scholarly journals Metabolically Healthy versus Unhealthy Morbidly Obese: Chronic Inflammation, Nitro-Oxidative Stress, and Insulin Resistance

Nutrients ◽  
2018 ◽  
Vol 10 (9) ◽  
pp. 1199 ◽  
Author(s):  
Adriana Cӑtoi ◽  
Alina Pârvu ◽  
Andra Andreicuț ◽  
Aurel Mironiuc ◽  
Alexandra Crӑciun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Chronic Inflammation ◽  
Fasting Blood Glucose ◽  
Morbidly Obese ◽  
Model Assessment ◽  
Metabolic Disturbances ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Metabolically Healthy

Metabolically heathy obesity is characterised by the presence of obesity in the absence of metabolic disturbances. The aim of our study was to analyse pro-inflammatory, nitro-oxidative stress, and insulin-resistance (IR) markers in metabolically healthy morbidly obese (MHMO) with respect to metabolically unhealthy morbidly obese (MUHMO) with metabolic syndrome (MS) and to identify the potential predictors of MS in the MHMO group. Two groups of MHMO and MUHMO with MS were analysed. We evaluated serum high sensitivity C reactive protein (hsCRP), tumor necrosis factor alpha (TNF-α), chemerin, nitrite and nitrate (NOx), total oxidant status (TOS), total antioxidant response (TAR), fasting blood glucose, insulin, and homeostasis model assessment of insulin resistance (HOMA-IR.) MHMO have similar hsCRP and TNF-α values as the MUHMO with MS, while chemerin was significantly lower in MHMO. NOx was higher in MUHMO with MS patients, while no difference regarding TOS and TAR was found between the two groups. HOMA-IR and insulin values were lower in MHMO as compared to the MUHMO with MS group. Insulin, HOMA-IR, and chemerin were identified predictors of MS in MHMO. In conclusion, MHMO and MUHMO display similarities and differences in terms of chronic inflammation, nitro-oxidative stress, and IR. Markers of IR and chemerin are possible predictors of MS in MHMO.

scholarly journals The Roles of Liver Inflammation and the Insulin Signaling Pathway in PM2.5 Instillation-Induced Insulin Resistance in Wistar Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Zhihua Zhang ◽  
Shujun Hu ◽  
Ping Fan ◽  
Ling Li ◽  
Shanshan Feng ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Rat Liver ◽  
Insulin Signaling ◽  
Glucose Transporter ◽  
Fasting Blood Glucose ◽  
Model Assessment ◽  
Glucose Transporter 2 ◽  
Systemic Insulin Resistance ◽  
Tnf Α ◽  
Phosphorylated Akt

To elucidate the mechanism of how the liver participates in PM2.5-caused insulin resistance. A novel Wistar rat model was developed in this study by instilling a suspension of lyophilized PM2.5 sample (2.5 mg/kg, 5 mg/kg, or 10 mg/kg) collected from the atmosphere. Systemic insulin resistance indicators, including serum fasting blood glucose (FBG), fasting insulin (FINS), Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), and hemoglobin A1 (HbA1), were upregulated by the PM2.5 instillation. The area under the curve (AUCglu) calculated by intraperitoneal glucose tolerance testing (IPGTT) was also significantly greater in the PM2.5 instillation groups. Additionally, PM2.5 instillation was found to cause liver damage and inflammation. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), total bilirubin (TBIL), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) were significantly elevated by PM2.5 instillation. PM2.5 also triggered IL-6 and TNF-α transcription but inhibited mRNA synthesis and suppressed signaling activation of the insulin-phosphoinositide 3-kinase- (PI3K-) Akt-glucose transporter 2 (GLUT2) pathway in the rat liver by reducing the ratio of phosphorylated Akt to phosphorylated insulin receptor substrate 1 (IRS-1). Thus, PM2.5-induced inflammation activation and insulin signaling inhibition in the rat liver contribute to the development of systemic insulin resistance.

scholarly journals Effects of sleeve gastrectomy on insulin resistance

2016 ◽  
Vol 89 (2) ◽  
pp. 267-272 ◽  
Author(s):  
Adriana Florinela Cătoi ◽  
Alina Pârvu ◽  
Aurel Mironiuc ◽  
Romeo Florin Galea ◽  
Adriana Mureşan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Sleeve Gastrectomy ◽  
Plasma Glucose ◽  
Fasting Blood Glucose ◽  
Morbidly Obese ◽  
Model Assessment ◽  
Mean Values ◽  
Significant Change ◽  
Change In Mean

Background and aim. Obesity is a major risk factor for the onset of insulin resistance (IR), hyperinsulinemia and type 2 diabetes mellitus (T2DM) Evidence data has proven that beyond important weight loss bariatric surgery especially Roux-en-Y gastric bypass (RYGB) and bilio-pancreatic diversion (BPD) leads to significant early reduction of insulinemia and of IR calculated through the homeostatic model assessment (HOMA-IR), independently of fat mass decrease. Sleeve gastrectomy (SG) is now used as a sole weight loss operation with good results. Therefore, the aim of the present study was to investigate the early changes of fasting blood glucose, insulin and HOMA-IR in a group of morbidly obese (MO) patients i.e. at 7, 30 and 90 days after SG. Methods. The study included 20 MO patients (7 male and 13 female) submitted to SG. Anthropometrical (weight, body mass index –BMI, percent excess BMI loss -%EBMIL) and biochemical (plasma glucose, insulin and calculated HOMA-IR ) evaluation were performed before and at 7, 30 and 90 days after SG. In addition, a second group of 10 normal weight healthy subjects with a BMI ranging form 19 kg/m² to 23.14 kg/m², matched for age and gender was investigated. Results. Plasma glucose (p=0.018), insulin (p=0.004) and HOMA-IR (p=0.006) values were statistically different between the studied groups. After surgery, at every follow-up point, there were statistically different weight and BMI mean values relative to the operation day (p<0.003). BMI, decreased at 7 days (estimated reduction=2.79; 95% CI:[2.12;3.45]), at 30 days (estimated reduction=5.65; 95% CI:[3.57;7.73]) and at 90 days (estimated reduction=10.88; 95% CI:[7.35;14.41]) respectively after SG. We noted a tendency toward statistical significant change of mean insulin values at 7 days after surgery (corrected p=0.075), no statistical change at 30 days (corrected p=0.327) and a significant change at 90 days (corrected p=0.027) after SG as compared to baseline. There was a significant change in mean values of HOMA-IR at 30 days (corrected p=0.009) and at 90 days (corrected p=0.021) after the operation day. Conclusions. The present study showed important early changes consisting in reductions of mean values of plasma insulin and HOMA-IR after SG.

scholarly journals Associations of Obesity-metabolic Status With Insulin Resistance and Chronic Inflammation Level: Results From the CNTR Study

2020 ◽  
Author(s):  
Chunxiao Liao ◽  
Wenjing Gao ◽  
Weihua Cao ◽  
Jun Lv ◽  
Canqing Yu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Waist Circumference ◽  
Chronic Inflammation ◽  
High Sensitivity ◽  
Metabolic Status ◽  
Model Assessment ◽  
Reactive Protein ◽  
Chinese Adult ◽  
Metabolically Healthy ◽  
Adult Twins

Abstract Background: Insulin resistance (IR) and inflammation are the potential mechanism linking obesity and cardiometabolic risk. The aim of this work was to examine the joint relations of obesity and metabolic status with IR and chronic inflammation level among Chinese adult twins.Methods: The analyses used data from 1113 adult twins in 4 provinces (Shandong, Zhejiang, Jiangsu and Sichuan) from Chinese National Twin Registry (CNTR) which collected detailed information. Those with 0 or 1 metabolic syndrome (MetS) components excluding waist circumference were considered metabolically healthy, and those with waist circumference≥90 cm in men and ≥85 cm in women as obese. All participants were categorized into four phenotypes: metabolically healthy non-obesity (MHNO), metabolically healthy obesity (MHO), metabolically unhealthy non- obesity (MUNO), metabolically unhealthy obesity (MUO). High sensitivity C reactive protein (hsCRP) was measured to assess underlying inflammation and homeostasis model assessment of insulin resistance (HOMA-IR) was calculated as surrogate measure of insulin resistance. Results: In observational analyses of 1113 individuals (mean [SD] age, 46.6 [12.9] years; 463 obese [41.6%]). 20.3% obese twins were metabolic healthy. Serum HOMA-IR level was higher in MUNO (β=0.42, 95% CI: 0.21–0.64), MHO (β=0.68, 95% CI: 0.36–1.00) and MUO (β=0.69, 95% CI: 0.46–0.91) twins, compared with their MHNO counterparts. The chronic inflammation level, evaluated by hsCRP was similar between MHO and MUO, which differed significantly to metabolic healthy non-obesity (MHNO). Within twin-pair analysis indicated there might exist common genetic influence between HOMA-IR and MHO/MUO phenotype.Conclusions: Among Chinese adult twins, metabolic status were independently associated with higher IR while development of chronic inflammation might closely relate to central obesity. It is necessary for the different risk assessment based on metabolic status in obese population.

scholarly journals Inflammation and Hypertension in Rheumatoid Arthritis

2013 ◽  
Vol 40 (11) ◽  
pp. 1806-1811 ◽  
Author(s):  
Siriporn Manavathongchai ◽  
Aihua Bian ◽  
Young Hee Rho ◽  
Annette Oeser ◽  
Joseph F. Solus ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Insulin Resistance ◽  
Cardiovascular Risk ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Joint Disease ◽  
Model Assessment ◽  
Antiinflammatory Drugs ◽  
Necrosis Factor Alpha ◽  
Mediators Of Inflammation ◽  
Tnf Α

Objective.Hypertension (HTN), a common modifiable cardiovascular risk factor, is more common in patients with rheumatoid arthritis (RA), but the underlying mechanisms are unclear. We examined the hypothesis that mediators of inflammation and markers of cardiovascular risk are associated with HTN in RA.Methods.We compared measures of inflammation [serum C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), homocysteine, and leptin concentrations] and insulin resistance [homeostasis model assessment index (HOMA)] in RA patients with (n = 90) and without HTN (n = 79). HTN was defined as blood pressure ≥ 140/90 mm Hg or treatment with antihypertensive therapy. The independent association of markers of interest with HTN was examined using multivariable logistic regression.Results.Patients with HTN were significantly older and had longer disease duration than those without HTN (both p < 0.001). Concentrations of homocysteine [11.1 (8.5–13.5) μmol/l vs 9.3 (7.8–11.0) μmol/l] were significantly higher in patients with HTN (p < 0.001). After adjustment for age, sex, race, smoking, body mass index, and corticosteroid and nonsteroidal antiinflammatory drugs (NSAID) use, increased concentrations of homocysteine (OR 2.9, 95% CI: 1.5–5.5, p = 0.001), and leptin (OR 2.0, 95% CI: 1.0–3.8, p = 0.046) were significantly associated with HTN, but the 28-joint Disease Activity Score, IL-6, CRP, TNF-α, and HOMA index were not (all p > 0.05).Conclusion.HTN in patients with RA is not associated with generalized systemic inflammation or insulin resistance, but is associated with increasing concentrations of homocysteine and leptin. The pathogenesis of HTN in RA may involve pathways more regularly associated with fat and vascular homeostasis.

Role of inflammation in the development of colorectal cancer

2020 ◽  
Vol 20 ◽  
Author(s):  
Sridhar Muthusami ◽  
R. Ileng Kumaran ◽  
Kokelavani Nampalli Babu ◽  
Sneha Krishnamoorthy ◽  
Akash Guruswamy ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Chronic Inflammation ◽  
Interleukin 1 ◽  
Cell Types ◽  
Model Systems ◽  
Cytokine Gene Expression ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Proinflammatory Molecules

: Chronic inflammation can lead to the development of many diseases including cancer. Inflammatory bowel disease (IBD) that includes both ulcerative colitis (UC) and Crohn's disease (CD) are risk factors for the development of colorectal cancer (CRC). Many cytokines produced primarily by the gut immune cells either during or in response to localized inflammation in the colon and rectum are known to stimulate the complex interactions between the different cell types in the gut environment resulting in acute inflammation. Subsequently, chronic inflammation together with genetic and epigenetic changes has been shown to lead to the development and progression of CRC. Various cell types present in the colon such as enterocytes, Paneth cells, goblet cells and macrophages express receptors for inflammatory cytokines and respond to tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), IL-6 and other cytokines. Among the several cytokines produced, TNF-α and IL-1β are the key proinflammatory molecules that play critical roles in the development of CRC. The current review is intended to consolidate the published findings to focus on the role of proinflammatory cytokines, namely TNF-α and IL-1β, on inflammation (and the altered immune response) in the gut, to better understand the development of CRC in IBD, using various experimental model systems, preclinical and clinical studies. Moreover, this review also highlights the current therapeutic strategies available (monotherapy and combination therapy), to alleviate the symptoms or treat inflammationassociated CRC by using monoclonal antibodies or aptamers to block proinflammatory molecules, inhibitors of tyrosine kinases in inflammatory signaling cascade, competitive inhibitors of proinflammatory molecules, and the nucleic acid drugs like small activating RNAs (saRNAs) or microRNA (miRNA) mimics to activate tumor suppressor or repress oncogene/proinflammatory cytokine gene expression.

scholarly journals Association of Metabolically Healthy and Unhealthy Obesity Phenotypes with Oxidative Stress Parameters and Telomere Length in Healthy Young Adult Men. Analysis of the MAGNETIC Study

Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 93
Author(s):  
Mateusz Lejawa ◽  
Kamila Osadnik ◽  
Tadeusz Osadnik ◽  
Natalia Pawlas
Keyword(s):  
Oxidative Stress ◽  
Telomere Length ◽  
Quantitative Polymerase Chain Reaction ◽  
Oxidative Stress Markers ◽  
Metabolic Disturbances ◽  
Total Oxidation ◽  
Stress Markers ◽  
Metabolic Dysregulation ◽  
Total Antioxidant ◽  
Metabolically Healthy

Obesity is a significant factor related to metabolic disturbances that can lead to metabolic syndrome (MetS). Metabolic dysregulation causes oxidative stress, which affects telomere structure. The current study aimed to evaluate the relationships between telomere length, oxidative stress and the metabolically healthy and unhealthy phenotypes in healthy young men. Ninety-eight participants were included in the study (49 healthy slim and 49 obese patients). Study participants were divided into three subgroups according to body mass index and metabolic health. Selected oxidative stress markers were measured in serum. Relative telomere length (rTL) was measured using quantitative polymerase chain reaction. The analysis showed associations between laboratory markers, oxidative stress markers and rTL in metabolically healthy and unhealthy participants. Total oxidation status (TOS), total antioxidant capacity (TAC) and rTL were significantly connected with metabolically unhealthy obesity. TAC was associated with metabolically healthy obesity. Telomeres shorten in patients with metabolic dysregulation related to oxidative stress and obesity linked to MetS. Further studies among young metabolically healthy and unhealthy individuals are needed to determine the pathways related to metabolic disturbances that cause oxidative stress that leads to MetS.

scholarly journals Twelve Weeks of Pioglitazone Therapy Significantly Attenuates Dysmetabolism and Reduces Inflammation in Continuous Ambulatory Peritoneal Dialysis Patients—A Randomized Crossover Trial

2012 ◽  
Vol 32 (5) ◽  
pp. 507-515 ◽  
Author(s):  
Yun Li ◽  
Qiong-Hong Xie ◽  
Huai-Zhou You ◽  
Jing Tian ◽  
Chuan-Ming Hao ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Peritoneal Dialysis ◽  
Continuous Ambulatory Peritoneal Dialysis ◽  
Crossover Trial ◽  
Fasting Blood Glucose ◽  
High Risk Patient ◽  
Model Assessment ◽  
Serum Triglycerides ◽  
Once Daily ◽  
Randomized Crossover Trial

BackgroundThe aim of the present study was to investigate the effect of oral pioglitazone (PIO) on lipid metabolism, insulin resistance, inflammation, and adipokine metabolism in continuous ambulatory peritoneal dialysis (CAPD) patients.MethodsIn this randomized crossover trial, 36 CAPD patients with serum triglyceride levels above 1.8 mmol/L were randomly assigned to receive either oral PIO 15 mg once daily or no PIO for 12 weeks. Then, after a 4-week washout, the patients were switched to the alternative regimen. The primary endpoint was change in serum triglycerides during the PIO regimen compared with no PIO. Secondary endpoints included changes in other lipid levels, homeostatic model assessment of insulin resistance (HOMA-IR), adipocytokines, and C-reactive protein (CRP).ResultsAll 36 CAPD patients (age: 64 ± 11 years; 33% men; 27.8% with diabetes mellitus) completed the study. Comparing patients after PIO and no PIO therapy, we found no significant differences in mean serum triglycerides (3.83 ± 1.49 mmol/L vs 3.51 ± 1.98 mmol/L, p = 0.2). However, mean high-density lipoprotein (0.94 ± 0.22 mmol/L vs 1.00 ± 0.21 mmol/L, p = 0.004) and median total adiponectin [10.34 μg/mL (range: 2.59 – 34.48 μg/mL) vs 30.44 μg/mL (3.47 – 93.41 μg/mL), p < 0.001] increased significantly. Median HOMA-IR [7.51 (1.39 – 45.23) vs 5.38 (0.97 – 14.95), p = 0.006], mean fasting blood glucose (7.31 ± 2.57 mmol/L vs 6.60 ± 2.45 mmol/L, p = 0.01), median CRP [8.78 mg/L (0.18 – 53 mg/L) vs 3.50 mg/L (0.17 – 26.30 mg/L), p = 0.005], and mean resistin (32.70 ± 17.17 ng/mL vs 28.79 ± 11.83 ng/mL, p = 0.02) all declined. The PIO was well tolerated, with only one adverse event: lower-extremity edema in a patient with low residual renal function.ConclusionsBlood triglycerides were not altered after 12 weeks of PIO 15 mg once daily in CAPD patients, but parameters of dysmetabolism were markedly improved, including insulin resistance, inflammation, and adipokine balance, suggesting that PIO could be of value for this high-risk patient group. Larger, more definitive studies are needed to confirm these findings.

scholarly journals Neurodegeneration in an animal model of Parkinson's disease is exacerbated by a high-fat diet

2010 ◽  
Vol 299 (4) ◽  
pp. R1082-R1090 ◽  
Author(s):  
Jill K. Morris ◽  
Gregory L. Bomhoff ◽  
John A. Stanford ◽  
Paige C. Geiger
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Animal Model ◽  
Locomotor Activity ◽  
Substantia Nigra ◽  
High Fat Diet ◽  
Model Assessment ◽  
High Fat

Despite numerous clinical studies supporting a link between type 2 diabetes (T2D) and Parkinson's disease (PD), the clinical literature remains equivocal. We, therefore, sought to address the relationship between insulin resistance and nigrostriatal dopamine (DA) in a preclinical animal model. High-fat feeding in rodents is an established model of insulin resistance, characterized by increased adiposity, systemic oxidative stress, and hyperglycemia. We subjected rats to a normal chow or high-fat diet for 5 wk before infusing 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle. Our goal was to determine whether a high-fat diet and the resulting peripheral insulin resistance would exacerbate 6-OHDA-induced nigrostriatal DA depletion. Prior to 6-OHDA infusion, animals on the high-fat diet exhibited greater body weight, increased adiposity, and impaired glucose tolerance. Two weeks after 6-OHDA, locomotor activity was tested, and brain and muscle tissue was harvested. Locomotor activity did not differ between the groups nor did cholesterol levels or measures of muscle atrophy. High-fat-fed animals exhibited higher homeostatic model assessment of insulin resistance (HOMA-IR) values and attenuated insulin-stimulated glucose uptake in fast-twitch muscle, indicating decreased insulin sensitivity. Animals in the high-fat group also exhibited greater DA depletion in the substantia nigra and the striatum, which correlated with HOMA-IR and adiposity. Decreased phosphorylation of HSP27 and degradation of IκBα in the substantia nigra indicate increased tissue oxidative stress. These findings support the hypothesis that a diet high in fat and the resulting insulin resistance may lower the threshold for developing PD, at least following DA-specific toxin exposure.

scholarly journals Relation of Endothelial Dysfunction and Adipokines Levels to Insulin Resistance in Metabolic Syndrome Patients

2009 ◽  
Vol 63 (4-5) ◽  
pp. 222-227
Author(s):  
Pēteris Tretjakovs ◽  
Antra Jurka ◽  
Inga Bormane ◽  
Indra Miķelsone ◽  
Dace Reihmane ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Endothelial Dysfunction ◽  
Doppler Imaging ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Cytokines And Chemokines ◽  
Tnf Α ◽  
Artery Disease ◽  
D 20

Relation of Endothelial Dysfunction and Adipokines Levels to Insulin Resistance in Metabolic Syndrome Patients Obese metabolic syndrome (MS) patients were categorised into three groups: 44 with type 2 diabetes mellitus (T2DM)(D); 20 with T2DM and coronary artery disease (CAD) (DC), and 26 with MS alone (M). Eighteen healthy subjects were selected as controls (C). Insulin resistance (IR) was assessed by HOMA-IR. Adiponectin, tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and interleukin-8 (IL-8) concentrations were measured by xMAP technology. Endothelin-1 (ET-1) was determined by ELISA. We used laser Doppler imaging for evaluating cutaneous endothelium-dependent vasodilatation in the hand. D and DC groups had significantly elevated IR compared with M or C group (P < 0.01). TNF-α, IL-6, IL-8, MCP-1 and ET-1 levels in DC were significantly elevated compared with other groups (P < 0.001). IL-6, IL-8, MCP-1 and ET-1 in D group were higher than those in C group (P < 0.05). TNF-α, IL-6, IL-8, MCP-1 and ET-1 concentrations were correlated with HOMA-IR indexes and adiponectin levels. All patients had lower adiponectin concentrations than controls (P < 0.001), but there were no differences between the patient groups. Only D and DC groups demonstrated a significant and similar decrease in LDI-Ach marker compared to C group (P < 0.001). LDI-Ach values were significantly correlated with HOMA-IR indexes and adiponectin levels (P < 0.001). Our findings show that obese MS patients have significantly increased HOMA-IR, TNF-α, IL-6, MCP-1 and IL-8 levels, decreased adiponectin concentration, and endothelial dysfunction, but the presence of T2DM and CAD in these patients is associated with more pronounced endothelial dysfunction and increased production of inflammatory cytokines and chemokines.

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