scholarly journals Adiponectin and Inflammation in Health and Disease: An Update

2018 ◽  
Vol 5 (1) ◽  
pp. 20-32 ◽  
Author(s):  
Alice G. Geagea ◽  
Samir Mallat ◽  
Charbel F. Matar ◽  
Raymond Zerbe ◽  
Estelle Filfili ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Medical Attention ◽  
Therapeutic Approaches ◽  
Major Health Problem ◽  
Major Health ◽  
Tnf Α ◽  
Inflammatory State ◽  
Health And Disease ◽  
Important Cytokine

Adiponectin, a protein secreted by adipocytes, gained a special medical attention in the past two decades mostly due to its relation to obesity, a major health problem worldwide. Moreover, adiponectin has shown to have a preventive effect on insulin resistance, diabetes and cardiovascular diseases. Lately, obesity has been classified as a chronic inflammatory state, whereby dysregulated adipocytes and high infiltration of macrophages shift toward the production of pro-inflammatory cytokines like TNF-α and IL-6 among others. This status contributes to a decrease in adiponectin levels, thus leading to the emergence of obesity related complications. This review will focus on the hormone adiponectin and its mechanisms of action in relation to insulin resistance, diabetes, cardiovascular effect and atherosclerosis. It will also cover the various therapeutic approaches aiming to increase the levels of this important cytokine, and to highlight the promising role of AdipoRon, an adiponectin receptor agonist, and of diet.

Wogonin Alleviates Hyperglycemia Through Increased Glucose Entry into Cells Via AKT/GLUT4 Pathway

2019 ◽  
Vol 25 (23) ◽  
pp. 2602-2606 ◽  
Author(s):  
Shahzad Khan ◽  
Mohammad A. Kamal
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Modern World ◽  
Major Health Problem ◽  
Major Health ◽  
Chronic Hyperglycemia ◽  
Main Factor

: Insulin resistance and type 2 Diabetes mellitus resulting in chronic hyperglycemia is a major health problem in the modern world. Many drugs have been tested to control hyperglycemia which is believed to be the main factor behind many of the diabetes-related late-term complications. Wogonin is a famous herbal medicine which has been shown to be effective in controlling diabetes and its complications. In our previous work, we showed that wogonin is beneficial in many ways in controlling diabetic cardiomyopathy. In this review, we mainly explained wogonin anti-hyperglycemic property through AKT/GLUT4 pathway. Here we briefly discussed that wogonin increases Glut4 trafficking to plasma membrane which allows increased entry of glucose and thus alleviates hyperglycemia. Conclusion: Wogonin can be used as an anti-diabetic and anti-hyperglycemic drug and works via AKT/GLUT4 pathway.

scholarly journals The Gut Ecosystem: A Critical Player in Stroke

2020 ◽  
Author(s):  
Rosa Delgado Jiménez ◽  
Corinne Benakis
Keyword(s):  
Current Knowledge ◽  
Critical Factor ◽  
Intestinal Microbiome ◽  
Brain Disorders ◽  
Therapeutic Approaches ◽  
Health And Disease ◽  
Brain Stroke ◽  
The Brain ◽  
Improve Patient

AbstractThe intestinal microbiome is emerging as a critical factor in health and disease. The microbes, although spatially restricted to the gut, are communicating and modulating the function of distant organs such as the brain. Stroke and other neurological disorders are associated with a disrupted microbiota. In turn, stroke-induced dysbiosis has a major impact on the disease outcome by modulating the immune response. In this review, we present current knowledge on the role of the gut microbiome in stroke, one of the most devastating brain disorders worldwide with very limited therapeutic options, and we discuss novel insights into the gut-immune-brain axis after an ischemic insult. Understanding the nature of the gut bacteria-brain crosstalk may lead to microbiome-based therapeutic approaches that can improve patient recovery.

scholarly journals Exploring the Role of Endothelial Cell Resilience in Cardiovascular Health and Disease

2020 ◽  
Author(s):  
Yunling Gao ◽  
Zorina S. Galis
Keyword(s):  
Risk Factors ◽  
Paradigm Shift ◽  
Cardiovascular Health ◽  
Research Effort ◽  
Future Research ◽  
Therapeutic Approaches ◽  
New Knowledge ◽  
Health And Disease ◽  
Disease Understanding

Traditionally, much research effort has been invested into focusing on disease, understanding pathogenic mechanisms, identifying risk factors, and developing effective treatments. A few recent studies unraveling the basis for absence of disease, including cardiovascular disease, despite existing risk factors, a phenomenon commonly known as resilience, are adding new knowledge and suggesting novel therapeutic approaches. Given the central role of endothelial function in cardiovascular health, we herein provide a number of considerations that warrant future research and considering a paradigm shift toward identifying the molecular underpinnings of endothelial resilience.

The Role of TNF-α in Insulin Resistance

Endocrine ◽  
2004 ◽  
Vol 23 (2-3) ◽  
pp. 177-182 ◽  
Author(s):  
Stephen E. Borst
Keyword(s):  
Insulin Resistance ◽  
Tnf Α

scholarly journals Precision Preventive Medicine of Relapse in Smoking Cessation: Can MRI Inform the Search of Intermediate Phenotypes?

Biology ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 35
Author(s):  
Yolaine Rabat ◽  
Sandra Chanraud ◽  
Majd Abdallah ◽  
Igor Sibon ◽  
Sylvie Berthoz
Keyword(s):  
Smoking Cessation ◽  
Meta Analysis ◽  
Major Health Problem ◽  
Major Health ◽  
Smoking Cessation Treatment ◽  
Intermediate Phenotypes ◽  
Prevention Therapy ◽  
Cessation Treatment ◽  
Magnetic Resonance Imaging Mri

Chronic tobacco smoking remains a major health problem worldwide. Numerous smokers wish to quit but most fail, even if they are helped. The possibility of identifying neuro-biomarkers in smokers at high risk of relapse could be of incredible progress toward personalized prevention therapy. Our aim is to provide a scoping review of this research topic in the field of Magnetic Resonance Imaging (MRI) and to review the studies that investigated if MRI defined markers predicted smoking cessation treatment outcome (abstainers versus relapsers). Based on the available literature, a meta-analysis could not be conducted. We thus provide an overview of the results obtained and take stock of methodological issues that will need to be addressed to pave the way toward precision medicine. Based on the most consistent findings, we discuss the pivotal role of the insula in light of the most recent neurocognitive models of addiction.

scholarly journals The Mechanistic and Pathophysiological Role of Adiponectin and Resistin Towards Regulation of Food Intake and Appetite in Cardiovascular Associated Risk Factor of Metabolic Syndrome

2021 ◽  
Author(s):  
Mimie Noratiqah Jumli ◽  
Muhammad Ilyas Nadeem
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Food Intake ◽  
Urban Population ◽  
Insulin Resistance Syndrome ◽  
Mediating Effect ◽  
Syndrome X ◽  
Therapeutic Approaches ◽  
Pathophysiological Role

Insulin resistance syndrome or syndrome X is also known as metabolic syndrome (MetS). It is an emerging problem globally with the surge of increasing prevalence among urban population of developing countries. The etiology of pathophysiology of metabolic syndrome includes the inflammatory pathways of insulin resistance, deregulated appetite, diet-induced, inflammation-induced obesity, and cardiovascular diseases (CVD). Adipose tissue is an endocrine organ that secrets adipokines like adiponectin and resistin during physiological and pathological states. Moreover, the adipokines associated with diet-induced and inflammation-induced obesity have secondary deteriorating effects on cardiovascular system. Although, the adiponectin and resistin were potentially found in regulating food intake and appetite but their mediating effect on pathophysiology of CVD still needs future investigations. However, the prior studies reported the association of adiponectin and resistin levels with CVD complications related to food intake but still there is need to understand its multifactorial heterogeneity. Therefore, literature suggests figuring out potential target mechanistic and therapeutic approaches of adiponectin and resistin hormone towards food intake and appetite involvement in metabolic syndrome and CVD.

scholarly journals TNF-α and Hyperandrogenism: A Clinical, Biochemical, and Molecular Genetic Study

2001 ◽  
Vol 86 (8) ◽  
pp. 3761-3767 ◽  
Author(s):  
Héctor F. Escobar-Morreale ◽  
Rosa M. Calvo ◽  
José Sancho ◽  
José L. San Millán
Keyword(s):  
Insulin Resistance ◽  
Body Mass Index ◽  
Body Mass ◽  
Molecular Genetic ◽  
Molecular Genetic Study ◽  
Tnf Α ◽  
Serum Androgens ◽  
17 Hydroxyprogesterone ◽  
The Relationship

To evaluate the role of TNF-α in the pathogenesis of hyperandrogenism, we have evaluated the serum TNF-α levels, as well as several polymorphisms in the promoter region of the TNF-α gene, in a group of 60 hyperandrogenic patients and 27 healthy controls matched for body mass index. Hyperandrogenic patients presented with mildly increased serum TNF-α levels as compared with controls (mean[median] ± sd: 7.2[7.0] ± 3.3 pg/ml vs. 5.6[4.4] ± 4.0 pg/ml, P < 0.02). Although no differences in body mass index and insulin resistance indexes were observed between patients and controls, when subjects were classified by body weight, serum TNF-α was increased only in lean patients as compared with lean controls, but this difference was not statistically significant when comparing obese patients with obese controls. The TNF-α gene polymorphisms studied here (−1196C/T, −1125G/C,− 1031T/C, −863C/A, −857C/T, −316G/A, −308G/A, −238G/A, and− 163G/A) were equally distributed in hyperandrogenic patients and controls. However, carriers of the −308A variant presented with increased basal and leuprolide-stimulated serum androgens and 17-hydroxyprogesterone levels when considering patients and controls as a group. No differences were observed in serum TNF-α levels, body mass index, and insulin resistance indexes, depending on the presence or absence of these variants. In conclusion, our present results suggest that the TNF-α system might contribute to the pathogenesis of hyperandrogenism, independent of obesity and insulin resistance. However, elucidation of the precise mechanisms underlying the relationship between the TNF-α system and androgen excess is needed before considering TNF-α as a significant contributing factor to the development of hyperandrogenism.

Abstract 15225: Post-ischemic Myocardial Insulin Resistance Induced by Tnf-α Overproduction Precipitates the Development of Heart Failure After Myocardial Infarction

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Feng Fu ◽  
Jia Li ◽  
Jie Xu ◽  
Yuan Zhang ◽  
Chao Gao ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Insulin Signaling ◽  
Left Ventricular ◽  
Separate Experiment ◽  
Tnf Α ◽  
Lv Remodeling ◽  
Myocardial Insulin Resistance

Objectives: Clinical evidence has demonstrated a decreased myocardial insulin response in HF patients. However, the role of myocardial insulin resistance and the underlying mechanisms in HF are largely unclear. Methods and Results: Sprague Dawley rats subjected to myocardial infarction (MI) resulted in a progressive left ventricular (LV) remodeling and dysfunction. Echocardiographic assessment showed preserved LV end-systolic dimension (LVESD 0.453 ± 0.027 cm) and ejection fraction (EF 57.03 ± 2.35%) at 1 wk after MI, and evident LV dilation (LVESD 0.612 ± 0.026 cm) and dysfunction (EF 40.21 ± 3.09%) at 4 wk after MI. Myocardial insulin sensitivity decreased significantly at 1 wk after MI as evidenced by reduced insulin-stimulated myocardial fluorodeoxyglucose uptake (Standardized Uptake Value: 2.71 ± 0.42 vs. 5.13 ± 0.51 of sham+insulin, n=6, P <0.01) and GLUT-4 translocation and altered insulin signaling, whereas systemic insulin sensitivity remained unchanged. Mechanistically, myocardial TNF-α production was increased following MI. Treatment with etanercept (a TNF-α inhibitor) post-MI improved myocardial insulin sensitivity, while adenovirus-mediated overexpression of TNF-α resulted in myocardial insulin resistance in non-MI hearts. In addition, TNF-α overexpressed rat hearts exhibited LV dysfunction (EF 41.32 ± 4.21%) and LV dilation as early as 1 wk after MI. Moreover, insulin treatment during the first week following MI suppressed myocardial TNF-α production and increased myocardial insulin sensitivity, resulting in alleviated cardiac dysfunction and remodeling at 4 wk after MI. Importantly, in a separate experiment, cardiomyocyte-specific insulin receptor knockout mice exhibited aggravated post-ischemic LV remodeling and dysfunction compared with littermate controls. Conclusions: Our data provide novel insights that myocardial insulin resistance, independently of systemic insulin resistance, precipitates the development of post-ischemic HF. Myocardial insulin resistance is an early event partly attributed to myocardial TNF-α overproduction following MI. This finding indicates the essential role of myocardial insulin signaling in protection against ischemic HF.

scholarly journals Inflammation as a potential link between nonalcoholic fatty liver disease and insulin resistance

2013 ◽  
Vol 218 (3) ◽  
pp. R25-R36 ◽  
Author(s):  
Mohamed Asrih ◽  
François R Jornayvaz
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Metabolic Energy ◽  
Hepatic Insulin Resistance ◽  
Major Health Problem ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) has become a major health problem in developed countries. It has affected more than 30% of the general population and is commonly associated with insulin resistance, which is a major risk factor for the development of type 2 diabetes and a central feature of the metabolic syndrome. Furthermore, accumulating evidences reveal that NAFLD as well as insulin resistance is strongly related to inflammation. Cytokines and adipokines play a pivotal role in inflammatory processes. In addition, these inflammatory mediators regulate various functions including metabolic energy balance, inflammation, and immune response. However, their role in modulating ectopic lipids involved in the development of insulin resistance, such as diacylglycerols and ceramides, remains unknown. The aim of this review is first to describe the pathophysiology of insulin resistance in NAFLD. In particular, we discuss the role of ectopic lipid accumulation in the liver. Secondly, we also summarize recent findings emphasizing the role of main inflammatory markers in both NAFLD and insulin resistance and their potential role in modulating hepatic fat content in NAFLD and associated hepatic insulin resistance.

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