scholarly journals Biotic elicitation as a tool to improve strawberry and raspberry extract potential on metabolic syndrome‐related enzymes in vitro

2019 ◽  
Vol 99 (6) ◽  
pp. 2939-2946 ◽  
Author(s):  
Enrique Gutierrez‐Albanchez ◽  
Ara Kirakosyan ◽  
Steven F Bolling ◽  
Ana García‐Villaraco ◽  
Javier Gutierrez‐Mañero ◽  
...  
2020 ◽  
Vol 26 (39) ◽  
pp. 4970-4981
Author(s):  
Yu-Tang Tung ◽  
Chun-Hsu Pan ◽  
Yi-Wen Chien ◽  
Hui-Yu Huang

Metabolic syndrome is an aggregation of conditions and associated with an increased risk of developing diabetes, obesity and cardiovascular diseases (CVD). Edible mushrooms are widely consumed in many countries and are valuable components of the diet because of their attractive taste, aroma, and nutritional value. Medicinal mushrooms are higher fungi with additional nutraceutical attributes having low-fat content and a transisomer of unsaturated fatty acids along with high fiber content, biologically active compounds such as polysaccharides or polysaccharide β-glucans, alkaloids, steroids, polyphenols and terpenoids. In vitro experiments, animal models, and even human studies have demonstrated not only fresh edible mushroom but also mushroom extract that has great therapeutic applications in human health as they possess many properties such as antiobesity, cardioprotective and anti-diabetic effect. They are considered as the unmatched source of healthy foods and drugs. The focus of this report was to provide a concise and complete review of the novel medicinal properties of fresh or dry mushroom and extracts, fruiting body or mycelium and its extracts, fiber, polysaccharides, beta-glucan, triterpenes, fucoidan, ergothioneine from edible mushrooms that may help to prevent or treat metabolic syndrome and associated diseases.


2021 ◽  
pp. 110101
Author(s):  
Aldo Leyva-Soto ◽  
Rocío Alejandra Chavez-Santoscoy ◽  
Omar Porras ◽  
Miltha Hidalgo-Ledesma ◽  
Aracely Serrano-Medina ◽  
...  

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Kaivan Khavandi ◽  
Adam Greenstein ◽  
Sarah Withers ◽  
Kazuhiko Sonoyama ◽  
Sarah Lewis ◽  
...  

In order to investigate the contribution of perivascular adipose tissue (PVAT) to arterial function, a total of 55 small arteries harvested from 35 skin biopsies of patients with Metabolic Syndrome and matched controls were mounted as ring preparations in a wire myograph. Contractility to cumulative doses of Norepinephrine in the presence or absence of PVAT showed an anticontractile effect in arteries from healthy volunteers (p=0.009), which was lost in patients with Metabolic Syndrome. Bioassay studies confirmed that PVAT releases a hydrophilic anticontractile factor in health, which is absent in obesity. Using a soluble fragment of the human Type 1 receptor, we identified that the anticontractile factor was adiponectin, which is the sole mediator of vasodilation, acting by increasing endothelial bioavailability of nitric oxide. Significant endothelial dysfunction was observed in patients with Metabolic Syndrome (p<0.001). Quantitative image analysis of adipose tissue revealed significantly increased adipocyte cell size in patients with Metabolic Syndrome, compared with healthy controls (p<0.006). There was immunohistochemical evidence of inflammation with upregulation of TNF-alpha receptor 1 in these patients (p<0.001). Application of exogenous TNF-alpha abolished the anticontractile effect of PVAT by reducing adiponectin bioavailability. Oxidative stress also induced by cytokines TNF-alpha and IL-6 but not IL-1, reduced adiponectin production from PVAT and increased basal tone. When the obese microenvironment was replicated in vitro by inflicting hypoxia on PVAT, adiponectin activity was lost but then rescued by incubation with cytokine antagonists. Further application of the adiponectin receptor fragment abolished PVAT relaxation. We conclude that in healthy arteries, PVAT releases adiponectin which reduces vascular tone. In obesity, this is lost by a cascade of adipocyte hypertrophy, hypoxia, inflammation and oxidative stress. The resulting vasoconstriction contributes to hypertension, hypertriglyceridaemia and insulin resistance. Direct targeting of adiponectin release from PVAT therefore provides a novel therapeutic opportunity in the Metabolic Syndrome.


2018 ◽  
Vol 120 (7) ◽  
pp. 751-762 ◽  
Author(s):  
Giorgio Biasiotto ◽  
Isabella Zanella ◽  
Federica Predolini ◽  
Ivonne Archetti ◽  
Moris Cadei ◽  
...  

Abstract7-Hydroxymatairesinol (7-HMR) is a plant lignan abundant in various concentrations in plant foods. The objective of this study was to test HMRLignan™, a purified form of 7-HMR, and the correspondingPicea abiesextract (total extractP. abies; TEP) as dietary supplements on a background of a high-fat diet (HFD)-induced metabolic syndrome in mice and in the 3T3-L1 adipogenesis model. Mice, 3 weeks old, were fed a HFD for 60 d. Subgroups were treated with 3 mg/kg body weight 7-HMR (HMRLignan™) or 10 mg/kg body weight TEP by oral administration. 7-HMR and TEP limited the increase in body weight (−11 and −13 %) and fat mass (−11 and −18 %) in the HFD-fed mice. Epididymal adipocytes were 19 and −12 % smaller and the liver was less steatotic (−62 and −65 %). Serum lipids decreased in TEP-treated mice (−11 % cholesterol, −23 % LDL and −15 % TAG) and sugar metabolism was ameliorated by both lignan preparations, as shown by a more than 70 % decrease in insulin secretion and insulin resistance. The expression of several metabolic genes was modulated by the HFD with an effect that was reversed by lignan. In 3T3-L1 cells, the 7-HMR metabolites enterolactone (ENL) and enterodiol (END) showed a 40 % inhibition of cell differentiation accompanied by the inhibited expression of the adipogenic genesPPARγ,C/EBPαandaP2. Furthermore, END and ENL caused a 10 % reduction in TAG uptake in HEPA 1–6 hepatoma cells. In conclusion, 7-HMR and TEP reduce metabolic imbalances typical of the metabolic syndrome and obesity in male mice, whereas their metabolites inhibit adipogenesis and lipid uptakein vitro.


2012 ◽  
Vol 123 (11) ◽  
pp. 635-647 ◽  
Author(s):  
Radko Komers ◽  
Shaunessy Rogers ◽  
Terry T. Oyama ◽  
Bei Xu ◽  
Chao-Ling Yang ◽  
...  

In the present study, we investigated the activity of the thiazide-sensitive NCC (Na+–Cl− co-transporter) in experimental metabolic syndrome and the role of insulin in NCC activation. Renal responses to the NCC inhibitor HCTZ (hydrochlorothiazide), as a measure of NCC activity in vivo, were studied in 12-week-old ZO (Zucker obese) rats, a model of the metabolic syndrome, and in ZL (Zucker lean) control animals, together with renal NCC expression and molecular markers of NCC activity, such as localization and phosphorylation. Effects of insulin were studied further in mammalian cell lines with inducible and endogenous expression of this molecule. ZO rats displayed marked hyperinsulinaemia, but no differences in plasma aldosterone, compared with ZL rats. In ZO rats, natriuretic and diuretic responses to NCC inhibition with HCTZ were enhanced compared with ZL rats, and were associated with a decrease in BP (blood pressure). ZO rats displayed enhanced Thr53 NCC phosphorylation and predominant membrane localization of both total and phosphorylated NCC, together with a different profile in expression of SPAK (Ste20-related proline/alanine-rich kinase) isoforms, and lower expression of WNK4. In vitro, insulin induced NCC phosphorylation, which was blocked by a PI3K (phosphoinositide 3-kinase) inhibitor. Insulin-induced reduction in WNK4 expression was also observed, but delayed compared with the time course of NCC phosphorylation. In summary, we report increased NCC activity in hyperinsulinaemic rodents in conjunction with the SPAK expression profile consistent with NCC activation and reduced WNK4, as well as an ability of insulin to induce NCC stimulatory phosphorylation in vitro. Together, these findings indicate that hyperinsulinaemia is an important driving force of NCC activity in the metabolic syndrome with possible consequences for BP regulation.


Author(s):  
О.В. Першина ◽  
А.В. Пахомова ◽  
Н.Н. Ермакова ◽  
О.Ю. Рыбалкина ◽  
В.А. Крупин ◽  
...  

Цель исследования состояла в выявлении информативных клеточных маркеров сосудистых осложнений, регенерации микрососудистой сети и воспаления в венозной крови здоровых волонтеров, больных с метаболическим синдромом, сахарным диабетом 1 и 2 типа. Методы. Обследованы больные с метаболическим синдромом (МС), диабетом 2 типа без осложнений, диабетом 1 типа средней степени тяжести и здоровые волонтеры. Диагноз пациентов подтвержден общеклиническими, биохимическими, коагулометрическими и иммуноферментными методами исследования, для оценки экспрессии антигенов использовался многопараметрический цитометрический анализ. Результаты. При анализе экспрессии маркеров показано изменение числа эндотелиальных клеток, мезенхимальных стволовых клеток (МСК) и гемопоэтических стволовых клеток (ГСК) в крови в зависимости от патологии. Эндотелиальные клетки миелоидного (CD45CD14CD34CD309CD144CD31) и немиелоидного (CD45CD14CD34CD309CD144CD31) происхождения, CD309-эндотелиальные клетки и МСК (CD44CD73CD90CD105) предлагаются в качестве маркеров повреждения эндотелия при диабетической симптоматике. При этом ГСК (CD45CD34) могут выступать ценным диагностическим и прогностическим маркером воспаления. Заключение. Для подтверждения сосудистых повреждений и прогноза развития осложнений при диабете 1 и 2 типа в венозной крови пациентов целесообразно оценивать эндотелиальные прогениторные клетки (ЭПК) не костномозговой локализации (CD31CD309CD144) и костномозговой локализации (CD34CD309), и ЭПК c высоким регенеративным потенциалом (CD45CD34CD31CD144). Циркулирующие ЭПК, формирующие колонии in vitro (CD45CD34CD31), рекомендуется использовать в качестве дифференциального маркера состояния регенерации эндотелия при диабете 2 типа. The aim of this study was to identify mesenchymal stem cells (MSC), hematopoietic stem cells (HSC), mature endothelial cells, and endothelial progenitor cells (EPC) in the blood of healthy volunteers, patients with metabolic syndrome, and type 1 and 2 diabetes mellitus as new, informative cellular markers of vascular complications, endothelial regeneration, and inflammation. Methods. The diagnosis was confirmed by general clinical, biochemical, coagulometeric and ELISA studies; multi-parameter cytometric assay was used for evaluation of antigen expression. Results. Changes in the count of MSC, HSC, mature endothelial cells, and endothelial progenitor cells in blood of patients with metabolic syndrome and type 1 and 2 diabetes depended on the type of pathology. We propose using endothelial cells of myeloid (CD45CD14CD34CD309CD144CD31) and non-myeloid origin (CD45CD14CD34CD309CD144CD31), CD309-endothelial cells, and MSCs with the CD44CD73CD90CD105 phenotype as nonspecific markers of endothelial damage in presence of diabetic symptoms. Furthermore, HSCs (CD45CD34) can be used as a valuable diagnostic and prognostic marker of inflammation. Conclusions. It is relevant to evaluate EPCs of non-bone marrow localization (CD31CD309CD144) and bone marrow localization (CD34CD309) and EPCs with a high regenerative potential (CD45CD34CD31CD144) in the blood of patients with type 1 and 2 diabetes to confirm the presence of vascular damage and predict development of complications. Circulating, in vitro colony-forming EPCs (CD45CD34CD31) are recommended as a differential marker for inhibition of endothelial regeneration in type 2 diabetes.


2018 ◽  
Vol 46 ◽  
pp. 185-194 ◽  
Author(s):  
Daniel Rico ◽  
Ana Belén Martín Diana ◽  
Iñaki Milton-Laskibar ◽  
Alfredo Fernández-Quintela ◽  
Jose Manuel Silván ◽  
...  

Antioxidants ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 554
Author(s):  
Anna Jakubczyk ◽  
Urszula Złotek ◽  
Urszula Szymanowska ◽  
Kamila Rybczyńska-Tkaczyk ◽  
Krystyna Jęderka ◽  
...  

Lovage seedlings were elicited with jasmonic acid (JA) and yeast extract (YE) to induce the synthesis of biologically active compounds. A simulated digestion process was carried out to determine the potential bioavailability of phenolic acids. Buffer extracts were prepared for comparison. The ability to neutralize ABTS radicals was higher in all samples after the in vitro digestion, compared to that in the buffer extracts. However, the elicitation resulted in a significant increase only in the value of the reduction power of the potentially bioavailable fraction of phenolic acids. The effect of the elicitation on the activity of the potentially bioavailable fraction of phenolic acids towards the enzymes involved in the pathogenesis of the metabolic syndrome, i.e., ACE, lipase, amylase, and glucosidase, was analyzed as well. The in vitro digestion caused a significant increase in the ability to inhibit the activity of these enzymes; moreover, the inhibitory activity against alpha-amylase was revealed only after the digestion process. The potential anti-inflammatory effect of the analyzed extracts was defined as the ability to inhibit key pro-inflammatory enzymes, i.e., lipoxygenase and cyclooxygenase 2. The buffer extracts from the YE-elicited lovage inhibited the LOX and COX-2 activity more effectively than the extracts from the control plants. A significant increase in the anti-inflammatory and antimicrobial properties was noted after the simulated digestion.


2018 ◽  
Vol 19 (10) ◽  
pp. 3068
Author(s):  
Katarzyna Kornicka ◽  
Agnieszka Śmieszek ◽  
Jolanta Szłapka-Kosarzewska ◽  
Jennifer Irwin Houston ◽  
Michael Roecken ◽  
...  

Endocrine disorders are becoming an increasing problem in both human and veterinary medicine. In recent years, more and more horses worldwide have been suffering from equine metabolic syndrome (EMS). This metabolic disorder is characterized by pathological obesity, hyperinsulinaemia, hyperglycaemia and insulin resistance. Although metabolic disorders, including diabetes, have been extensively studied, there are still no data on the molecular effects of EMS in horses. Thus, the aim of this study was to evaluate apoptosis, oxidative stress, autophagy and microRNA (miR) expression in multipotent intestinal epithelial stem cells (IECs) and pancreatic islets (PIs) isolated post mortem form healthy and EMS diagnosed horses. Our group was the first to describe how EMS affects IEC and PI aging and senescence. First, we evaluated isolation and culture protocol for these cells and subsequently established their metabolic status in vitro. Both IECs and PIs isolated from EMS horses were characterized by increased apoptosis and senescence. Moreover, they accumulated elevated levels of reactive oxygen species (ROS). Here we have observed that autophagy/mitophagy may be a protective mechanism which allows those cells to maintain their physiological function, clear protein aggregates and remove damaged organelles. Furthermore, it may play a crucial role in reducing endoplasmic reticulum (ER) stress. This protective mechanism may help to overcome the harmful effects of ROS and provide building blocks for protein and ATP synthesis.


Planta Medica ◽  
2019 ◽  
Vol 86 (01) ◽  
pp. 78-84 ◽  
Author(s):  
Omar Estrada ◽  
Camilo Di Giulio ◽  
Radharani Dorta-Ledezma ◽  
Freddy Gonzalez-Mujica ◽  
Norma Motta ◽  
...  

AbstractCommon chronic conditions such as metabolic syndrome and diabetes are increasingly associated to metabolic and cardiovascular complications. Although Phyllanthus tenellus leaves have been used in decoctions as a popular remedy to control blood glucose levels and hypertension, its use needs a scientific basis. This study was therefore undertaken to report a phytochemical analysis of P. tenellus leaves and to test if the main active compound has potential to simultaneously tackle several pathophysiological features of metabolic syndrome and diabetes-related metabolic and vascular disorders such as hyperglycaemia, increased platelet activation, and endothelial dysfunction. We performed a partition of the methanolic extract of P. tenellus leaves among different organic solvents followed by chromatographic separation guided by the rat liver microsomal glucose-6-phosphatase assay. Two known tannins were identified by spectroscopic methods as pinocembrin-7-O-[3″-O-galloyl-4″,6″-(S)-hexahydroxydiphenoyl]-α-D-glucose, named P7OG by us, and gemin D. The structural determination of the isolated compounds was based on spectral data. The ability of the main active component, P7OG, to inhibit human platelet aggregation and to modify vascular reactivity of rat aortic rings incubated with high glucose (D-glucose 55 mM) was then evaluated. P7OG was further able to inhibit platelet aggregation induced by adenosine 5′-diphosphate and collagen, showed vasorelaxant effects in arteries precontracted with phenylephrine, and reverted the endothelium-dependent impairment effect of high glucose in rat aortic rings. In conclusion, one tannin isolated from P. tenellus showed promising metabolic, antiaggregant, and vascular effects, which suggests the potential beneficial use of P. tenellus to tackle complex cardiometabolic diseases.


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