scholarly journals Cardioprotection conferred by rooibos (Aspalathus linearis): A mini review to highlight a potential mechanism of action

2019 ◽  
Vol 115 (7/8) ◽  
Author(s):  
Gerald J. Maarman
Keyword(s):  
Cardiac Disease ◽  
Energy Homeostasis ◽  
Natural Antioxidants ◽  
Potential Mechanism ◽  
Energy Usage ◽  
Ischaemic Injury ◽  
Adjunct Treatment ◽  
Aspalathus Linearis ◽  
Cardiac Energy ◽  
Underlying Mechanisms

A number of cardioprotective interventions have been identified throughout the years, and these include the use of natural antioxidants in sources like rooibos (Aspalathus linearis) tea. Recent studies have demonstrated that rooibos (either its isolated components or the crude rooibos extract/tea) confers cardioprotection in diabetic cardiomyopathy and myocardial ischaemic injury. In addition, a clinical study has shown that regular rooibos consumption reduces the risk for cardiovascular disease in adults. However, rooibos is currently not considered an official treatment against cardiac disease, mainly because the underlying mechanisms for rooibos-induced cardioprotection are not fully elucidated. Physiological actions of rooibos must be well investigated before rooibos can be used in a clinical setting as adjunct treatment for patients with heart disease. Thus, research to delineate the underlying mechanisms of rooibos-induced cardioprotection is key. In the light of the aforementioned, the available literature on rooibos-induced cardioprotection is reviewed here, highlighting the fact that rooibos preserves and maintains cardiac energy homeostasis. It is postulated that rooibos activates an AMPK-GLUT-4 glucose oxidation (cardiac energy-shortage sensing) pathway to shift cardiac energy usage, thereby conferring cardioprotection.

Novel Non-invasive Approaches to the Treatment of Obesity: From Pharmacotherapy to Gene Therapy

2021 ◽  
Author(s):  
Angeliki M Angelidi ◽  
Matthew J Belanger ◽  
Alexander Kokkinos ◽  
Chrysi C Koliaki ◽  
Christos S Mantzoros
Keyword(s):  
Gene Therapy ◽  
Drug Targets ◽  
Energy Homeostasis ◽  
Treatment Options ◽  
Gastrointestinal Hormones ◽  
Interindividual Variation ◽  
Obesity Epidemic ◽  
Treatment Of Obesity ◽  
Underlying Mechanisms ◽  
Novel Therapeutic Strategies

Abstract Recent insights into the pathophysiologic underlying mechanisms of obesity have led to the discovery of several promising drug targets and novel therapeutic strategies to address the global obesity epidemic and its comorbidities. Current pharmacologic options for obesity management are largely limited in number and of modest efficacy/safety profile. Therefore, the need for safe and more efficacious new agents is urgent. Drugs which are currently under investigation modulate targets across a broad range of systems and tissues, including the central nervous system, gastrointestinal hormones, adipose tissue, kidney, liver, and skeletal muscle. Beyond pharmacotherapeutics, other potential antiobesity strategies are being explored, including novel drug delivery systems, vaccines, modulation of the gut microbiome, and gene therapy. The present review summarizes the pathophysiology of energy homeostasis, and highlights pathways being explored in the effort to develop novel antiobesity medications and interventions but does not cover devices and bariatric methods. Emerging pharmacologic agents and alternative approaches targeting these pathways and relevant research in both animals and humans are presented in detail. Special emphasis is given to treatment options at the end of the development pipeline and closer to the clinic, i.e., compounds that have a higher chance to be added to our therapeutic armamentarium in the near future. Ultimately, advancements in our understanding of the pathophysiology and interindividual variation of obesity may lead to multimodal and personalized approaches to obesity treatment that will result in safe, effective and sustainable weight loss until the root causes of the problem are identified and addressed.

scholarly journals Broken Energy Homeostasis and Obesity Pathogenesis: The Surrounding Concepts

2018 ◽  
Vol 7 (11) ◽  
pp. 453 ◽  
Author(s):  
Abdelaziz Ghanemi ◽  
Mayumi Yoshioka ◽  
Jonny St-Amand
Keyword(s):  
Energy Balance ◽  
Population Health ◽  
Clinical Evaluation ◽  
Health Problem ◽  
Psychological Factors ◽  
Energy Homeostasis ◽  
Fat Accumulation ◽  
Underlying Mechanisms ◽  
Diagnosis Classification

Obesity represents an abnormal fat accumulation resulting from energy imbalances. It represents a disease with heavy consequences on population health and society economy due to its related morbidities and epidemic proportion. Defining and classifying obesity and its related parameters of evaluation is the first challenge toward understanding this multifactorial health problem. Therefore, within this review we report selected illustrative examples of the underlying mechanisms beyond the obesity pathogenesis which is systemic rather than limited to fat accumulation. We also discuss the gut-brain axis and hormones as the controllers of energy homeostasis and report selected impacts of obesity on the key metabolic tissues. The concepts of “broken energy balance” is detailed as the obesity starting key step. Sleep shortage and psychological factors are also reported with influences on obesity development. Importantly, describing such mechanistic pathways would allow clinicians, biologists and researchers to develop and optimize approaches and methods in terms of diagnosis, classification, clinical evaluation, treatment and prognosis of obesity.

Abstract 274: Spatiotemporal Regulation of β Adrenergic Signaling In Heart failure

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Yang K Xiang ◽  
Federica Barbagallo ◽  
Bing Xu ◽  
Qin Fu
Keyword(s):  
Heart Failure ◽  
Plasma Membrane ◽  
Sarcoplasmic Reticulum ◽  
Cardiac Myocytes ◽  
Cardiac Disease ◽  
Spatiotemporal Regulation ◽  
Disease Therapy ◽  
Functional Implications ◽  
Underlying Mechanisms

Our long-term goal is to understand mechanisms that govern spatiotemporal regulation of cAMP/PKA signaling in cardiac myocytes under physiological and pathophysiological conditions, and their implication in cardiac disease therapy. Here we use a series of biosensors to measure cAMP/PKA activity under βAR subtype regulation. In failing cardiac myocytes, the cAMP and PKA activity are shifted from the plasma membrane to the intracellular sarcoplasmic reticulum and the myofilaments. Meanwhile, β2AR displays an increased role in signaling to the myofilaments in failing myocytes when compared to the control myocytes. Moreover, we show that an increased βAR association with phosphodiesterases promotes the alteration in spatiotemporal propagation of cAMP/PKA signaling in failing myocytes. These observations and the underlying mechanisms and functional implications will be discussed.

Bioinformatics-based Prediction of the mechanism and targets for BushenjieduDecoction in preventing relapse of acute leukemia

2020 ◽  
Author(s):  
Weilong Sun ◽  
Fujun Yang ◽  
Weipeng Shi ◽  
Xia Tao ◽  
Zhiwei Xi ◽  
...  
Keyword(s):  
Bioinformatics Analysis ◽  
Topological Analysis ◽  
Traditional Chinese Medicines ◽  
Potential Mechanism ◽  
Ppi Network ◽  
Chinese Medicines ◽  
Kegg Pathways ◽  
Long Time ◽  
Underlying Mechanisms

Abstract Background: Leukemia is a lethal myeloproliferative disorder, its’ relapse following chemotherapy is the major concern in clinical practice. For a long time, we found that traditional Chinese medicines such as Bushenjiedudecoction (BSJD) have significant effects on delaying relapse. However, the underlying mechanisms are not clear, which limits the clinical application of BSJD decoction. Methods: Therefore, we tried to make some explorations in this study. We isolated mesenchymal stem cells (MSC) after treated them with BSJD for proteomic analysis. And then 109 targets were screened out through analysis of the shared proteins of that affected by BSJD and those related to leukemia. Subsequently, the data were analyzed by GO functions, KEGG pathways, PPI network and topological analysis, and then some nodes were selected for animal experiment. Results: As a result, we demonstrated the effective targets of BSJD on MSC through bioinformatics analysis and explored the potential mechanism of BSJD from its influence on niches.These targets contains Hspb1、Dnmt1、Mmp2、Thbs1、Crebbp、Hmgb1、Acta2、Cdkn1b、Atg7、Tsc2 and Icam1. Afterwards, we confirmed BSJD reduced the gene expression of ICAM-1 through cultured MSC in vitro.Conclusions: We screened the potential targets of BSJD on MSC through proteomics and bioinformatics analysis, and selected some genes for experimental verification. These studies demonstrated the effect of BSJD on MSC. We hope that this research method could provide a new way of systematically studying the effects of traditional Chinese medicine on diseases.

scholarly journals Metabolic tuning of inhibition regulates hippocampal neurogenesis in the adult brain

2020 ◽  
Vol 117 (41) ◽  
pp. 25818-25829
Author(s):  
Xinxing Wang ◽  
Hanxiao Liu ◽  
Johannes Morstein ◽  
Alexander J. E. Novak ◽  
Dirk Trauner ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Energy Homeostasis ◽  
Inhibitory Neuron ◽  
Hippocampal Neurogenesis ◽  
Adult Brain ◽  
Adult Hippocampal Neurogenesis ◽  
Neuron Activity ◽  
Adult Mice ◽  
Sphingosine 1 Phosphate ◽  
Underlying Mechanisms

Hippocampus-engaged behaviors stimulate neurogenesis in the adult dentate gyrus by largely unknown means. To explore the underlying mechanisms, we used tetrode recording to analyze neuronal activity in the dentate gyrus of freely moving adult mice during hippocampus-engaged contextual exploration. We found that exploration induced an overall sustained increase in inhibitory neuron activity that was concomitant with decreased excitatory neuron activity. A mathematical model based on energy homeostasis in the dentate gyrus showed that enhanced inhibition and decreased excitation resulted in a similar increase in neurogenesis to that observed experimentally. To mechanistically investigate this sustained inhibitory regulation, we performed metabolomic and lipidomic profiling of the hippocampus during exploration. We found sustainably increased signaling of sphingosine-1-phosphate, a bioactive metabolite, during exploration. Furthermore, we found that sphingosine-1-phosphate signaling through its receptor 2 increased interneuron activity and thus mediated exploration-induced neurogenesis. Taken together, our findings point to a behavior-metabolism circuit pathway through which experience regulates adult hippocampal neurogenesis.

The influence of insulin on circulating ghrelin

2003 ◽  
Vol 284 (2) ◽  
pp. E313-E316 ◽  
Author(s):  
Daniel E. Flanagan ◽  
Mark L. Evans ◽  
Teresa P. Monsod ◽  
Frances Rife ◽  
Rubina A. Heptulla ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Energy Homeostasis ◽  
Insulin Infusion ◽  
Significant Rise ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Physiological Regulator ◽  
Underlying Mechanisms ◽  
Mean Glucose

Ghrelin is a novel peptide that acts on the growth hormone (GH) secretagogue receptor in the pituitary and hypothalamus. It may function as a third physiological regulator of GH secretion, along with GH-releasing hormone and somatostatin. In addition to the action of ghrelin on the GH axis, it appears to have a role in the determination of energy homeostasis. Although feeding suppresses ghrelin production and fasting stimulates ghrelin release, the underlying mechanisms controlling this process remain unclear. The purpose of this study was to test the hypotheses, by use of a stepped hyperinsulinemic eu- hypo- hyperglycemic glucose clamp, that either hyperinsulinemia or hypoglycemia may influence ghrelin production. Having been stable in the period before the clamp, ghrelin levels rapidly fell in response to insulin infusion during euglycemia (baseline ghrelin 207 ± 12 vs. 169 ± 10 fmol/ml at t = 30 min, P < 0.001). Ghrelin remained suppressed during subsequent periods of hypoglycemia (mean glucose 53 ± 2 mg/dl) and hyperglycemia (mean glucose 163 ± 6 mg/dl). Despite suppression of ghrelin, GH showed a significant rise during hypoglycemia (baseline 4.1 ± 1.3 vs. 28.2 ± 3.9 μg/l at t = 120 min, P < 0.001). Our data suggest that insulin may suppress circulating ghrelin independently of glucose, although glucose may have an additional effect. We conclude that the GH response seen during hypoglycemia is not regulated by circulating ghrelin.

scholarly journals FOXO1, a Potential Therapeutic Target, Regulates Autophagic Flux, Oxidative Stress, Mitochondrial Dysfunction, and Apoptosis in Human Cholangiocarcinoma QBC939 Cells

2018 ◽  
Vol 45 (4) ◽  
pp. 1506-1514 ◽  
Author(s):  
Wei He ◽  
Aiqing Zhang ◽  
Lei Qi ◽  
Chen Na ◽  
Rui Jiang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Therapeutic Target ◽  
Energy Homeostasis ◽  
Serum Starvation ◽  
Autophagic Flux ◽  
Potential Therapeutic Target ◽  
New Strategy ◽  
Underlying Mechanisms ◽  
Foxo1 Gene

Background/Aims: Autophagy is an evolutionarily conserved catabolic mechanism to maintain energy homeostasis and to remove damaged cellular components, which plays an important role in the survival of various cells. Inhibiting autophagy is often applied as a new strategy to halt the growth of cancer cells. Methods: The effect of FOXO1 gene on cellular function and apoptosis and its underlying mechanisms were investigated in cultured QBC939 cells by the methylthiazoletetrazolium (MTT) assay, western blot, DCFDA mitochondrial membrane potential, and ATP content measurement. FOXO1 siRNA was applied to down-regulate FOXO1 expression in QBC939 cells. Results: Here we reported that FOXO1, acetylation of FOXO1 (Ac-FOXO1) and the following interaction between Ac-FOXO1 and Atg7 regulated the basal and serum starvation (SS)-induced autophagy as evidenced by light chain 3 (LC3) accumulation and p62 degration. Either treatment with FOXO1 siRNA or resveratrol, a sirt1 agonist, inhibited autophagic flux, resulting in oxidative stress, mitochondrial dysfunction (MtD) and apoptosis in QBC939 cells, which were attenuated by enhancing autophagy with rapamycin. On the contrary, inhibiting autophagic flux with 3-MA worsened all these effects in QBC939 cells. Conclusions: Taken together, our study for the first time identified FOXO1 as a potential therapeutic target to cure against human cholangiocarcinoma via regulation of autophagy, oxidative stress and MtD.

scholarly journals Hypothalamic AMPK as a Mediator of Hormonal Regulation of Energy Balance

2018 ◽  
Vol 19 (11) ◽  
pp. 3552 ◽  
Author(s):  
Baile Wang ◽  
Kenneth Cheng
Keyword(s):  
Energy Balance ◽  
Hormonal Regulation ◽  
Energy Homeostasis ◽  
Adenosine Monophosphate ◽  
Acid Oxidation ◽  
Peripheral Tissues ◽  
Adaptive Thermogenesis ◽  
Increase Food Intake ◽  
Regulatory Effects ◽  
Underlying Mechanisms

As a cellular energy sensor and regulator, adenosine monophosphate (AMP)-activated protein kinase (AMPK) plays a pivotal role in the regulation of energy homeostasis in both the central nervous system (CNS) and peripheral organs. Activation of hypothalamic AMPK maintains energy balance by inducing appetite to increase food intake and diminishing adaptive thermogenesis in adipose tissues to reduce energy expenditure in response to food deprivation. Numerous metabolic hormones, such as leptin, adiponectin, ghrelin and insulin, exert their energy regulatory effects through hypothalamic AMPK via integration with the neural circuits. Although activation of AMPK in peripheral tissues is able to promote fatty acid oxidation and insulin sensitivity, its chronic activation in the hypothalamus causes obesity by inducing hyperphagia in both humans and rodents. In this review, we discuss the role of hypothalamic AMPK in mediating hormonal regulation of feeding and adaptive thermogenesis, and summarize the diverse underlying mechanisms by which central AMPK maintains energy homeostasis.

Exercise as Therapy for Schizophrenia: An Ethnographic Study

1999 ◽  
Vol 21 (1) ◽  
pp. 52-69 ◽  
Author(s):  
Guy Faulkner ◽  
Andrew Sparkes
Keyword(s):  
Participant Observation ◽  
Psychiatric Rehabilitation ◽  
Exercise Program ◽  
Self Esteem ◽  
Ethnographic Study ◽  
Primary Sources ◽  
Adjunct Treatment ◽  
Research Paradigms ◽  
Alternative Research ◽  
Underlying Mechanisms

As part of the emergence of alternative research paradigms in exercise and sport psychology, we draw upon data from an ethnographic study of 3 individuals with schizophrenia to explore the use of exercise as an adjunct therapy for schizophrenia. A 10-week exercise program of twice-weekly sessions was implemented. Participant observation and interviews with participants and their assigned key-workers were the primary sources of data collection used. The influence of exercise on the lives of participants and their mental health and the underlying mechanisms of change were explored. Our findings indicate that exercise has the potential to help reduce participants’ perceptions of auditory hallucinations, raise self-esteem, and improve sleep patterns and general behavior. The process of exercising, via the provision of distraction and social interaction rather than the exercise itself, was very influential in providing these benefits. In conclusion, we strongly recommend the inclusion of exercise as an adjunct treatment in psychiatric rehabilitation.

scholarly journals Current Landscape: The Mechanism and Therapeutic Impact of Obesity for Breast Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Chongru Zhao ◽  
Weijie Hu ◽  
Yi Xu ◽  
Dawei Wang ◽  
Yichen Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Energy Homeostasis ◽  
Treatment Strategies ◽  
Therapeutic Interventions ◽  
Novel Treatment ◽  
Common Cancer ◽  
Prevalence Of Obesity ◽  
Novel Treatment Strategies ◽  
Underlying Mechanisms ◽  
The Impact

Obesity is defined as a chronic disease induced by an imbalance of energy homeostasis. Obesity is a widespread health problem with increasing prevalence worldwide. Breast cancer (BC) has already been the most common cancer and one of the leading causes of cancer death in women worldwide. Nowadays, the impact of the rising prevalence of obesity has been recognized as a nonnegligible issue for BC development, outcome, and management. Adipokines, insulin and insulin-like growth factor, sex hormone and the chronic inflammation state play critical roles in the vicious crosstalk between obesity and BC. Furthermore, obesity can affect the efficacy and side effects of multiple therapies such as surgery, radiotherapy, chemotherapy, endocrine therapy, immunotherapy and weight management of BC. In this review, we focus on the current landscape of the mechanisms of obesity in fueling BC and the impact of obesity on diverse therapeutic interventions. An in-depth exploration of the underlying mechanisms linking obesity and BC will improve the efficiency of the existing treatments and even provide novel treatment strategies for BC treatment.

Sign in / Sign up

Export Citation Format

Share Document