Circulating Chemerin, Oxidative Stress, Inflammation and Insulin Resistance in Morbid Obesity

2017 ◽  
Vol 68 (5) ◽  
pp. 1014-1018 ◽  
Author(s):  
Viviana Aursulesei ◽  
Siminela Bulughiana ◽  
Bogdan Alexandru Stoica ◽  
Ecaterina Anisie

Chemerin is a relatively novel adipokine with controversial pathophysiological role in obesity. Our study aimed to investigate the relationship of serum chemerin level with inflammation, oxidative stress and insulin resistance in morbidly obese subjects. Circulating chemerin was an independent predictor of TNF-Q level, superoxide dismutase activity and lipid peroxidation, but no relation with insulin resistance could be sustained. Taken together chemerin could be a marker of dysfunctional adipose tissue, but its serum level does not reflect properly the metabolic phenotype in morbid obesity.

2018 ◽  
Vol 15 (3) ◽  
pp. 14-20
Author(s):  
Yassine Chahirou ◽  
Abdelhalim Mesfioui ◽  
Ali Ouichou ◽  
Aboubaker Hessni

Current studies show that metabolic and behavioral disorders represent severe health problems. Several questions arise about the molecular relationship of metabolic and behavioral disorders. This review will discuss the relationship of lipid metabolism and fructose consumption accompanied by an increase in weight as well as associated disorders: hypertension, insulin-resistance, oxidative stress and depression. Adipose tissue is considered as an endocrine tissue with intense secretory activities (metabolic and inflammatory). These adipokines are responsible for an alteration of several physiological functions. In this review we will try to understand how lipogenesis that causes dyslipidemia can influence insulin resistance, hypertension, oxidative stress, depression and the relationship between these various disorders.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1812-P
Author(s):  
MARIA D. HURTADO ◽  
J.D. ADAMS ◽  
MARCELLO C. LAURENTI ◽  
CHIARA DALLA MAN ◽  
CLAUDIO COBELLI ◽  
...  

2003 ◽  
Vol 149 (4) ◽  
pp. 331-335 ◽  
Author(s):  
JV Silha ◽  
M Krsek ◽  
JV Skrha ◽  
P Sucharda ◽  
BL Nyomba ◽  
...  

OBJECTIVE: Adipose tIssue regulates insulin sensitivity via the circulating adipocytokines, leptin, resistin and adiponectin. The objective of this study was to compare the levels of resistin, adiponectin and leptin in lean and obese subjects and determine the relationship between circulating adipocytokines and insulin resistance. METHODS: We examined plasma levels of resistin, adiponectin and leptin in 17 lean subjects with a mean body mass index (BMI) of approximately 23 and 34 non-diabetic obese individuals with a mean BMI approximately 33. Insulin resistance was assessed using the homeostasis model assessment ratio (HOMA-R) formula derived from fasting insulin and glucose levels. RESULTS: Resistin levels were not significantly different between the two groups but were significantly higher in women compared with men, 35.4+/-6.5 (s.e.) vs 15.4+/-2.9 microg/L, P<0.01. Resistin did not correlate with BMI but did significantly correlate with HOMA-R, P<0.01, and this correlation remained significant after adjustment for gender and BMI. Adiponectin levels were significantly lower in obese compared with lean subjects, P<0.005, and higher in women, P<0.001, but showed no significant correlation with HOMA-R. Leptin levels were significantly higher in obese subjects and women and correlated with HOMA-R and resistin. DISCUSSION: In this small group of patients we demonstrated that insulin resistance correlated most strongly with leptin levels. A significant correlation between resistin levels and insulin resistance was also observed. Although a similar trend was apparent for adiponectin, the correlation with insulin resistance did not achieve statistical significance.


2011 ◽  
Vol 31 (5) ◽  
pp. 1208-1214 ◽  
Author(s):  
Sander J. Robins ◽  
Asya Lyass ◽  
Justin P. Zachariah ◽  
Joseph M. Massaro ◽  
Ramachandran S. Vasan

2009 ◽  
Vol 66 (3) ◽  
pp. 346-349 ◽  
Author(s):  
Elvira Verduci ◽  
Silvia Scaglioni ◽  
Carlo Agostoni ◽  
Giovanni Radaelli ◽  
Marialuisa Biondi ◽  
...  

2021 ◽  
Vol 10 (10) ◽  
pp. 1326-1336
Author(s):  
Nannan Bian ◽  
Xiaomeng Sun ◽  
Biao Zhou ◽  
Lin Zhang ◽  
Qiu Wang ◽  
...  

Objective Bariatric surgery has become the most effective treatment for morbid obesity. Increasing evidence showed that bariatric surgery can alleviate insulin resistance and influence thyroid function. This study aimed to investigate the relationship between changes in thyroid function and adipose tissue insulin resistance (adipo-IR) after bariatric surgery. Methods A total of 287 non-diabetic participants with regular thyroid function were recruited and divided into the lean, overweight and obese groups. Among them, 50 morbidly obese patients submitted to bariatric surgery. Results The obese group had a higher level of adipo-IR, thyroid-stimulating hormone (TSH), free triiodothyronine (FT3), FT3/free thyroxine (FT4) and metabolism disorders than the lean and overweight groups. BMI was correlated with TSH, FT3, FT3/FT4 and adipo-IR (r = 0.309, 0.315, 0.322 and 0.651, respectively, all P < 0.001). Adipo-IR was significantly correlated with TSH (r = 0.402, P < 0.001), FT3 (r = 0.309, P < 0.001), and FT3/FT4 (r = 0.228, P < 0.05). Bariatric surgery resulted in a sharp decline in BMI, adipo-IR, TSH, FT3 and FT3/FT4 levels, meanwhile, metabolic disorders improved. The decrease in BMI after bariatric surgery was significantly correlated with reductions in adipo-IR (r = 0.577, P < 0.001) and TSH (r = 0.401, P = 0.005). Interestingly, the fasting blood glucose, fasting insulin, adipo-IR and TSH in the higher TSH group decreased more remarkably than in the lower TSH group. Conclusion Obese individuals with higher TSH levels had an obvious metabolic improvement after bariatric surgery.


2021 ◽  
Vol 20 (4) ◽  
pp. 2746
Author(s):  
A. V. Svarovskaya ◽  
A. A. Garganeeva

Adipose tissue is currently regarded as a key organ for excess dietary lipids, which determine whether the body will maintain normal homeostasis or whether inflammation and insulin resistance will develop. In recent years, there is more information about novel prognostic models — the visceral adiposity index and the lipid accumulation product. The aim of this review was to analyze the results of studies examining the relationship between various indices of obesity and cardiometabolic risk. We analyzed 105 literature sources, 53 of which were ruled out, becausethe processes of interest were not described in detail or included anassessment of the relationship of various obesity indices with metabolic parameters. The results obtained indicate the advisability of using novel obesity indices, which have a good predictive ability and are simple and convenient to use. It is necessary to use additional methods of anthropometric and clinical examination in order to assess the metabolic phenotype of obesity, which will make it possible to stratify patients by the level of cardiometabolic risk.


2019 ◽  
Vol 8 (9) ◽  
pp. 1385 ◽  
Author(s):  
Burgos-Morón ◽  
Abad-Jiménez ◽  
Marañón ◽  
Iannantuoni ◽  
Escribano-López ◽  
...  

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.


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