scholarly journals Visfatin levels in non-obese, obese, and insulin resistant adolescents

2017 ◽  
Vol 56 (5) ◽  
pp. 291
Author(s):  
Indra Ihsan ◽  
Eka Agustia Rini ◽  
Rismawati Yaswir
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Serum Insulin ◽  
Enzyme Linked Immunosorbent Assay ◽  
Model Assessment ◽  
Fasting Serum ◽  
Obese Adolescents ◽  
Insulin Resistant ◽  
Resistant Group ◽  
Visfatin Level

Background Adipose tissue is not merely a site for energy storage, but is also the largest endocrine organ, secreting various adipocytokines. Plasma visfatin, an adipocytokine predominantly secreted from visceral adipose tissue, has insulin-mimetic effects, and has been closely linked to insulin resistance.Objective To compare plasma visfatin levels between obese and non-obese adolescents, as well as between obese adolecents with and without insulin resistance.Methods This cross-sectional study was conducted in students who attended three senior high schools in Padang. Subjects comprised 28 obese and 28 non-obese adolescents. The age of the subjects ranged from 14-18 years. Obesity criteria were based on body mass index (BMI) measurements. Fasting serum glucose level was measured by glucose hexokinase photometry and serum insulin was measured by chemiluminesence immunoassay. Plasma visfatin was measured by enzyme-linked immunosorbent assay (ELISA). The insulin resistance index was estimated from fasting serum insulin and glucose levels using the homeostatic model assessment for insulin resistance (HOMA-IR). Differences in the variables were tested using independent T-test and Mann-Whitney test, depending on the distribution of the variables.Results The mean plasma visfatin level was significantly higher in the obese than in the control group [2.55 (SD 1.54) vs. 1.61 (SD 0.64) ng/mL, respectively; (P=0.005)]. The insulin resistant group had significantly higher mean plasma visfatin level than the non-resistant group [3.61 (SD 1.59) vs. 1.96 (SD 1.18) ng/mL, respectively; (P=0.004)].Conclusion Obese adolescents with insulin resistance have signifcantly higher plasma visfatin levels compared to those without insulin resistance.

The relationship between insulin resistance and endothelial dysfunction in obese adolescents

2017 ◽  
Vol 30 (6) ◽  
Author(s):  
Preneet Cheema Brar ◽  
Payal Patel ◽  
Stuart Katz
Keyword(s):  
Insulin Resistance ◽  
Endothelial Dysfunction ◽  
Intima Media Thickness ◽  
Microvascular Function ◽  
Reciprocal Relationship ◽  
Model Assessment ◽  
Obese Adolescents ◽  
Insulin Resistant ◽  
Ldl Particles ◽  
Vessel Structure

AbstractBackground:Insulin resistance and endothelial dysfunction share a reciprocal relationship that links the metabolic and cardiovascular sequelae of obesity. We characterized the brachial artery reactivity testing (BART) and carotid artery-intima media thickness (CIMT) in adolescents categorized as obese insulin resistant (OIR) and obese not insulin resistant (ONIR). Lipoprotein particle (p) analysis and inflammatory cytokines in OIR and ONIR groups were also analyzed.Methods:Obese adolescents (n=40; mean body mass index [BMI] 35.6) were categorized as ONIR and OIR based on their homeostatic model assessment of insulin resistance (HOMA-IR) calculation (≤or> than 3.4). Ultrasound measured conduit arterial function BART, microvascular function (post-ischemic hyperemia) and conduit artery structure CIMT.Results:BART did not differ according to IR status (mean±SD: 7.0±4.3% vs. 5.9±3.4% in ONIR and OIR, respectively, p=0.3, but post-ischemic hyperemia was significantly greater in the ONIR group (4.5±2.2 vs. 3.5±3, p=0.04). Atherogenic lipoprotein particles; large VLDL particles and small LDL particles were higher in the OIR compared to ONIR group.Conclusions:OIR adolescents demonstrate an inflamed atherogenic milieu compared to the ONIR adolescents. Microvascular function, but not conduit vessel structure or function, was impaired in association with IR.

scholarly journals Adipose tissue gene expression of CXCL10 and CXCL11 modulates inflammatory markers in obesity: implications for metabolic inflammation and insulin resistance

2020 ◽  
Vol 11 ◽  
pp. 204201882093090
Author(s):  
Shihab Kochumon ◽  
Ashraf Al Madhoun ◽  
Fatema Al-Rashed ◽  
Rafaat Azim ◽  
Ebaa Al-Ozairi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Inflammatory Markers ◽  
Fasting Blood Glucose ◽  
Subcutaneous Fat ◽  
Family Members ◽  
Enzyme Linked Immunosorbent Assay ◽  
Model Assessment ◽  
Metabolic Inflammation

Background: The CXCL subfamily of chemokines (CXCL9, CXCL10, and CXCL11; angiostatic chemokines) plays a key role in many inflammatory diseases. However, the expression of CXCLs in adipose tissue (AT) during obesity and association of these CXCLs with inflammatory markers and insulin resistance are poorly understood. Therefore, this study aimed to investigate the effects of CXCL gene expression on subcutaneous AT inflammatory markers and insulin resistance. Methods: Subcutaneous-fat biopsies were collected from 59 nondiabetic (lean/overweight/obese) individuals for RNA isolation. Expression levels of AT CXCL and inflammatory markers were determined by quantitative reverse transcriptase polymerase chain reaction (RT-qPCR). Biomedical parameters in the plasma were measured by enzyme-linked immunosorbent assay (ELISA). Insulin resistance was estimated using homeostatic model assessment (HOMA-IR). Results: AT CXCL expression was higher in obese compared with lean individuals ( p < 0.05) and positively correlated with body mass index (BMI; r ⩾ 0.269, p < 0.05). Expression of CXCL9, CXCL10, and CXCL11 correlated significantly with various pro-inflammatory markers, including family members of interleukins, chemokines, and their prospective receptors ( r ⩾ 0.339, p ⩽ 0.009), but not anti-inflammatory markers. CXCL11 expression correlated specifically with the expression of CCL5, CCL18, TLR3, TLR4, TLR8, IRF5, and NF-κB ( r ⩾ 0.279, p ⩽ 0.039). Notably, CXCL11 was correlated with C-reactive protein (CRP), fasting blood glucose (FBG), and HOMA-IR. In multiple regression analysis, CXCL11 was identified as an independent predictor of CCL19, CCL5, IL-6, and TLR3. Conclusion: These data suggest that the CXCL family members, specifically CXCL10 and CXCL11, are potential biomarkers for the onset of AT inflammation during obesity.

scholarly journals Maternal Protein Restriction Altered Insulin Resistance and Inflammation-Associated Gene Expression in Adipose Tissue of Young Adult Mouse Offspring in Response to a High-Fat Diet

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1103 ◽  
Author(s):  
Juhae Kim ◽  
Alee Choi ◽  
Young Hye Kwon
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Serum Insulin ◽  
Protein Restriction ◽  
Epididymal Adipose Tissue ◽  
Model Assessment ◽  
High Fat ◽  
Maternal Protein Restriction ◽  
Increased Risk

Maternal protein restriction is associated with increased risk of insulin resistance and inflammation in adulthood offspring. Here, we investigated whether maternal protein restriction could alter the risk of metabolic syndrome in postweaning high-fat (HF)-diet-challenged offspring, with focus on epididymal adipose tissue gene expression profile. Female ICR mice were fed a control (C) or a low-protein (LP) diet for two weeks before mating and throughout gestation and lactation, and their male offspring were fed an HF diet for 22 weeks (C/HF and LP/HF groups). A subset of offspring of control dams was fed a low-fat control diet (C/C group). In response to postweaning HF diet, serum insulin level and the homeostasis model assessment of insulin resistance (HOMA-IR) were increased in control offspring. Maternal LP diet decreased HOMA-IR and adipose tissue inflammation, and increased serum adiponectin level in the HF-diet-challenged offspring. Accordingly, functional analysis revealed that differentially expressed genes (DEGs) enriched in cytokine production were downregulated in the LP/HF group compared to the C/HF group. We also observed the several annotated gene ontology terms associated with innate immunity and phagocytosis in down-regulated DEGs between LP/HF and C/C groups. In conclusion, maternal protein restriction alleviated insulin resistance and inflammation in young offspring mice fed a HF diet but may impair development of immune system in offspring.

scholarly journals Association of Osteocalcin with Metabolic Syndrome and its Correlation with Insulin Resistance

2021 ◽  
Author(s):  
Nehali Pattanayak ◽  
Anuva Mishra ◽  
Sucharita Mohanty ◽  
Pramila Kumari Mishra ◽  
Putul Bara
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Blood Sugar ◽  
Serum Insulin ◽  
Fasting Blood Sugar ◽  
Enzyme Linked Immunosorbent Assay ◽  
Model Assessment ◽  
Serum Osteocalcin ◽  
Public Health Burden ◽  
Cardio Vascular

Introduction: Metabolic Syndrome (MetS) is an important public health burden associated with five-fold risk of developing Type 2 Diabetes Mellitus (T2DM) and two fold risk of Cardio Vascular Disease (CVD). Recent studies described that osteoblasts produce osteocalcin which increases insulin secretion and adiponectin production resulting in insulin sensitivity. Aim: To determine the association of serum osteocalcin with MetS and to assess the correlation of insulin resistance Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) with osteocalcin. Materials and Methods: This case-control study was carried out in the Department of Biochemistry at MKCG Medical College, Brahmapur, Odisha, India. By observing the mean and standard deviation from previous studies, with 95% Confidence Interval (CI) and 80% power of study, the sample size was calculated to be 45. Forty eight cases between 20-45 years of age meeting the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criteria of MetS and 50 age and sex matched healthy individuals were taken as controls. Individuals with any systemic illness or on any kind of medications were excluded from the study. Fasting blood sugar, lipid profile were measured by standard procedures. Serum osteocalcin and serum insulin was estimated by Enzyme-linked Immunosorbent Assay (ELISA) LISA SCAN READER and ROCHE e COBAS 411 electrochemiluminiscence, respectively. Statistical analysis was done in Statistical Package for the Social Sciences (SPSS) 22.0 version software. Results: Serum osteocalcin was found to be lower in cases as compared to controls (7.74±4.62 ng/mL and 23.24±9.74 ng/mL) respectively. Osteocalcin was also found to be significantly negatively correlated with HOMA-IR, Waist Circumference (WC), triglyceride and fasting blood sugar in cases with (r=-0.322, p=0.025), (r=-0.519, p<0.001), (r=-0.401, p=0.005), (r=-0.539, p<0.001), respectively and also in controls with (r=-0.494, p<0.001), (r=-0.176, p=0.245), (r=-0.398, p<0.05), (r=-0.141, p<0.05), respectively. Conclusion: Serum osteocalcin being negatively correlated with insulin resistance may have therapeutic role in prevention of MetS which may be substantiated with further study.

scholarly journals Retinol binding protein 4, obesity, and insulin resistance in adolescents

2017 ◽  
Vol 57 (1) ◽  
pp. 1
Author(s):  
Ronaldi Noor ◽  
Eka Agustria Rini ◽  
Eti Yerizel
Keyword(s):  
Insulin Resistance ◽  
Binding Protein ◽  
Cross Sectional Study ◽  
Normal Weight ◽  
Retinol Binding Protein ◽  
Model Assessment ◽  
Cross Sectional ◽  
Obese Adolescents ◽  
Insulin Resistant ◽  
Significant Difference

Background Obesity is a global problem. Even in poor and developing countries, obesity has reached alarming levels. In childhood, obesity may lead to insulin resistance. Retinol binding protein (RBP4), secreted primarily by liver and adipose tissues, was recently proposed as a link between obesity and insulin resistance. The role of RBP4 in pediatric obesity and its relationship with insulin resistance have not been well elucidated.Objective To compare RBP4 levels in obese and lean adolescents and to assess for a relationship between RBP4 levels and insulin resistance. Method This cross-sectional study was conducted in three senior high schools in Padang, West Sumatera, Indonesia. Subjects were adolescents aged 14-18 years, who were obese or normal weight (n=56). We measured subjects’ body mass index (BMI) and serum RBP4 concentrations. Insulin resistance was assessed using the homeostasis model assessment of insulin resistance (HOMA-IR) index.Results Similar RBP4 levels were found in the obese and normoweight groups (P>0.05). Higher RBP4 levels were found in the insulin resistant compared to the non-insulin resistant group, but the difference was not significant (P > 0.05).Conclusion There is no significant difference in mean RBP4 levels in obese adolescents compared to normoweight adolescents. Nor are mean RBP4 levels significantly different between obese adolescents with and without insulin resistance.  

scholarly journals A Role for Oncostatin M in the Impairment of Glucose Homeostasis in Obesity

2019 ◽  
Vol 105 (3) ◽  
pp. e337-e348 ◽  
Author(s):  
Irene Piquer-Garcia ◽  
Laura Campderros ◽  
Siri D Taxerås ◽  
Aleix Gavaldà-Navarro ◽  
Rosario Pardo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Glucose Homeostasis ◽  
Serum Insulin ◽  
Oncostatin M ◽  
Mrna Levels ◽  
Model Assessment ◽  
Human Adipocytes ◽  
Glucose Levels ◽  
Inflammatory State

Abstract Context Oncostatin M (OSM) plays a key role in inflammation, but its regulation and function during obesity is not fully understood. Objective The aim of this study was to evaluate the relationship of OSM with the inflammatory state that leads to impaired glucose homeostasis in obesity. We also assessed whether OSM immunoneutralization could revert metabolic disturbances caused by a high-fat diet (HFD) in mice. Design 28 patients with severe obesity were included and stratified into two groups: (1) glucose levels &lt;100 mg/dL and (2) glucose levels &gt;100 mg/dL. White adipose tissue was obtained to examine OSM gene expression. Human adipocytes were used to evaluate the effect of OSM in the inflammatory response, and HFD-fed C57BL/6J mice were injected with anti-OSM antibody to evaluate its effects. Results OSM expression was elevated in subcutaneous and visceral fat from patients with obesity and hyperglycemia, and correlated with Glut4 mRNA levels, serum insulin, homeostatic model assessment of insulin resistance, and inflammatory markers. OSM inhibited adipogenesis and induced inflammation in human adipocytes. Finally, OSM receptor knockout mice had increased Glut4 mRNA levels in adipose tissue, and OSM immunoneutralization resulted in a reduction of glucose levels and Ccl2 expression in adipose tissue from HFD-fed mice. Conclusions OSM contributes to the inflammatory state during obesity and may be involved in the development of insulin resistance.

scholarly journals A Model of Insulin Resistance in Mice, Born to Diabetic Pregnancy, Is Associated with Alterations of Transcription-Related Genes in Pancreas and Epididymal Adipose Tissue

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Akadiri Yessoufou ◽  
Kabirou Moutairou ◽  
Naim Akhtar Khan
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Transcription Factors ◽  
Serum Insulin ◽  
Diabetic Pregnancy ◽  
Epididymal Adipose Tissue ◽  
Insulin Resistant ◽  
Macrophage Marker ◽  
Tnf Α ◽  
And Control

Objective. This study is conducted on a model of insulin-resistant (IR) mice born to dams which were rendered diabetic by the administration of streptozotocin.Methods. Adult IR and control offspring were selected and we determined the mRNA expression of transcription factors known to modulate pancreatic and adipose tissue activities and inflammation.Results. We observed that serum insulin increased, and the mRNA of insulin gene transcription factors, Pdx-1, Nkx6.1 and Maf-A, were upregulated in IR mice pancreas. Besides, their pancreatic functional capacity seemed to be exhausted as evidenced by low expression of pancreatic Glut2 and glucokinase mRNA. Though IR offspring exhibited reduced epididymal adipose tissue, their adipocytes seemed to be differentiated into macrophage-like cells, as they exhibited upregulated CD14 and CD68 antigens, generally expressed by macrophages. However, there was no peripheral macrophages infiltration into epididymal adipose tissue, as the expression of F4/80, a true macrophage marker, was undetectable. Furthermore, the expression of IL-6, TNF-α and TLR-2, key players of insulin resistance, was upregulated in the adipose tissue of IR offspring.Conclusion. Insulin resistant state in mice, born to diabetic pregnancy, alters the expression of function-related genes in pancreas and epididymal adipose tissue and these offspring are prone to develop metabolic syndrome.

scholarly journals Myricetin Ameliorates Defective Post-Receptor Insulin Signaling via β-Endorphin Signaling in the Skeletal Muscles of Fructose-Fed Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Thing-Fong Tzeng ◽  
Shorong-Shii Liou ◽  
I-Min Liu
Keyword(s):  
Insulin Resistance ◽  
Insulin Receptor ◽  
Plasma Levels ◽  
Glucose Transporter ◽  
Insulin Receptors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Model Assessment ◽  
Homeostasis Model Assessment ◽  
Insulin Resistant ◽  
Glucose Plasma

β-Endorphin plays a major role in the amelioration of insulin resistance. The present study documents that myricetin (3,5,7,-hexahydroxyflavone) ameliorates insulin resistance by enhancingβ-endorphin production in insulin-resistant rats. The rats were induced for insulin resistance by feeding them a diet containing 60% fructose for 6 weeks. The degree of insulin resistance was measured by the homeostasis model assessment of basal insulin resistance (HOMA-IR). The plasma levels of insulin andβ-endorphin were measured by an enzyme-linked immunosorbent assay. The insulin receptor-related signaling mediators in the soleus muscles of rats were evaluated by immunoprecipitation or immunoblotting. Myricetin was injected daily (1 mg kg−1per injection, thrice daily) for 14 days. Consequently, the high-glucose plasma levels in fructose-fed rats decreased significantly concomitant with an increase in plasmaβ-endorphin. The reduction of the elevated HOMA-IR index following treatment with myricetin was subsequently inhibited by the administration ofβ-funaltrexamine hydrochloride (β-FNA) at doses sufficient to blockμ-opioid receptors (MOR). The myricetin treatment was also observed to affect the phosphorylation of the insulin receptor, insulin receptor substrate-1, Akt and Akt substrate of 160 kDa, with subsequent effects on glucose-transporter subtype 4 translocation, all of which were blocked byβ-FNA pretreatment. These results indicated that enhancement ofβ-endorphin secretion, which in turn leads to peripheral MOR activation, is involved in the action of myricetin on the amelioration of impaired signaling intermediates downstream of insulin receptors.

Evaluation of Mn-superoxide dismutase and catalase gene expression in childhood obesity: its association with insulin resistance

2018 ◽  
Vol 31 (7) ◽  
pp. 727-732 ◽  
Author(s):  
Roohollah Mohseni ◽  
Zahra Arab Sadeghabadi ◽  
Mohammad Taghi Goodarzi ◽  
Maryam Teimouri ◽  
Mitra Nourbakhsh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Insulin Resistance ◽  
Superoxide Dismutase ◽  
Biochemical Parameters ◽  
Mononuclear Cells ◽  
Serum Insulin ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Model Assessment

Abstract Background Obesity is associated with oxidative stress. Superoxide dismutase (SOD) is the first line of defense against reactive oxygen species (ROS), eliminating the strong superoxide radical and producing H2O2, which can then be degraded by catalase (CAT). The main objective of this study was to evaluate the gene expression antioxidant enzymes (Mn-SOD and CAT) in peripheral blood mononuclear cells (PBMCs) of obese and normal-weight children, and its association with anthropometric and biochemical parameters. Methods Thirty obese and 30 control subjects between the ages of 8 and 16 years were enrolled in this study. Serum insulin levels were measured using enzyme-linked immunosorbent assay (ELISA), and insulin resistance was calculated using the homeostasis model assessment of insulin resistance (HOMA-IR). Biochemical parameters were also measured. PBMCs of the subjects were separated and Mn-SOD and CAT gene expression was measured using real-time polymerase chain reaction (PCR). Results Mn-SOD and CAT gene expression was significantly lower in the obese group compared with the control group (p<0.01). Also, a positive correlation was observed between the gene expression of Mn-SOD and CAT and body mass index (BMI), fasting blood sugar, insulin resistance, low density lipoprotein-cholesterol (LDL-C) cholesterol, triglycerides (TG) and systolic blood pressure (SBP). Conclusions Induction of antioxidants, especially Mn-SOD and CAT, can lead to reduction of oxidative stress and prevent the complications of obesity in children.

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