Plant Compounds for the Treatment of Diabetes, a Metabolic Disorder: NF-κB as a Therapeutic Target

2020 ◽  
Vol 26 (39) ◽  
pp. 4955-4969
Author(s):  
Ravi Sahukari ◽  
Jyothi Punabaka ◽  
Shanmugam Bhasha ◽  
Venkata S. Ganjikunta ◽  
Shanmugam K. Ramudu ◽  
...  
Keyword(s):  
Diabetic Complications ◽  
Current Knowledge ◽  
World Population ◽  
Future Studies ◽  
Expression Of Genes ◽  
Treatment Of Diabetes ◽  
Online Library ◽  
And Oxidative Stress ◽  
Stress Activation ◽  
Plant Compounds

Background: The prevalence of diabetes in the world population hás reached 8.8 % and is expected to rise to 10.4% by 2040. Hence, there is an urgent need for the discovery of drugs against therapeutic targets to sojourn its prevalence. Previous studies proved that NF-κB serves as a central agent in the development of diabetic complications. Objectives: This review intended to list the natural plant compounds that would act as inhibitors of NF-κB signalling in different organs under the diabetic condition with their possible mechanism of action. Methods: Information on NF-κB, diabetes, natural products, and relation in between them, was gathered from scientific literature databases such as Pubmed, Medline, Google scholar, Science Direct, Springer, Wiley online library. Results and Conclusion: NF-κB plays a crucial role in the development of diabetic complications because of its link in the expression of genes that are responsible for organs damage such as kidney, brain, eye, liver, heart, muscle, endothelium, adipose tissue and pancreas by inflammation, apoptosis and oxidative stress. Activation of PPAR-α, SIRT3/1, and FXR through many cascades by plant compounds such as terpenoids, iridoids, flavonoids, alkaloids, phenols, tannins, carbohydrates, and phytocannabinoids recovers diabetic complications. These compounds also exhibit the prevention of NF-κB translocation into the nucleus by inhibiting NF-κB activators, such as VEGFR, RAGE and TLR4 receptors, which in turn, prevent the activation of many genes involved in tissue damage. Current knowledge on the treatment of diabetes by targeting NF-κB is limited, so future studies would enlighten accordingly.

Mesophyll conductance: the leaf corridors for photosynthesis

2020 ◽  
Vol 48 (2) ◽  
pp. 429-439 ◽  
Author(s):  
Jorge Gago ◽  
Danilo M. Daloso ◽  
Marc Carriquí ◽  
Miquel Nadal ◽  
Melanie Morales ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Main Role ◽  
Mesophyll Conductance ◽  
Future Studies ◽  
Cell Structures ◽  
Leaf Tissues ◽  
Change Framework ◽  
Chloroplast Stroma

Besides stomata, the photosynthetic CO2 pathway also involves the transport of CO2 from the sub-stomatal air spaces inside to the carboxylation sites in the chloroplast stroma, where Rubisco is located. This pathway is far to be a simple and direct way, formed by series of consecutive barriers that the CO2 should cross to be finally assimilated in photosynthesis, known as the mesophyll conductance (gm). Therefore, the gm reflects the pathway through different air, water and biophysical barriers within the leaf tissues and cell structures. Currently, it is known that gm can impose the same level of limitation (or even higher depending of the conditions) to photosynthesis than the wider known stomata or biochemistry. In this mini-review, we are focused on each of the gm determinants to summarize the current knowledge on the mechanisms driving gm from anatomical to metabolic and biochemical perspectives. Special attention deserve the latest studies demonstrating the importance of the molecular mechanisms driving anatomical traits as cell wall and the chloroplast surface exposed to the mesophyll airspaces (Sc/S) that significantly constrain gm. However, even considering these recent discoveries, still is poorly understood the mechanisms about signaling pathways linking the environment a/biotic stressors with gm responses. Thus, considering the main role of gm as a major driver of the CO2 availability at the carboxylation sites, future studies into these aspects will help us to understand photosynthesis responses in a global change framework.

scholarly journals MicroRNAs and Oxidative Stress: An Intriguing Crosstalk to Be Exploited in the Management of Type 2 Diabetes

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 802
Author(s):  
Teresa Vezza ◽  
Aranzazu M. de Marañón ◽  
Francisco Canet ◽  
Pedro Díaz-Pozo ◽  
Miguel Marti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Signaling Pathways ◽  
Current Knowledge ◽  
Critical Role ◽  
Cell Dysfunction ◽  
Non Coding Rnas ◽  
And Oxidative Stress ◽  
Molecular Crosstalk

Type 2 diabetes is a chronic disease widespread throughout the world, with significant human, social, and economic costs. Its multifactorial etiology leads to persistent hyperglycemia, impaired carbohydrate and fat metabolism, chronic inflammation, and defects in insulin secretion or insulin action, or both. Emerging evidence reveals that oxidative stress has a critical role in the development of type 2 diabetes. Overproduction of reactive oxygen species can promote an imbalance between the production and neutralization of antioxidant defence systems, thus favoring lipid accumulation, cellular stress, and the activation of cytosolic signaling pathways, and inducing β-cell dysfunction, insulin resistance, and tissue inflammation. Over the last few years, microRNAs (miRNAs) have attracted growing attention as important mediators of diverse aspects of oxidative stress. These small endogenous non-coding RNAs of 19–24 nucleotides act as negative regulators of gene expression, including the modulation of redox signaling pathways. The present review aims to provide an overview of the current knowledge concerning the molecular crosstalk that takes place between oxidative stress and microRNAs in the physiopathology of type 2 diabetes, with a special emphasis on its potential as a therapeutic target.

scholarly journals Molecular Mechanisms of Obesity-Linked Cardiac Dysfunction: An Up-Date on Current Knowledge

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 629
Author(s):  
Jorge Gutiérrez-Cuevas ◽  
Ana Sandoval-Rodriguez ◽  
Alejandra Meza-Rios ◽  
Hugo Christian Monroy-Ramírez ◽  
Marina Galicia-Moreno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Dysfunction ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Peroxisome Proliferator ◽  
White Adipocyte ◽  
Peroxisome Proliferator Activated Receptors ◽  
And Oxidative Stress

Obesity is defined as excessive body fat accumulation, and worldwide obesity has nearly tripled since 1975. Excess of free fatty acids (FFAs) and triglycerides in obese individuals promote ectopic lipid accumulation in the liver, skeletal muscle tissue, and heart, among others, inducing insulin resistance, hypertension, metabolic syndrome, type 2 diabetes (T2D), atherosclerosis, and cardiovascular disease (CVD). These diseases are promoted by visceral white adipocyte tissue (WAT) dysfunction through an increase in pro-inflammatory adipokines, oxidative stress, activation of the renin-angiotensin-aldosterone system (RAAS), and adverse changes in the gut microbiome. In the heart, obesity and T2D induce changes in substrate utilization, tissue metabolism, oxidative stress, and inflammation, leading to myocardial fibrosis and ultimately cardiac dysfunction. Peroxisome proliferator-activated receptors (PPARs) are involved in the regulation of carbohydrate and lipid metabolism, also improve insulin sensitivity, triglyceride levels, inflammation, and oxidative stress. The purpose of this review is to provide an update on the molecular mechanisms involved in obesity-linked CVD pathophysiology, considering pro-inflammatory cytokines, adipokines, and hormones, as well as the role of oxidative stress, inflammation, and PPARs. In addition, cell lines and animal models, biomarkers, gut microbiota dysbiosis, epigenetic modifications, and current therapeutic treatments in CVD associated with obesity are outlined in this paper.

scholarly journals Physiological roles of tryptophan in teleosts: current knowledge and perspectives for future studies

2017 ◽  
Vol 11 (1) ◽  
pp. 3-24 ◽  
Author(s):  
Seyyed Morteza Hoseini ◽  
Amalia Pérez-Jiménez ◽  
Benjamin Costas ◽  
Rita Azeredo ◽  
Manuel Gesto
Keyword(s):  
Current Knowledge ◽  
Future Studies

Mechanisms involved in developmental programming of hypertension and renal diseases. Gender differences

2014 ◽  
Vol 18 (2) ◽  
Author(s):  
Analia Lorena Tomat ◽  
Francisco Javier Salazar
Keyword(s):  
Metabolic Diseases ◽  
Current Knowledge ◽  
Adult Life ◽  
Developmental Programming ◽  
Renal Diseases ◽  
Future Studies ◽  
Functional Changes ◽  
Regulatory Systems ◽  
Increased Risk ◽  
Renal Changes

AbstractA substantial body of epidemiological and experimental evidence suggests that a poor fetal and neonatal environment may “program” susceptibility in the offspring to later development of cardiovascular, renal and metabolic diseases.This review focuses on current knowledge from the available literature regarding the mechanisms linking an adverse developmental environment with an increased risk for cardiovascular, renal and metabolic diseases in adult life. Moreover, this review highlights important sex-dependent differences in the adaptation to developmental insults.Developmental programming of several diseases is secondary to changes in different mechanisms inducing important alterations in the normal development of several organs that lead to significant changes in birth weight. The different diseases occurring as a consequence of an adverse environment during development are secondary to morphological and functional cardiovascular and renal changes, to epigenetic changes and to an activation of several hormonal and regulatory systems, such as angiotensin II, sympathetic activity, nitric oxide, COX2-derived metabolites, oxidative stress and inflammation. The important sex-dependent differences in the developmental programming of diseases seem to be partly secondary to the effects of sex hormones. Recent studies have shown that the progression of these diseases is accelerated during aging in both sexes.The cardiovascular, renal and metabolic diseases during adult life that occur as a consequence of several insults during fetal and postnatal periods are secondary to multiple structural and functional changes. Future studies are needed in order to prevent the origin and reduce the incidence and consequences of developmental programmed diseases.

scholarly journals Interaction between Parkin and α-Synuclein in PARK2-Mediated Parkinson’s Disease

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 283
Author(s):  
Daniel Aghaie Madsen ◽  
Sissel Ida Schmidt ◽  
Morten Blaabjerg ◽  
Morten Meyer
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Ubiquitin Ligase ◽  
Current Knowledge ◽  
Lewy Bodies ◽  
Ubiquitin Proteasome System ◽  
Loss Of Function ◽  
Functional Interaction ◽  
Future Studies ◽  
Ubiquitin Proteasome

Parkin and α-synuclein are two key proteins involved in the pathophysiology of Parkinson’s disease (PD). Neurotoxic alterations of α-synuclein that lead to the formation of toxic oligomers and fibrils contribute to PD through synaptic dysfunction, mitochondrial impairment, defective endoplasmic reticulum and Golgi function, and nuclear dysfunction. In half of the cases, the recessively inherited early-onset PD is caused by loss of function mutations in the PARK2 gene that encodes the E3-ubiquitin ligase, parkin. Parkin is involved in the clearance of misfolded and aggregated proteins by the ubiquitin-proteasome system and regulates mitophagy and mitochondrial biogenesis. PARK2-related PD is generally thought not to be associated with Lewy body formation although it is a neuropathological hallmark of PD. In this review article, we provide an overview of post-mortem neuropathological examinations of PARK2 patients and present the current knowledge of a functional interaction between parkin and α-synuclein in the regulation of protein aggregates including Lewy bodies. Furthermore, we describe prevailing hypotheses about the formation of intracellular micro-aggregates (synuclein inclusions) that might be more likely than Lewy bodies to occur in PARK2-related PD. This information may inform future studies aiming to unveil primary signaling processes involved in PD and related neurodegenerative disorders.

The essential role of nesfatin-1 as a biological signal on the body systems

2021 ◽  
pp. 113-118
Keyword(s):  
Metabolic Disorders ◽  
Clinical Medicine ◽  
The Body ◽  
World Population ◽  
Peripheral Tissues ◽  
Future Studies ◽  
Body Organ ◽  
Regulate Food Intake ◽  
System Today

Nesfatin-1is first described in 2006 as an anorectic peptide and regulate food intake. In following years, the studies demonstrated the presence of nesfatin-1 in central and various peripheral tissues. Thus, nesfatin-1 popularity increasing widely in clinical medicine, especially in cardiology, neurology, reproduction, metabolic disorders, psychiatric disorders, gastrointestinal system. Today, the main point concerning nesfatin-1 action in body organ and systems is concentrate its biological signals effects. Thus the increasing knowledge in these area will be highlighted for future studies especially in serious health problem all over the world population.

scholarly journals Relationship Between Oxidative Stress, ER Stress, and Inflammation in Type 2 Diabetes: The Battle Continues

2019 ◽  
Vol 8 (9) ◽  
pp. 1385 ◽  
Author(s):  
Burgos-Morón ◽  
Abad-Jiménez ◽  
Marañón ◽  
Iannantuoni ◽  
Escribano-López ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Current Knowledge ◽  
Β Cells ◽  
The Relationship ◽  
And Oxidative Stress

Type 2 diabetes (T2D) is a metabolic disorder characterized by hyperglycemia and insulin resistance in which oxidative stress is thought to be a primary cause. Considering that mitochondria are the main source of ROS, we have set out to provide a general overview on how oxidative stress is generated and related to T2D. Enhanced generation of reactive oxygen species (ROS) and oxidative stress occurs in mitochondria as a consequence of an overload of glucose and oxidative phosphorylation. Endoplasmic reticulum (ER) stress plays an important role in oxidative stress, as it is also a source of ROS. The tight interconnection between both organelles through mitochondrial-associated membranes (MAMs) means that the ROS generated in mitochondria promote ER stress. Therefore, a state of stress and mitochondrial dysfunction are consequences of this vicious cycle. The implication of mitochondria in insulin release and the exposure of pancreatic β-cells to hyperglycemia make them especially susceptible to oxidative stress and mitochondrial dysfunction. In fact, crosstalk between both mechanisms is related with alterations in glucose homeostasis and can lead to the diabetes-associated insulin-resistance status. In the present review, we discuss the current knowledge of the relationship between oxidative stress, mitochondria, ER stress, inflammation, and lipotoxicity in T2D.

scholarly journals Enantiomers of Carbohydrates and Their Role in Ecosystem Interactions: A Review

Symmetry ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 470 ◽  
Author(s):  
Lea Lojkova ◽  
Valerie Vranová ◽  
Pavel Formánek ◽  
Ida Drápelová ◽  
Martin Brtnicky ◽  
...  
Keyword(s):  
Abiotic Stress ◽  
Plant Nutrition ◽  
Current Knowledge ◽  
Genetic Regulation ◽  
Future Research ◽  
Knowledge Gaps ◽  
Research Knowledge ◽  
Critical Knowledge ◽  
Ecosystem Interactions ◽  
Plant Compounds

D- and most L-enantiomers of carbohydrates and carbohydrate-containing compounds occur naturally in plants and other organisms. These enantiomers play many important roles in plants including building up biomass, defense against pathogens, herbivory, abiotic stress, and plant nutrition. Carbohydrate enantiomers are also precursors of many plant compounds that significantly contribute to plant aroma. Microorganisms, insects, and other animals utilize both types of carbohydrate enantiomers, but their biomass and excrements are dominated by D-enantiomers. The aim of this work was to review the current knowledge about carbohydrate enantiomers in ecosystems with respect to both their metabolism in plants and occurrence in soils, and to identify critical knowledge gaps and directions for future research. Knowledge about the significance of D- versus L-enantiomers of carbohydrates in soils is rare. Determining the mechanism of genetic regulation of D- and L-carbohydrate metabolism in plants with respect to pathogen and pest control and ecosystem interactions represent the knowledge gaps and a direction for future research.

scholarly journals Topiramate: use in binge eating disorder?

2012 ◽  
pp. 282-287
Author(s):  
Mauro Gentile ◽  
Giovanni Scanelli
Keyword(s):  
Eating Disorder ◽  
Side Effects ◽  
Binge Eating ◽  
Binge Eating Disorder ◽  
Search Strategy ◽  
Current Knowledge ◽  
Significant Weight Loss ◽  
Good Tool ◽  
Randomized Controlled ◽  
Treatment Of Diabetes

Introduction: Topiramate was serendipitously synthesized in 1979 during research aimed at developing a fructose-1,6-diphosphatase inhibitor that might be used in the treatment of diabetes mellitus. Some investigators have suggested it might be used in the treatment of binge eating disorder (BED). The aim of this review was to evaluate current knowledge and opinions on this topic. Materials and methods: We conducted a search of five electronic databases (PubMed, Embase, Nice, Cochrane, Cinahl) using the search strategy ‘‘topiramate’’ AND ‘‘binge’’, ‘‘binge eating disorder.’’ No time limits were applied, and only reports of randomized controlled trials were included in our analysis. Results: In clinical studies, topiramate use has been associated with significant weight loss mediated by reductions in the frequency of bingeing episodes. The most common side effects of the drug are paresthesias, but nephrolithiasis, oligohydrosis, and dizziness have also been described. Conclusions: Available data are limited, but the literature we reviewed suggests that topiramate can be useful in the medical treatment of BED, reducing both body weight and binge episodes. Side effects are not negligible. Before topiramate can be regarded as a good tool for the treatment of BED, further data must be obtained from longer, methodologically correct studies of larger populations.

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