Rhodiola and salidroside in the treatment of metabolic disorders

2019 ◽  
Vol 19 (19) ◽  
pp. 1611-1626 ◽  
Author(s):  
Xiang-Li Bai ◽  
Xiu-Ling Deng ◽  
Guang-Jie Wu ◽  
Wen-Jing Li ◽  
Si Jin
Keyword(s):  
Metabolic Disorders ◽  
Energy Homeostasis ◽  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Ex Vivo ◽  
Treatment Strategies ◽  
Ampk Signaling ◽  
Beneficial Effects

Over the past three decades, the knowledge gained about the mechanisms that underpin the potential use of Rhodiola in stress- and ageing-associated disorders has increased, and provided a universal framework for studies that focused on the use of Rhodiola in preventing or curing metabolic diseases. Of particular interest is the emerging role of Rhodiola in the maintenance of energy homeostasis. Moreover, over the last two decades, great efforts have been undertaken to unravel the underlying mechanisms of action of Rhodiola in the treatment of metabolic disorders. Extracts of Rhodiola and salidroside, the most abundant active compound in Rhodiola, are suggested to provide a beneficial effect in mental, behavioral, and metabolic disorders. Both in vivo and ex vivo studies, Rhodiola extracts and salidroside ameliorate metabolic disorders when administered acutely or prior to experimental injury. The mechanism involved includes multi-target effects by modulating various synergistic pathways that control oxidative stress, inflammation, mitochondria, autophagy, and cell death, as well as AMPK signaling that is associated with possible beneficial effects on metabolic disorders. However, evidence-based data supporting the effectiveness of Rhodiola or salidroside in treating metabolic disorders is limited. Therefore, a comprehensive review of available trials showing putative treatment strategies of metabolic disorders that include both clinical effective perspectives and fundamental molecular mechanisms is warranted. This review highlights studies that focus on the potential role of Rhodiola extracts and salidroside in type 2 diabetes and atherosclerosis, the two most common metabolic diseases.

scholarly journals Metformin-stimulated AMPK-α1 promotes microvascular repair in acute lung injury

2013 ◽  
Vol 305 (11) ◽  
pp. L844-L855 ◽  
Author(s):  
Ming-Yuan Jian ◽  
Mikhail F. Alexeyev ◽  
Paul E. Wolkowicz ◽  
Jaroslaw W. Zmijewski ◽  
Judy R. Creighton
Keyword(s):  
Endothelial Cells ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Ex Vivo ◽  
Endothelial Permeability ◽  
Beneficial Effects ◽  
Isolated Lung

Acute lung injury secondary to sepsis is a leading cause of mortality in sepsis-related death. Present therapies are not effective in reversing endothelial cell dysfunction, which plays a key role in increased vascular permeability and compromised lung function. AMP-activated protein kinase (AMPK) is a molecular sensor important for detection and mediation of cellular adaptations to vascular disruptive stimuli. In this study, we sought to determine the role of AMPK in resolving increased endothelial permeability in the sepsis-injured lung. AMPK function was determined in vivo using a rat model of endotoxin-induced lung injury, ex vivo using the isolated lung, and in vitro using cultured rat pulmonary microvascular endothelial cells (PMVECs). AMPK stimulation using N1-(α-d-ribofuranosyl)-5-aminoimidizole-4-carboxamide or metformin decreased the LPS-induced increase in permeability, as determined by filtration coefficient ( Kf) measurements, and resolved edema as indicated by decreased wet-to-dry ratios. The role of AMPK in the endothelial response to LPS was determined by shRNA designed to decrease expression of the AMPK-α1 isoform in capillary endothelial cells. Permeability, wounding, and barrier resistance assays using PMVECs identified AMPK-α1 as the molecule responsible for the beneficial effects of AMPK in the lung. Our findings provide novel evidence for AMPK-α1 as a vascular repair mechanism important in the pulmonary response to sepsis and identify a role for metformin treatment in the management of capillary injury.

scholarly journals Regulation of TRH neurons and energy homeostasis-related signals under stress

2015 ◽  
Vol 224 (3) ◽  
pp. R139-R159 ◽  
Author(s):  
Patricia Joseph-Bravo ◽  
Lorraine Jaimes-Hoy ◽  
Jean-Louis Charli
Keyword(s):  
Energy Homeostasis ◽  
Molecular Mechanisms ◽  
Cell Types ◽  
Cellular Phenotype ◽  
Energy Demands ◽  
Rapid Responses ◽  
Hpt Axis

Energy homeostasis relies on a concerted response of the nervous and endocrine systems to signals evoked by intake, storage, and expenditure of fuels. Glucocorticoids (GCs) and thyroid hormones are involved in meeting immediate energy demands, thus placing the hypothalamo–pituitary–thyroid (HPT) and hypothalamo–pituitary–adrenal axes at a central interface. This review describes the mode of regulation of hypophysiotropic TRHergic neurons and the evidence supporting the concept that they act as metabolic integrators. Emphasis has been be placed on i) the effects of GCs on the modulation of transcription ofTrhin vivoandin vitro, ii) the physiological and molecular mechanisms by which acute or chronic situations of stress and energy demands affect the activity of TRHergic neurons and the HPT axis, and iii) the less explored role of non-hypophysiotropic hypothalamic TRH neurons. The partial evidence gathered so far is indicative of a contrasting involvement of distinct TRH cell types, manifested through variability in cellular phenotype and physiology, including rapid responses to energy demands for thermogenesis or physical activity and nutritional status that may be modified according to stress history.

Gum Acacia Functional Significance in the Management of Obesity

2019 ◽  
Vol 25 ◽  
Author(s):  
Surender Jangra ◽  
Ramesh Pothuraju
Keyword(s):  
Metabolic Disorders ◽  
Molecular Mechanisms ◽  
Guar Gum ◽  
Metabolic Diseases ◽  
The United States ◽  
Epidemiologic Studies ◽  
Beneficial Effects ◽  
Gum Acacia ◽  
Acacia Gum ◽  
United States Food

: Consumption of diets rich in fat and refined sugars are recognized to be the cause of altered intestinal functionality and metabolic disorders like obesity, insulin resistance, type 2 diabetes and cardiovascular diseases. Different epidemiologic studies have shown a significant relationship between lower intake of fibre and metabolic disorders. There are many naturally occurring dietary fibres among which gums are utmost important class e.g. guar gum, locust bean gum, tara gum, gellan gum, and gum acacia. Gum acacia has been considered as a safe dietary fibre by the United States, Food and Drug Administration and it is used widely as a stabilizer, thickening agent, and emulsifier in the food industry. Though gum acacia feeding has been reported to exert many beneficial effects in both rodents and humans, the underpinning for the different proposed molecular mechanisms are still elusive. So it would be of great relevance to conduct studies to understand the molecular mechanism of action of such fibres in the management of metabolic diseases.

scholarly journals Metabolic signaling functions of ER–mitochondria contact sites: role in metabolic diseases

2017 ◽  
Vol 58 (2) ◽  
pp. R87-R106 ◽  
Author(s):  
Emily Tubbs ◽  
Jennifer Rieusset
Keyword(s):  
Cell Fate ◽  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Treatment Strategies ◽  
Contact Sites ◽  
Novel Treatment ◽  
Functional Features ◽  
Novel Treatment Strategies

Beyond the maintenance of cellular homeostasis and the determination of cell fate, ER–mitochondria contact sites, defined as mitochondria-associated membranes (MAM), start to emerge as an important signaling hub that integrates nutrient and hormonal stimuli and adapts cellular metabolism. Here, we summarize the established structural and functional features of MAM and mainly focus on the latest breakthroughs highlighting a crucial role of organelle crosstalk in the control of metabolic homeostasis. Lastly, we discuss recent studies that have revealed the importance of MAM in not only metabolic diseases but also in other pathologies with disrupted metabolism, shedding light on potential common molecular mechanisms and leading hopefully to novel treatment strategies.

scholarly journals Metabolic Perturbations and Severe COVID-19 Disease: Implication of Molecular Pathways

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Ersilia Nigro ◽  
Fabio Perrotta ◽  
Rita Polito ◽  
Vito D’Agnano ◽  
Filippo Scialò ◽  
...  
Keyword(s):  
Respiratory Failure ◽  
Metabolic Disorders ◽  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Respiratory Illnesses ◽  
Receptor Modulation ◽  
High Incidence ◽  
The Impact

Coronavirus disease (COVID-19) is caused by SARS-CoV-2 virus, which can result in serious respiratory illnesses such as pneumonia leading to respiratory failure. It was first reported in Wuhan, Hubei, China, in December 2019 and rapidly spread globally, becoming a pandemic in March 2020. Among comorbidities observed in SARS-CoV-2 positive patients, hypertension (68.3%) and type 2-diabetes (30.1%) are the most frequent conditions. Although symptoms are highly heterogeneous (ranging from absence of symptoms to severe acute respiratory failure), patients with metabolic-associated diseases often experience worse COVID-19 outcomes. This review investigates the association between metabolic disorders and COVID-19 severity, exploring the molecular mechanisms potentially underlying this relationship and those that are responsible for more severe COVID-19 outcomes. In addition, the role of the main biological processes that may connect metabolic alterations to SARS-CoV-2 infection such as hyperglycemia, immune system deregulation, ACE-2 receptor modulation, and inflammatory response is described. The impact of metabolic disorders on the prognosis of COVID-19 has major implications in public health especially for countries affected by a high incidence of metabolic diseases.

scholarly journals Effects of Treatment with the Hypomethylating Agent 5-aza-2′-deoxycytidine in Murine Type II Collagen-Induced Arthritis

2019 ◽  
Vol 12 (4) ◽  
pp. 174 ◽  
Author(s):  
Maria Cristina Petralia ◽  
Emanuela Mazzon ◽  
Maria Sofia Basile ◽  
Marco Cutuli ◽  
Roberto Di Marco ◽  
...  
Keyword(s):  
Myeloid Leukemia ◽  
Ex Vivo ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Beneficial Effects ◽  
Significant Amelioration ◽  
Pro Inflammatory Cytokines

The emerging role of epigenetics in the pathogenesis of autoimmune diseases has recently attracted much interest on the possible use of epigenetic modulators for the prevention and treatment of these diseases. In particular, we and others have shown that drugs that inhibit DNA methylation, such as azacitidine (AZA) and decitabine (DAC), already used for the treatment of acute myeloid leukemia, exert powerful beneficial effects in rodent models of type 1 diabetes, multiple sclerosis, and Guillain Barrè syndrome. Along this line of research, we have presently studied the effects of DAC in a murine model of rheumatoid arthritis induced by type II collagen and have demonstrated that DAC administration was associated with a significant amelioration of the clinical condition, along with in vivo and ex vivo modification of the immunological profile of the so-treated mice, that exhibited a diminished production of Th1 and Th17 pro-inflammatory cytokines and reduction of anti-type II collagen autoantibodies.

scholarly journals miR-22-3p is involved in gluconeogenic pathway modulated by 3,5-diiodo-L-thyronine (T2)

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Rosalba Senese ◽  
Federica Cioffi ◽  
Giuseppe Petito ◽  
Pieter de Lange ◽  
Aniello Russo ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Tolerance Test ◽  
High Fat ◽  
Beneficial Effects ◽  
Insulin Tolerance

Abstract The 3,5-diiodo-L-thyronine (T2) has emerged as an active iodothyronine and its beneficial effects on glucose metabolism including glucose tolerance and insulin resistance is well established. However, little is known about its molecular mechanisms. Given the emerging importance of microRNAs in various metabolic diseases, in this study a possible link between the effects of T2 on glucose metabolism and miRNA expression was investigated by using an in vivo model in which T2 was administered in rats receiving a high fat diet, a condition known to impair glucose homeostasis. The results showed that T2-treated rats had a better tolerance to glucose load and a better performance at the insulin tolerance test in comparison to high fat diet animals. Interestingly, in the serum of the animals treated with T2 there was a general decrease of miRNAs with miR-22a-3p, miR-34c-5p and miR-33a-3p significantly downregulated. Furthermore, miR-22a-3p had the largest variation pointing toward its preeminent role in T2 metabolic effect. In fact, in liver there was an up-regulation of its target (Transcription Factor 7) Tcf7, which had an important impact on gluconeogenesis. This study provide, for the first time, evidences that miRNAs are involved in the effects exerted by T2 on glucose homeostasis.

scholarly journals Role of exercise-induced hepatokines in metabolic disorders

2019 ◽  
Vol 317 (1) ◽  
pp. E11-E24 ◽  
Author(s):  
Gaël Ennequin ◽  
Pascal Sirvent ◽  
Martin Whitham
Keyword(s):  
Metabolic Disease ◽  
Metabolic Disorders ◽  
Molecular Mechanisms ◽  
Acute Exercise ◽  
Whole Body ◽  
Fibroblast Growth Factor 21 ◽  
Beneficial Effects ◽  
Future Challenges ◽  
Exercise Induced

The health-promoting effects of physical activity to prevent and treat metabolic disorders are numerous. However, the underlying molecular mechanisms are not yet completely deciphered. In recent years, studies have referred to the liver as an endocrine organ, since it releases specific proteins called hepatokines. Some of these hepatokines are involved in whole body metabolic homeostasis and are theorized to participate in the development of metabolic disease. In this regard, the present review describes the role of Fibroblast Growth Factor 21, Fetuin-A, Angiopoietin-like protein 4, and Follistatin in metabolic disease and their production in response to acute exercise. Also, we discuss the potential role of hepatokines in mediating the beneficial effects of regular exercise and the future challenges to the discovery of new exercise-induced hepatokines.

scholarly journals Cross-Presenting XCR1+ Dendritic Cells as Targets for Cancer Immunotherapy

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 565 ◽  
Author(s):  
Katherine M. Audsley ◽  
Alison M. McDonnell ◽  
Jason Waithman
Keyword(s):  
Dendritic Cells ◽  
T Cell ◽  
Ex Vivo ◽  
Treatment Strategies ◽  
Vital Role ◽  
Cell Responses ◽  
Cell Immunity ◽  
Patient Responses

The use of dendritic cells (DCs) to generate effective anti-tumor T cell immunity has garnered much attention over the last thirty-plus years. Despite this, limited clinical benefit has been demonstrated thus far. There has been a revival of interest in DC-based treatment strategies following the remarkable patient responses observed with novel checkpoint blockade therapies, due to the potential for synergistic treatment. Cross-presenting DCs are recognized for their ability to prime CD8+ T cell responses to directly induce tumor death. Consequently, they are an attractive target for next-generation DC-based strategies. In this review, we define the universal classification system for cross-presenting DCs, and the vital role of this subset in mediating anti-tumor immunity. Furthermore, we will detail methods of targeting these DCs both ex vivo and in vivo to boost their function and drive effective anti-tumor responses.

The Role of Polyphenols in the Modulation of Plasma Non-Enzymatic Antioxidant Capacity (NEAC)

2012 ◽  
Vol 82 (3) ◽  
pp. 228-232 ◽  
Author(s):  
Mauro Serafini ◽  
Giuseppa Morabito
Keyword(s):  
Antioxidant Capacity ◽  
Dietary Intervention ◽  
Ex Vivo ◽  
The Body ◽  
Dietary Polyphenols ◽  
Enzymatic Antioxidant ◽  
Endogenous Antioxidant

Dietary polyphenols have been shown to scavenge free radicals, modulating cellular redox transcription factors in different in vitro and ex vivo models. Dietary intervention studies have shown that consumption of plant foods modulates plasma Non-Enzymatic Antioxidant Capacity (NEAC), a biomarker of the endogenous antioxidant network, in human subjects. However, the identification of the molecules responsible for this effect are yet to be obtained and evidences of an antioxidant in vivo action of polyphenols are conflicting. There is a clear discrepancy between polyphenols (PP) concentration in body fluids and the extent of increase of plasma NEAC. The low degree of absorption and the extensive metabolism of PP within the body have raised questions about their contribution to the endogenous antioxidant network. This work will discuss the role of polyphenols from galenic preparation, food extracts, and selected dietary sources as modulators of plasma NEAC in humans.

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