerides, insulin resistance and inflammatory markers. The HFHS + SBp diet increased the Bacteroidetes/Firmicutes (B/F) ratio and relative abundance of Muriculaceae family bacteria in mouse feces detected using 16S rRNA gene sequencing. The HFHS + SBp or HFHS + C3G diet attenuated glucose, lipids, insulin resistance and inflammatory markers, and increased the B/F ratio and Muriculaceae relative abundance compared to the HFHS diet alone. The relative abundances of Muriculaceae negatively correlated with body weight, glucose, lipids, insulin resistance and inflammatory mediators. Functional predication analysis suggested that the HFHS diet upregulated gut bacteria genes involved in inflammation, and downregulated bacteria involved in metabolism. C3G and SBp partially neutralized HFHS diet-induced alterations of gut bacteria. The results suggest that C3G is a potential prebiotic, mitigating HFHS diet-induced disorders in metabolism, inflammation and gut dysbiosis, and that C3G contributes to the metabolic beneficial effects of SBp.

scholarly journals Influence of Saskatoon Berry and Cyanidin-3-Glucoside on Gut Microbiota and Relationship with Metabolism and Inflammation in High Fat-High Sucrose Diet-Induced Insulin Resistant Mice

2020 ◽  
Author(s):  
Fei Huang ◽  
Ruozhi Zhao ◽  
Mi Xia ◽  
Garry Shen
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Gut Microbiota ◽  
Inflammatory Mediators ◽  
Inflammatory Markers ◽  
High Fat ◽  
Insulin Resistant ◽  
Sucrose Diet ◽  
High Sucrose Diet ◽  
High Sucrose

Abstract Background Type 2 Diabetes (T2D) has become one of most common and harmful chronic diseases worldwide. T2D is characterized as insulin resistant and is often associated with unhealthy dietary habits. The present study assessed the effects of freeze-dried Saskatoon berry powder (SBp) and cyanidin-3-glucoside (C3G, an anthocyanin enriched in SBp) on metabolism, inflammatory markers and gut microbiota in high fat-high sucrose diet (HFHS) diet induced insulin resistant mice. Results Male C57 BL/6J mice received control, HFHS, HFHS + SBp (8.0 g/kg body weight/day) or HFHS + C3G (7.2 mg/kg/day, equal amount of C3G in 8.0 g/kg/day SBp) diet for 11 weeks. HFHS diet significantly increased the levels of glucose, cholesterol, triglycerides, insulin resistance and inflammatory mediators in plasma. The results of 16S rRNA gene sequencing demonstrated that HFHS diet increased the ratio of Bacteroidetes/Firmicutes (B/F) phylum bacteria and an elevated abundance of Muriculaceae family bacteria in the feces of mice. SBp or C3G supplementation attenuated HFHS diet-induced disorders in metabolism and inflammatory markers, and increased B/F ratio and Muriculaceae abundance in mouse gut compared to HFHS diet alone. The abundance of Muriculaceae in the gut microbiota negatively correlated with body weight, glucose, lipids, insulin resistance and inflammatory mediators in mice. The results of functional predication analysis suggest that HFHS diet upregulated the genes of gut bacteria involved in inflammation-related cellular processes, and inhibited bacteria involved in metabolism. SBp and C3G partially neutralized the alterations induced by HFHS diet in gut microbiota implicated in metabolism or inflammation. Conclusion The findings of the present study suggest that SBp is a potential prebiotic food mitigating Western diet-induced disorders in metabolism, inflammation and gut dysbiosis, and C3G possibly contributes to the beneficial effects of SBp.

Strong parent-child correlation in circulating vitamin B12 levels and its association with inflammatory markers in Saudi families

2020 ◽  
Vol 90 (5-6) ◽  
pp. 430-438
Author(s):  
Nasser M Al-Daghri ◽  
Sherif Abd-Alrahman ◽  
Kaiser Wani ◽  
Soundararajan Krishnaswamy ◽  
Amal Alenad ◽  
...  
Keyword(s):  
Vitamin B12 ◽  
Inflammatory Markers ◽  
Vitamin B12 Deficiency ◽  
Inverse Correlation ◽  
Plasminogen Activator Inhibitor ◽  
Limited Information ◽  
Plasminogen Activator Inhibitor 1 ◽  
Clinical Benefits ◽  
Factor Α ◽  
Circulating Levels

Abstract. Vitamin B12 deficiency leads to adverse effects on human health, but limited information is available as to whether abnormal vitamin B12 levels are associated between parents and offspring. The present study aimed to assess the association between circulating levels of vitamin B12 in Saudi parents and their children as well as its association with pro-inflammatory markers. A total of 104 Saudi families: 49 fathers, 63 mothers, 94 sons and 79 daughters were selected for the study. Fasting blood samples and anthropometrics were collected. Biochemical parameters, various pro-inflammatory markers and vitamin B12 were measured. Results showed a significant positive correlation between B12 levels in most parent-offspring pairs: mother-daughter (N = 46 pairs, r = 0.72, p < 0.0001); father-daughter (N = 39, r = 0.62, p < 0.0001) and mother-son (N = 51, r = 0.42, p < 0.01). This association was absent in father-son pairs (N = 48, r = 0.26, p = 0.09). Also, B12 was inversely associated with tumor necrosis factor-α and plasminogen activator inhibitor-1 in parents (r = −0.32; p < 0.01 and r = −0.31; p < 0.01 respectively) and children (r = −0.14; p < 0.01 and r = −0.19; p < 0.01 respectively). A significant inverse correlation was found between vitamin B12 and leptin in mothers (r = −0.31, p < 0.05). Our study suggests a strong familial component between B12 levels indicating a possible genetic influence on individual B12 status. Our study also suggests an inverse correlation between circulating levels of vitamin B12 and pro-inflammatory markers. The present study highlights the importance of extending screening in families of patients with abnormal B12 levels and expanding treatment, if necessary, to maximize clinical benefits.

scholarly journals Combined but not single treatment with ethinylestradiol/levonorgestrel and spironolactone reduces plasminogen activator inhibitor-1 in insulin-resistant ovariectomised rats

2019 ◽  
Vol 20 (4) ◽  
pp. 147032031989593
Author(s):  
Adeyanju Oluwaseun Aremu ◽  
Dibia Chinaza Lilian ◽  
Soladoye Ayodele Olufemi ◽  
Olatunji Lawrence Aderemi
Keyword(s):  
Plasminogen Activator ◽  
Density Lipoprotein ◽  
Plasminogen Activator Inhibitor ◽  
Dependent Manner ◽  
Model Assessment ◽  
Plasminogen Activator Inhibitor 1 ◽  
Insulin Resistant ◽  
Ovx Rats ◽  
Activator Inhibitor ◽  
Pai 1

Objective: Increased circulating level of plasminogen activator inhibitor-1 (PAI-1) is associated with menopausal oestrogen deficiency. We therefore hypothesised that the combined oral contraceptive (COC) with spironolactone (SPL) improves insulin resistance (IR) in ovariectomised (OVX) rats by reducing circulating PAI-1. Methods: Twelve-week-old female Wistar rats were divided into sham-operated (SHM), OVX, OVX+SPL (0.25 mg/kg), COC (1.0 µg ethinylestradiol and 5.0 µg levonorgestrel) and OVX+COC+SPL rats treated with COC and SPL daily for eight weeks. IR was assessed by homeostatic model assessment of IR (HOMA-IR). Results: Data showed that OVX rats had a higher HOMA-IR value that is associated with increased visceral adiposity, triglycerides (TG), total cholesterol/high-density lipoprotein cholesterol (HDL-C), TG/HDL-C, plasma insulin, GSK-3, corticosterone and decreased 17β-oestradiol. However, these effects were attenuated in OVX+COC, OVX+SPL and OVX+COC+SPL rats compared to OVX rats. OVX rats had lower PAI-1 than SHM rats, whereas the beneficial effect on IR and other parameters by COC or SPL was accompanied with increased PAI-1. Improvement of IR and other parameters with combined COC and SPL in OVX rats was accompanied with reduced PAI-1. Conclusion: Taken together, COC or SPL improves IR independent of PAI-1, whereas a combination of COC and SPL in OVX rats ameliorates IR in a PAI-1-dependent manner.

scholarly journals Emerging Role of Endothelial and Inflammatory Markers in Preeclampsia

2009 ◽  
Vol 26 (3) ◽  
pp. 127-133 ◽  
Author(s):  
Menha Swellam ◽  
Nervana Samy ◽  
Susan Abdl Wahab ◽  
Mohamed Saeed Ibrahim
Keyword(s):  
Inflammatory Markers ◽  
Linear Regression Analysis ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
New Approach ◽  
Reactive Protein ◽  
Diagnostic Role ◽  
Activator Inhibitor ◽  
Pai 1

Objectives:Endothelial disturbance and excess inflammatory response are pathogenic mechanisms in pre-eclampsia (PE). Authors determine the clinical diagnostic role for thrombomodulin (TM), plasminogen activator inhibitor-1 (PAI-1) as endothelial markers and C-reactive protein (CRP), and interlukin-6 (IL-6) as inflammatory markers when tested independently or in combinations.Materials and methods:We conducted a retrospective study in a cohort of 185 women grouped as 80 women with PE, 55 normotensive pregnant and 50 healthy non-pregnant. Plasma levels of TM, PAI-1, CRP and IL-6 were examined using enzyme linked immunosorbent assays.Results:Median levels and the positivity rates for the investigated markers were higher in PE as compared to the other groups (P< 0.0001). Using linear regression analysis, the investigated markers were significantly correlated regarding healthy nonpregnantvsPE or normotensive pregnantvsPE. The sensitivity of PAI-1 was the highest (98%) among the tested biomarkers. Combination between the investigated markers revealed absolute sensitivity (100%) and reliable specificity especially when PAI-1 was combined with CRP at 83% specificity.Conclusions:Investigated endothelial and inflammatory markers revealed sensitive diagnostic test for PE. However, coupled combination between PAI-1 with CRP showed superior both sensitivity and specificity which represent a promising new approach for detection of PE.

Differential Mechanisms of Plasminogen Activator Inhibitor-1 Gene Activation by Transforming Growth Factor-β and Tumor Necrosis Factor-α in Endothelial Cells

2001 ◽  
Vol 86 (12) ◽  
pp. 1563-1572 ◽  
Author(s):  
Yan Chen ◽  
Joanne Sloan-Lancaster ◽  
David Berg ◽  
Mark Richardson ◽  
Brian Grinnell ◽  
...  
Keyword(s):  
Map Kinases ◽  
Transforming Growth Factor ◽  
Gene Activation ◽  
Plasminogen Activator Inhibitor ◽  
Transforming Growth Factor Β ◽  
Promoter Activation ◽  
Plasminogen Activator Inhibitor 1 ◽  
Tnf Α ◽  
Factor Α ◽  
Pai 1

SummaryPlasminogen activator inhibitor-1 (PAI-1) is a serine protease inhibitor (SERPIN) specific for tissue-type and urokinase-like plasminogen activators. High plasma PAI-1 activity is a risk factor for thrombotic diseases. Due to the short half-life of PAI-1, regulation of PAI-1 gene expression and secretion of active PAI-1 into the blood stream is important for hemostatic balance. We have investigated transcriptional control of PAI-1 gene expression in bovine aortic endothelial cells (BAECs) and human cell lines using PAI-1 5’ promoter-luciferase reporter assays. Contrary to the cytokine-induced up-regulation of PAI-1 mRNA and protein levels, we found that only transforming growth factor-β (TGF-β) was efficient in inducing PAI-1 promoter activation. Tissue necrosis factor-α (TNF-α) induced a small luciferase activity with the 2.5 kb PAI-1 promoter, but not with the PAI-800/4G/5G and p3TP-lux promoters. Next we investigated whether a lack of response to TNF-α was due to deficient signaling pathways. BAECs responded to TNF-α with robust NFκB promoter activation. TGF-β activated the p38 MAP kinase, while TNF-α activated both the SAPK/JNK and p38 MAP kinases. The ERK1/2 MAP kinases were constitutively activated in BAECs. BAEC therefore responded to TNF-α stimulation with activation of the MAP kinases and the NFκB transcriptional factors. We further measured the messenger RNA stability under the influence by TGF-β and TNF-α and found no difference. PAI-1 gene activation by TNF-α apparently is yet to be defined for the location of the response element and/or the signaling pathway, while TGF-β is the most important cytokine for PAI-1 transcriptional activation through its 5’ proximal promoter.

scholarly journals Water-Pipe Smoke Exposure-Induced Circulatory Disturbances in Mice, and the Influence of Betaine Supplementation Thereon

2017 ◽  
Vol 41 (3) ◽  
pp. 1098-1112 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Suhail Al-Salam ◽  
Sumaya Beegam ◽  
Priya Yuvaraju ◽  
Abderrahim Oulhaj ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Plasma Concentrations ◽  
Immunohistochemical Analysis ◽  
Plasminogen Activator Inhibitor ◽  
Water Pipe ◽  
Plasminogen Activator Inhibitor 1 ◽  
Factor Α ◽  
Air Control

Background/Aims: It has been shown, both experimentally and clinically, that water-pipe smoke (WPS) exposure adversely affects the cardiovascular system (CVS) through the generation of oxidative stress and inflammation. Betaine, a naturally occurring compound in common foods, has antioxidant and anti-inflammatory actions. However, its potential to mitigate the adverse effect of WPS on the CVS has never been reported before. This is the subject of this study in mice. Methods: Mice were exposed daily for 30 min to either normal air (control), or to WPS for two consecutive weeks. Betaine was administered daily by gavage at a dose of 10mg/kg, 1h before either air or WPS exposure. Results: Betaine mitigated the in vivo prothrombotic effect of WPS in pial arterioles and venules. Moreover, it reversed the WPS-induced decrease in circulating platelets. Likewise, betaine alleviated platelet aggregation in vitro, and the shortening of activated partial thromboplastin time and prothrombin time induced by WPS. Betaine reduced the increase of plasminogen activator inhibitor-1 and fibrinogen concentrations in plasma induced by WPS. Betaine also diminished the WPS-induced increase of plasma concentrations of interleukin 6 and tumor necrosis factor α, and attenuated the increase of lipid peroxidation and superoxide dismutase. Immunohistochemical analysis of the heart revealed an increase in the expression of inducible nitric oxide synthase and cytochrome C by cardiomyocytes of the WPS-exposed mice. These effects were averted by betaine. Conclusion: Our findings suggest that betaine treatment significantly mitigated WPS-induced hypercoagulability, and inflammation, as well as systemic and cardiac oxidative stress.

Abstract 43: Association of Plasminogen Activator Inhibitor-1 with Prevalent and Incident Obesity is Independent of Inflammatory Markers: The Multi-Ethnic Study of Atherosclerosis (MESA)

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Sadiya S Khan ◽  
Donald M Lloyd-Jones ◽  
Cheelin Chan ◽  
Kiang Liu ◽  
Mary Cushman ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Inflammatory Markers ◽  
Smoking Status ◽  
Plasminogen Activator Inhibitor ◽  
Cox Proportional Hazards ◽  
Plasminogen Activator Inhibitor 1 ◽  
Ethnic Study ◽  
Activator Inhibitor ◽  
Pai 1

Background: In experimental animal models, deficiency of plasminogen activator inhibitor-1 (PAI-1) protects against development of obesity. In addition, elevated circulating levels of PAI-1 are associated in cross-sectional studies with prevalent obesity in humans. However, no studies have investigated the prospective association between PAI-1 and incident obesity. Methods: Plasma PAI-1 levels were measured in a random sample of men and women at baseline (2000-2002) in the Multi-Ethnic Study of Atherosclerosis. Obesity was defined as body mass index (BMI) > 30kg/m2. Incident obesity was identified at four follow-up exams (2002-2011) among those who were not obese at baseline. Logistic regression was used to examine the odds ratios (OR) and 95% confidence intervals (CI) of prevalent obesity at baseline. Cox proportional hazards regression was used to estimate hazard ratios (HR) for time to incident obesity. The covariates used for adjustment included baseline demographics (age, race, sex, center), lifestyle risk factors (physical activity, dietary energy intake, smoking status, alcohol consumption, education), and inflammatory markers (CRP and IL-6). Results: In 839 participants mean age was 59 years old; 59% and 47% of the cohort were female and white, respectively. At baseline, each standard deviation (SD) increase in log(PAI-1) level was associated with an odds ratio (OR) for adjusted prevalent obesity of 2.70 (95% CI: 2.21 - 3.30, p<0.001. This association remained significant after further adjustment for IL-6 and CRP with OR 2.39 (95% CI: 1.94-2.94, p<0.001). Over a median follow-up of 8.5 years, 16% of participants developed obesity. The multivariable adjusted hazard ratio for incident obesity was 1.36 (95% CI 1.09-1.69, p<0.001) per 1 SD increase in log(PAI-1). (Table). Conclusions: Elevated PAI-1 levels are associated with prevalent and incident obesity. These findings are consistent with results from murine studies and provide evidence suggesting a potential role of PAI-1 in the pathogenesis of obesity.

Resistance of adipose tissue lipoprotein lipase to insulin action in rats fed an obesity-promoting diet

2002 ◽  
Vol 282 (2) ◽  
pp. E412-E418 ◽  
Author(s):  
Frédéric Picard ◽  
André Boivin ◽  
Josée Lalonde ◽  
Yves Deshaies
Keyword(s):  
Insulin Resistance ◽  
Lipoprotein Lipase ◽  
Sprague Dawley ◽  
High Fat ◽  
Insulin Resistant ◽  
Nutritional Conditions ◽  
Sprague Dawley Rats ◽  
Postprandial Hypertriglyceridemia ◽  
Adipose Tissue Lipoprotein Lipase ◽  
High Sucrose

This study aimed to assess whether adipose lipoprotein lipase (LPL) becomes resistant to insulin in a nutritional model of resistance of glucose metabolism to insulin. Sprague-Dawley rats were fed for 4 wk chow or a purified high-sucrose, high-fat (HSHF) diet that induced overt insulin resistance. Rats were fasted for 24 h and then refed chow for 1, 3, or 6 h. The postprandial rise in insulinemia was similar in both dietary cohorts, whereas glycemia was higher in HSHF-fed than in chow-fed animals, indicating glucose intolerance and insulin resistance. In chow-fed rats, adipose LPL activity increased two- to fourfold postprandially, but only minimally (30%) in HSHF-fed rats. Muscle LPL decreased postprandially in HSHF-fed rats, suggesting intact sensitivity to insulin, but it increased in chow-fed animals. Peak postprandial triglyceridemia was higher (+70%) in insulin-resistant than in control rats. The postprandial rate of appearance of triglycerides in the circulation was similar in control and insulin-resistant rats, indicating that hypertriglyceridemia of the latter was the result of impaired clearance. These results demonstrate that adipose LPL becomes resistant to insulin in diet-induced IR and further suggest that, under certain nutritional conditions, modifications in adipose LPL modulation associated with insulin resistance, along with low muscle LPL, heightens postprandial hypertriglyceridemia through attenuated triglyceride clearance.

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