scholarly journals Adiposopathy as a key factor in the development of insulin resistance

2012 ◽  
Vol 18 (2) ◽  
pp. 164-176 ◽  
Author(s):  
E. I. Krasilnikova ◽  
YA. V. Blagosklonnaya ◽  
A. A. Bystrova ◽  
E. I. Baranova ◽  
M. A. Chilashvili ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Endothelial Dysfunction ◽  
Target Therapy ◽  
Metabolic Abnormalities ◽  
Key Factor ◽  
Underlying Mechanisms ◽  
Obesity Hypertension ◽  
Genetically Determined ◽  
Metabolic Cardiovascular Syndrome ◽  
Main Factor

The metabolic cardiovascular syndrome (MS) is a common cluster of metabolic abnormalities (abdominal obesity, hypertension, dyslipidemia and carbohydrate metabolism disorders) that are related to insulin resistance and hyperinsulinemia and are associated with accelerated atherogenesis. Insulin excess is known to promote the development of the whole metabolic cascade. Recently it has been shown that the inflammatory and hemostatic abnormalities, immunological disorders, endothelial dysfunction, hyperhomocysteinemia and hyperuricemia are also important features of MS. Despite the numerous studies of MS its underlying cause is still not established. The dysfunction of visceral adipocytes (adiposopathy) might be genetically determined, and is considered nowadays as the main factor contributing to the development of the MS. Understanding the underlying mechanisms is of particular interest for prevention and target therapy of all the components of MS.

Abstract 118: Adipose Inflammation Is Critically Involved in the Progression of Heart Failure During Pressure Overload

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Ippei Shimizu ◽  
Tohru Minamino ◽  
Yohko Yoshida ◽  
Taro Katsuno ◽  
Issei Komuro ◽  
...  
Keyword(s):  
Heart Failure ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Cardiac Function ◽  
Systolic Dysfunction ◽  
Pressure Overload ◽  
Chronic Phase ◽  
Metabolic Abnormalities ◽  
Underlying Mechanisms ◽  
Adipose Inflammation

Several clinical studies have shown that insulin resistance is prevalent among patients with impaired cardiac function and that systemic insulin resistance is the risk factor for the development of heart failure; however, underlying mechanisms have not been fully elucidated. We have previously reported that increased p53 level in adipose tissue is crucially involved in adipose inflammation and insulin resistance during pressure overload. Here we show that . Pressure overload increased sympathetic activity and promoted lipolysis in adipose tissue. Accelerated lipolysis resulted in increases of reactive oxygen species and DNA damage, leading to up-regulation of adipose p53. This up-regulation activated the NF-kappaB pathway and induced adipose inflammation and insulin resistance. Genetic disruption of adipose p53 markedly attenuated adipose inflammation and metabolic abnormalities associated with heart failure. We also observed that cardiac function and survival in the chronic phase of heart failure were significantly better in adipose tissue p53-deficient mice than control littermates. Pharmacological inhibition of adipose p53 after imposing pressure overload also improved cardiac dysfunction as well as insulin resistance in the chronic phase of heart failure. These results suggest that inhibition of adipose inflammation is a potential target for treating metabolic abnormalities and systolic dysfunction in patients with heart failure.

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.

Endothelial Dysfunction, Obesity and Insulin Resistance

2014 ◽  
Vol 12 (3) ◽  
pp. 412-426 ◽  
Author(s):  
Dolores Prieto ◽  
Cristina Contreras ◽  
Ana Sanchez
Keyword(s):  
Insulin Resistance ◽  
Endothelial Dysfunction

Increased Endothelial Dysfunction and Insulin Resistance in Patients with Klinefelter Syndrome

2018 ◽  
Vol 18 (4) ◽  
pp. 401-406 ◽  
Author(s):  
Cem Haymana ◽  
Aydogan Aydogdu ◽  
Ibrahim Demirci ◽  
Mustafa Dinc ◽  
Orhan Demir ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Endothelial Dysfunction ◽  
Klinefelter Syndrome

Insulin Resistance and Glucose Homeostasis in Peritoneal Dialysis

2009 ◽  
Vol 29 (2_suppl) ◽  
pp. 145-148 ◽  
Author(s):  
Paulo Cezar Fortes ◽  
Thyago Proença de Moraes ◽  
Jamille Godoy Mendes ◽  
Andrea E. Stinghen ◽  
Silvia Carreira Ribeiro ◽  
...  
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Peritoneal Dialysis ◽  
Metabolic Disorders ◽  
Patient Survival ◽  
Metabolic Abnormalities ◽  
Dialysis Fluid ◽  
Altered Glucose ◽  
Insulin Homeostasis ◽  
Therapeutic Measures

Cardiovascular disease (CVD) is the main cause of death in peritoneal dialysis (PD) patients, a situation that can be explained by a combination of traditional and nontraditional risk factors for CVD in these patients. Glucose and insulin homeostasis are altered in chronic kidney disease (CKD) patients even in the early stages of CKD, leading to insulin resistance by various pathways. Several factors have been implicated in the pathogenesis of insulin resistance, including anemia, dyslipidemia, uremia, malnutrition, excess of parathyroid hormone, vitamin D deficiency, metabolic acidosis, and increase in plasma free fatty acids and proinflammatory cytokines. Insulin resistance and dyslipidemia are observed and increase with the progression of CKD, playing an important role in the pathogenesis of hypertension and atherosclerosis. Particularly in PD patients, exposure to glucose from dialysis fluid accentuates the foregoing metabolic abnormalities. In conclusion, insulin resistance and altered glucose metabolism are frequently observed in CKD, and although dialysis partly corrects those disturbances, the use of glucose PD solutions intensifies a series of harmful metabolic consequences. New therapeutic measures aimed at reducing metabolic disorders are urgently needed and perhaps will improve PD patient survival.

Magnesium intake, insulin resistance and markers of endothelial function among women

2021 ◽  
pp. 1-9
Author(s):  
Narges Ghorbani Bavani ◽  
Parvane Saneei ◽  
Ammar Hassanzadeh Keshteli ◽  
Ahmadreza Yazdannik ◽  
Ebrahim Falahi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Adhesion Molecule ◽  
Cell Function ◽  
Intercellular Adhesion Molecule ◽  
Model Assessment ◽  
Serum Concentrations ◽  
Homeostasis Model Assessment

Abstract Objective: We investigated the association of dietary Mg intake with insulin resistance and markers of endothelial function among Iranian women. Design: A cross-sectional study. Setting: Usual dietary intakes were assessed using a validated FFQ. Dietary Mg intake was calculated by summing up the amount of Mg in all foods. A fasting blood sample was taken to measure serum concentrations of glycemic indices (fasting plasma glucose and insulin) and endothelial function markers (E-selectin, soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1). Insulin resistance and sensitivity were estimated using the Homeostasis Model Assessment-Insulin Resistance (HOMA-IR), Homeostasis Model Assessment β-cell function (HOMA-β) and quantitative insulin sensitivity check index (QUICKI). Participants: Iranian female nurses (n 345) selected by a multistage cluster random sampling method. Results: The Mg intake across energy-adjusted quartiles was 205 (se 7), 221·4 (se 8), 254·3 (se 7) and 355·2 (se 9) mg/d, respectively. After adjustments for potential confounders, QUICKI level was significantly different across quartiles of Mg intake (Q1: 0·34 (se 0·02), Q2: 0·36 (se 0·01), Q3: 0·40 (se 0·01), and Q4: 0·39 (se 0·02), P = 0·02); however, this association disappeared after considering markers of endothelial function, indicating that this relation might be mediated through endothelial dysfunction. After controlling for all potential confounders, Mg intake was inversely, but not significantly, associated with serum concentrations of sICAM (Q1: 239 (se 17), Q2: 214 (se 12), Q3: 196 (se 12), and Q4: 195 (se 17), P = 0·29). There was no other significant association between dietary Mg intake and other indicators of glucose homoeostasis or endothelial markers. Conclusions: Higher dietary Mg intake was associated with better insulin sensitivity in Iranian females. This linkage was mediated through reduced endothelial dysfunction.

scholarly journals Vitamin E beyond Its Antioxidant Label

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 634
Author(s):  
Anca Ungurianu ◽  
Anca Zanfirescu ◽  
Georgiana Nițulescu ◽  
Denisa Margină
Keyword(s):  
Vitamin E ◽  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Protective Effects ◽  
Cellular Effects ◽  
Inflammatory Status ◽  
Anti Cancer ◽  
Key Factor ◽  
Exciting Potential ◽  
Underlying Mechanisms

Vitamin E, comprising tocopherols and tocotrienols, is mainly known as an antioxidant. The aim of this review is to summarize the molecular mechanisms and signaling pathways linked to inflammation and malignancy modulated by its vitamers. Preclinical reports highlighted a myriad of cellular effects like modulating the synthesis of pro-inflammatory molecules and oxidative stress response, inhibiting the NF-κB pathway, regulating cell cycle, and apoptosis. Furthermore, animal-based models have shown that these molecules affect the activity of various enzymes and signaling pathways, such as MAPK, PI3K/Akt/mTOR, JAK/STAT, and NF-κB, acting as the underlying mechanisms of their reported anti-inflammatory, neuroprotective, and anti-cancer effects. In clinical settings, not all of these were proven, with reports varying considerably. Nonetheless, vitamin E was shown to improve redox and inflammatory status in healthy, diabetic, and metabolic syndrome subjects. The anti-cancer effects were inconsistent, with both pro- and anti-malignant being reported. Regarding its neuroprotective properties, several studies have shown protective effects suggesting vitamin E as a potential prevention and therapeutic (as adjuvant) tool. However, source and dosage greatly influence the observed effects, with bioavailability seemingly a key factor in obtaining the preferred outcome. We conclude that this group of molecules presents exciting potential for the prevention and treatment of diseases with an inflammatory, redox, or malignant component.

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