China
Africa
Explore chapters and articles related to this topic
Medicinal Mushrooms
Published in Anil K. Sharma, Raj K. Keservani, Surya Prakash Gautam, Herbal Product Development, 2020
Temitope A. Oyedepo, Adetoun E. Morakinyo
Research studies on some mushrooms have reported their hypoglycemic and antidiabetic activities in type 2 diabetic patients (Kim et al., 2010a; Li et al., 2011; Lu et al., 2010; Shokrzadeh et al., 2017). The possible mechanisms for antidiabetic effects of mushrooms may include: Increased adiponectin concentrations after taking fruiting body extract (Hsu et al., 2007). Plasma adiponectin concentrations predict insulin sensitivity toward glucose metabolism.Inhibition of glucose absorptionProtection of β-cell damageIncrease of insulin releaseEnhancement of antioxidant defense. Oxidative stress is a mainstream effect of the metabolic mechanisms by which alimentation can lead to insulin resistance (Zhai et al., 2011).Attenuation of inflammation. A study by Niwa et al. (2011) suggested that the antidiabetic effects exhibited by mushrooms are through the suppression of oxidative stress and pro-inflammatory cytokine, TNF-α.Modulation of carbohydrate metabolism pathway. Diabetic patients with dysfuntional metabolic control are susceptible to pulmonary complications with micro- and macro vascular disorders (Kaparianos et al., 2008).Regulation of insulin-dependent and insulin-independent signaling pathways. (Lo and Wasser, 2011; Oh et al., 2010).
Hydroxychloroquine improves high-fat-diet-induced obesity and organ dysfunction via modulation of lipid level, oxidative stress, and inflammation
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Mohamed A Hasan, Omar A. Ammar, Maher A Amer, Azza I Othman, Fawzia Zigheber, Mohamed A El-Missiry
The improvement in adiponectin levels in HCQ-treated obese rats has a fundamental and beneficial effect. The ability of adiponectin to control obesity consequences is attributed to several mechanisms [8]. It can suppress the induction of TNF-α and enhance the level of anti-inflammatory IL-10. Moreover, adiponectin decreases the amount of adipose tissue TG and improves insulin signaling and sensitivity. It also activates β-oxidation through enhancing peroxisome proliferator-activated receptor alpha (PPAR-α) receptor phosphorylation and stimulating AMP-activated protein kinase (AMPK) cascade [8]. Thus, these findings indicate that the effect of HCQ on obesity is mediated by adiponectin. In patients with systemic lupus erythematosus, treatment with HCQ controls adipokines [39]. In general, obesity is characterized by hyperleptinemia and resistance to weight loss [40]. Thus, we suggest that HCQ might normalize leptin levels, suppress leptin resistance, and/or restore the balance between leptin and adiponectin in rats treated with HFD+HCQ. These data indicate that HCQ intervention in obese rats improved oxidative stress status, declined production of inflammatory adipokines and reduced fat storage.
Associations of physical activity, sedentary time, and diet quality with biomarkers of inflammation in children
Published in European Journal of Sport Science, 2022
Eero A. Haapala, Juuso Väistö, Johanna K. Ihalainen, Claudia Tomaselli González, Marja H. Leppänen, Aapo Veijalainen, Taisa Sallinen, Aino-Maija Eloranta, Ulf Ekelund, Ursula Schwab, Soren Brage, Mustafa Atalay, Timo A. Lakka
Venous blood samples were taken the children having fasted for 12 h. Blood was immediately centrifuged and stored at a temperature of −75°C until biochemical analyses. Plasma hs-CRP was measured using an enhanced immunoturbidimetric assay with the CRP (Latex) High Sensitive Assay reagent (Roche Diagnostics GmbH, Mannheim, Germany) and the limit of quantitation of 0.3 mg/l. Plasma leptin concentration was measured by a competitive radioimmunoassay (Multigamma 1261-001, PerkinElmer Wallac Oy, Turku, Finland). Commercially available ELISA kits were employed for the measurement of plasma IL-6 and TNF-α concentrations (Sanquin Reagents, Amsterdam, The Netherlands). Serum high-molecular-weight adiponectin concentration was analysed using an ELISA kit after a specific proteolytic digestion of other multimeric adiponectin forms (Millipore, Billerica, MA, USA). The Nightingale high-throughput NMR metabolomics platform was used to quantify plasma glycoprotein acetyls (Soininen et al., 2015).
Biochanin A prevents 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced adipocyte dysfunction in cultured 3T3-L1 cells
Published in Journal of Environmental Science and Health, Part A, 2019
Eun Mi Choi, Kwang Sik Suh, So Young Park, Sang Ouk Chin, Sang Youl Rhee, Suk Chon
As PPARγ plays an important role in adipocyte differentiation, it is recognized as the master regulator of adipogenesis. Activation of PPARγ triggers the expression of various genes that are closely related to lipogenesis, fatty acid synthesis, and energy metabolism.[19] Adiponectin, an adipocyte-derived hormone that is expressed in differentiated adipocytes, stimulates lipid accumulation and insulin-responsive transporters.[20] Adiponectin plays an important role in the regulation of glucose and lipid metabolism. In differentiated adipocytes, adiponectin over-expressing cells exhibit greater fat accumulation, and stimulate glucose uptake by activating GLUT4. Because adiponectin is induced by PPAR-γ activity, adiponectin is used as a marker of PPAR-γ efficacy.[21] Thus, an increase in adiponectin secretion has more favorable effects against insulin resistance.[22] Here, we found that biochanin A partially reverses the TCDD-induced decrease in PPARγ and adiponectin levels during differentiation of 3T3-L1 adipocytes, suggesting that biochanin A affects adipogenesis and lipid accumulation by modulating PPAR-γ signaling and adiponectin production.