scholarly journals Molecular and Cellular Mechanisms of Electronegative Lipoproteins in Cardiovascular Diseases

Biomedicines ◽  
2020 ◽  
Vol 8 (12) ◽  
pp. 550
Author(s):  
Liang-Yin Ke ◽  
Shi Hui Law ◽  
Vineet Kumar Mishra ◽  
Farzana Parveen ◽  
Hua-Chen Chan ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Cardiovascular Diseases ◽  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Chemical Properties ◽  
Endothelial Damage ◽  
Cellular Mechanisms ◽  
Glucose And Lipid Metabolism ◽  
Markers Of Inflammation ◽  
Atherosclerotic Cardiovascular Diseases

Dysregulation of glucose and lipid metabolism increases plasma levels of lipoproteins and triglycerides, resulting in vascular endothelial damage. Remarkably, the oxidation of lipid and lipoprotein particles generates electronegative lipoproteins that mediate cellular deterioration of atherosclerosis. In this review, we examined the core of atherosclerotic plaque, which is enriched by byproducts of lipid metabolism and lipoproteins, such as oxidized low-density lipoproteins (oxLDL) and electronegative subfraction of LDL (LDL(−)). We also summarized the chemical properties, receptors, and molecular mechanisms of LDL(−). In combination with other well-known markers of inflammation, namely metabolic diseases, we concluded that LDL(−) can be used as a novel prognostic tool for these lipid disorders. In addition, through understanding the underlying pathophysiological molecular routes for endothelial dysfunction and inflammation, we may reassess current therapeutics and might gain a new direction to treat atherosclerotic cardiovascular diseases, mainly targeting LDL(−) clearance.

scholarly journals Antioxidant and Anti-inflammatory Mechanisms of Astaxanthin in Cardiovascular Diseases

2020 ◽  
Author(s):  
Carolina Parga Martins Pereira ◽  
Ana Carolina Remondi Souza ◽  
Andrea Rodrigues Vasconcelos ◽  
Pietra Sacramento Prado ◽  
José João Name
Keyword(s):  
Cardiovascular Diseases ◽  
Molecular Mechanisms ◽  
Cardiovascular Health ◽  
Redox Balance ◽  
Cellular Mechanisms ◽  
Positive Effects ◽  
Antioxidant Agents ◽  
Therapeutic Properties ◽  
Anti Inflammatory ◽  
Preclinical And Clinical Studies

Cardiovascular disease is the most common cause of death. Oxidative stress and inflammation are pathophysiological processes involved in the development of cardiovascular diseases, so anti-inflammatory and antioxidant agents that modulate redox balance have become the targets of research to evaluate their molecular mechanisms and therapeutic properties. Astaxanthin, a carotenoid of the xanthophyll group, has potent antioxidant effects due to its molecular structure and its arrangement in the plasma membrane, factors that favor the neutralization of reactive oxygen and nitrogen species. This carotenoid also stands out for its anti-inflammatory activity, possibly interrelated with its antioxidant effect, as well as for its modulation of lipid and glucose metabolism. Considering the potential positive effects of astaxanthin on cardiovascular health evidenced by preclinical and clinical studies, this paper describes the molecular and cellular mechanisms related to the antioxidant and anti-inflammatory properties of this carotenoid in cardiovascular diseases, especially atherosclerosis.

scholarly journals Effects on Liver Lipid Metabolism of the Naturally Occurring Dietary Flavone Luteolin-7-glucoside

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Carla Sá ◽  
Ana Rita Oliveira ◽  
Cátia Machado ◽  
Marisa Azevedo ◽  
Cristina Pereira-Wilson
Keyword(s):  
Lipid Metabolism ◽  
Fatty Acid Synthase ◽  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Regulatory Element ◽  
Lipid Lowering ◽  
Whole Body ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Hepatic Expression

Disruptions in whole-body lipid metabolism can lead to the onset of several pathologies such as nonalcoholic fatty liver disease (NAFLD) and cardiovascular diseases (CVDs). The present study aimed at elucidating the molecular mechanisms behind the lipid-lowering effects of the flavone luteolin-7-glucoside (L7G) which we previously showed to improve plasma lipid profile in rats. L7G is abundant in plant foods of Mediterranean diet such as aromatic plants used as herbs. Results show that dietary supplementation with L7G for one week induced the expression of peroxisome proliferator-activated receptor-alpha (PPAR-α) and of its target gene carnitine palmitoyl transferase 1 (CPT-1) in rat liver. L7G showed a tendency to decrease the hepatic expression of sterol regulatory element-binding protein-1 (SREBP-1), without affecting fatty acid synthase (FAS) protein levels. Although SREBP-2 and LDLr mRNA levels did not change, the expression of HMG CoA reductase (HMGCR) was significantly repressed by L7G. L7G also inhibited this enzyme’sin vitroactivity in a dose dependent manner, but only at high and not physiologically relevant concentrations. These results add new evidence that the flavone luteolin-7-glucoside may help in preventing metabolic diseases and clarify the mechanisms underlying the beneficial health effects of diets rich in fruits and vegetables.

scholarly journals Convergence of IPMK and LKB1-AMPK Signaling Pathways on Metformin Action

2014 ◽  
Vol 28 (7) ◽  
pp. 1186-1193 ◽  
Author(s):  
Sookhee Bang ◽  
Yong Chen ◽  
Rexford S. Ahima ◽  
Sangwon F. Kim
Keyword(s):  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Dominant Negative ◽  
Acid Oxidation ◽  
Ampk Activation ◽  
Inositol Polyphosphate ◽  
Murine Embryonic Fibroblast ◽  
Ampk Signaling ◽  
Protein Protein Interaction ◽  
Glucose And Lipid Metabolism

Metformin is a biguanide drug that is widely prescribed for type 2 diabetes. Metformin suppresses hepatic gluconeogenesis and increases fatty acid oxidation. Although studies have suggested that metformin acts, at least in part, via activation of the liver kinase B1 (LKB1)/AMP-activated protein kinase (AMPK) pathway, the specific molecular mechanisms underlying metformin's regulation of glucose and lipid metabolism have not been well delineated. Recently, we have shown that inositol polyphosphate multikinase (IPMK) plays an important role in cellular energy metabolism and glucose-mediated AMPK regulation. Here we investigated the role of IPMK in metformin-induced AMPK activation. We observed that metformin-mediated activation of AMPK was impaired in the absence of IPMK. Overexpression of wild-type IPMK was sufficient to restore LKB1-AMPK activation by either metformin or AICAR in IPMK−/− murine embryonic fibroblast cells, suggesting that IPMK may act as an upstream regulator of LKB1-AMPK signaling in response to metformin. Moreover, this regulation was mediated by protein-protein interaction between IPMK and LKB1 as a dominant-negative peptide, which abrogates this interaction, attenuated metformin's ability to activate AMPK. Our data demonstrate that IPMK plays an important role in LKB1/AMPK signaling and may be targeted for treatment of metabolic diseases.

scholarly journals Fibroblast growth factor 21: a regulator of metabolic disease and health span

2017 ◽  
Vol 313 (3) ◽  
pp. E292-E302 ◽  
Author(s):  
Ting Xie ◽  
Po Sing Leung
Keyword(s):  
Lipid Metabolism ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Metabolic Diseases ◽  
Scientific Basis ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Glucose And Lipid Metabolism ◽  
Care Guidelines

Fibroblast growth factor 21 (FGF21) is a potent endocrine regulator with physiological effects on glucose and lipid metabolism and thus garners much attention for its translational potential for the management of obesity and related metabolic syndromes. FGF21 is mainly expressed in several metabolically active tissue organs, such as the liver, adipose tissue, skeletal muscle, and pancreas, with profound effects and therapeutic relevance. Emerging experimental and clinical data point to the demonstrated metabolic benefits of FGF21, which include, but are not limited to, weight loss, glucose and lipid metabolism, and insulin sensitivity. In addition, FGF21 also acts directly through its coreceptor β-klotho in the brain to alter light-dark cycle activity. In this review, we critically appraise current advances in understanding the physiological actions of FGF21 and its role as a biomarker of various metabolic diseases, especially type 2 diabetes mellitus. We also discuss the potentially exciting role of FGF21 in improving our health and prolonging our life span. This information will provide a fuller understanding for further research into FGF21, as well as providing a scientific basis for potentially establishing health care guidelines for this promising molecule.

scholarly journals FGF21 as an Endocrine Regulator in Lipid Metabolism: From Molecular Evolution to Physiology and Pathophysiology

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Yusuke Murata ◽  
Morichika Konishi ◽  
Nobuyuki Itoh
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Molecular Evolution ◽  
Ketogenic Diet ◽  
Metabolic Diseases ◽  
Cultured Cells ◽  
Pharmacological Effects ◽  
Glucose And Lipid Metabolism ◽  
Physiological Regulator ◽  
Related Proteins

The FGF family comprises twenty-two structurally related proteins with functions in development and metabolism. TheFgf21gene was generated early in vertebrate evolution. FGF21 acts as an endocrine regulator in lipid metabolism. HepaticFgf21expression is markedly induced in mice by fasting or a ketogenic diet. Experiments withFgf21transgenic mice and cultured cells indicate that FGF21 exerts pharmacological effects on glucose and lipid metabolism in hepatocytes and adipocytes via cell surface FGF receptors. However, experiments withFgf21knockout mice indicate that FGF21 inhibits lipolysis in adipocytes during fasting and attenuates torpor induced by a ketogenic diet but maybe not a physiological regulator for these hepatic functions. These findings suggest the pharmacological effects to be distinct from the physiological roles. Serum FGF21 levels are increased in patients with metabolic diseases having insulin resistance, indicating that FGF21 is a metabolic regulator and a biomarker for these diseases.

scholarly journals Diabetic and Metabolic Programming: Mechanisms Altering the Intrauterine Milieu

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Claudia Eberle ◽  
Christoph Ament
Keyword(s):  
Metabolic Syndrome ◽  
Cardiovascular Diseases ◽  
Maternal Health ◽  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Experimental Studies ◽  
Cardiovascular Changes ◽  
Thrifty Phenotype ◽  
The Metabolic Syndrome ◽  
Thrifty Phenotype Hypothesis

A wealth of epidemiological, clinical, and experimental studies have been linked to poor intrauterine conditions as well as metabolic and associated cardiovascular changes postnatal. These are novel perspectives connecting the altered intrauterine milieu to a rising number of metabolic diseases, such as diabetes, obesity, and hypercholesterolemia as well as the Metabolic Syndrome (Met S). Moreover, metabolic associated atherosclerotic diseases are connected to perigestational maternal health. The “Thrifty Phenotype Hypothesis” introduced cross-generational links between poor conditions during gestation and metabolic as well as cardiovascular alterations postnatal. Still, mechanisms altering the intrauterine milieu causing metabolic and associated atherosclerotic diseases are currently poorly understood. This paper will give novel insights in fundamental concepts connected to specific molecular mechanisms “programming” diabetes and associated metabolic as well as cardiovascular diseases.

scholarly journals Potential anti-obesogenic properties of non-digestible carbohydrates: specific focus on resistant dextrin

2015 ◽  
Vol 74 (3) ◽  
pp. 258-267 ◽  
Author(s):  
Mark R. Hobden ◽  
Laetitia Guérin-Deremaux ◽  
Ian Rowland ◽  
Glenn R. Gibson ◽  
Orla B. Kennedy
Keyword(s):  
Lipid Metabolism ◽  
Gut Microbiota ◽  
Intervention Studies ◽  
Metabolic Diseases ◽  
Metabolic Effects ◽  
Appetite Regulation ◽  
Bacterial Populations ◽  
Glucose And Lipid Metabolism ◽  
Resistant Dextrin ◽  
The Impact

Alterations in the composition and metabolic activity of the gut microbiota appear to contribute to the development of obesity and associated metabolic diseases. However, the extent of this relationship remains unknown. Modulating the gut microbiota with non-digestible carbohydrates (NDC) may exert anti-obesogenic effects through various metabolic pathways including changes to appetite regulation, glucose and lipid metabolism and inflammation. The NDC vary in physicochemical structure and this may govern their physical properties and fermentation by specific gut bacterial populations. Much research in this area has focused on established prebiotics, especially fructans (i.e. inulin and fructo-oligosaccharides); however, there is increasing interest in the metabolic effects of other NDC, such as resistant dextrin. Data presented in this review provide evidence from mechanistic and intervention studies that certain fermentable NDC, including resistant dextrin, are able to modulate the gut microbiota and may alter metabolic process associated with obesity, including appetite regulation, energy and lipid metabolism and inflammation. To confirm these effects and elucidate the responsible mechanisms, further well-controlled human intervention studies are required to investigate the impact of NDC on the composition and function of the gut microbiota and at the same time determine concomitant effects on host metabolism and physiology.

scholarly journals The Roles and Pharmacological Effects of FGF21 in Preventing Aging-Associated Metabolic Diseases

2021 ◽  
Vol 8 ◽  
Author(s):  
Junbin Yan ◽  
Yunmeng Nie ◽  
Jielu Cao ◽  
Minmin Luo ◽  
Maoxiang Yan ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Metabolic Diseases ◽  
Cellular Aging ◽  
Fibroblast Growth Factor 21 ◽  
Aging Effects ◽  
Dark Cloud ◽  
Alcoholic Fatty Liver ◽  
Glucose And Lipid Metabolism ◽  
Theoretical Support

With the continuous improvement of living standards but the lack of exercise, aging-associated metabolic diseases such as obesity, type 2 diabetes mellitus (T2DM), and non-alcoholic fatty liver disease (NAFLD) are becoming a lingering dark cloud over society. Studies have found that metabolic disorders are near related to glucose, lipid metabolism, and cellular aging. Fibroblast growth factor 21 (FGF21), a member of the FGFs family, efficiently regulates the homeostasis of metabolism and cellular aging. By activating autophagy genes and improving inflammation, FGF21 indirectly delays cellular aging and directly exerts anti-aging effects by regulating aging genes. FGF21 can also regulate glucose and lipid metabolism by controlling metabolism-related genes, such as adipose triglyceride lipase (ATGL) and acetyl-CoA carboxylase (ACC1). Because FGF21 can regulate metabolism and cellular aging simultaneously, FGF21 analogs and FGF21 receptor agonists are gradually being valued and could become a treatment approach for aging-associated metabolic diseases. However, the mechanism by which FGF21 achieves curative effects is still not known. This review aims to interpret the interactive influence between FGF21, aging, and metabolic diseases and delineate the pharmacology of FGF21, providing theoretical support for further research on FGF21.

The Role of Adiponectin in Maintaining Metabolic Homeostasis

2020 ◽  
Vol 16 (2) ◽  
pp. 95-103 ◽  
Author(s):  
Suleyman Cem Adiyaman ◽  
Muhammet Ozer ◽  
Basak Ozgen Saydam ◽  
Baris Akinci
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Cardiovascular Health ◽  
Metabolic Diseases ◽  
Metabolic Homeostasis ◽  
Glucose And Lipid Metabolism ◽  
Treatment Of Diabetes ◽  
Novel Targets

Background: Adiponectin is an adipocyte-derived cytokine closely associated with obesity, altered body adipose tissue distribution, insulin resistance, and cardiovascular diseases. Introduction: Evidence from animal and human studies demonstrate that adiponectin plays an important role in the regulation of glucose and lipid metabolism. Adiponectin increases insulin sensitivity and improves systemic lipid metabolism. Although research efforts on adiponectin mostly aim towards its endocrine functions, this adipocyte-derived molecule also has profound autocrine and paracrine functions. Conclusion: In this review, our aim is to discuss the role of adiponectin in maintaining metabolic homeostasis and its association with cardiovascular health. The proper identification of these roles is of great importance, which has the potential to identify a wealth of novel targets for the treatment of diabetes and related cardio-metabolic diseases.

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