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Hyperleptinemia is associated with parameters of low-grade systemic inflammation and metabolic dysfunction in obese human beings  [PDF]
Sonia Leon-Cabrera,Lourdes Solís-Lozano,Karina Suárez-álvarez,Antonio González-Chávez,Galileo Escobedo
Frontiers in Integrative Neuroscience , 2013, DOI: 10.3389/fnint.2013.00062
Abstract: Leptin is an adipose tissue-derived hormone that has been involved in hypothalamic and systemic inflammation, altered food-intake patterns, and metabolic dysfunction in obese mice. However, it remains unclear whether leptin has a relationship with parameters of systemic inflammation and metabolic dysfunction in humans. We thus evaluated in a cross-sectional study the circulating levels of leptin in 40 non-obese and 41 obese Mexican individuals, examining their relationship with tumor necrosis factor alpha (TNF-α), interleukin (IL) 12, IL-10, central obesity, serum glucose and insulin levels, and serum triglyceride and cholesterol concentrations. Circulating levels of leptin, TNF-α, IL-12, IL-10, and insulin were measured by ELISA, while concentrations of glucose, triglyceride, and cholesterol were determined by enzymatic assays. As expected, serum levels of leptin exhibited a significant elevation in obese individuals as compared to non-obese subjects, showing a clear association with increased body mass index (r = 0.4173), central obesity (r = 0.4678), and body fat percentage (r = 0.3583). Furthermore, leptin also showed a strong relationship with serum TNF-α (r = 0.6989), IL-12 (r = 0.3093), and IL-10 (r = ?0.5691). Interestingly, leptin was also significantly related with high concentrations of fasting glucose (r = 0.5227) and insulin (r = 0.2229), as well as elevated levels of insulin resistance (r = 0.3611) and circulating triglyceride (r = 0.4135). These results suggest that hyperleptinemia is strongly associated with the occurrence of low-grade systemic inflammation and metabolic alteration in obese subjects. Further clinical research is still needed to determine whether hyperleptinemia may be a potential marker for recognizing the advent of obesity-related metabolic disorders in human beings.
Cereal based diets modulate some markers of oxidative stress and inflammation in lean and obese Zucker rats
Damien P Belobrajdic, Yan Y Lam, Mark Mano, Gary A Wittert, Anthony R Bird
Nutrition & Metabolism , 2011, DOI: 10.1186/1743-7075-8-27
Abstract: Seven wk old, lean and obese male Zucker rats (n = 8/group) were fed diets that contained wheat bran, barley or α-cellulose (control). After 3 months on these diets, systolic blood pressure was measured and plasma was analysed for glucose, insulin, lipids, oxygen radical absorbance capacity (ORAC), malondialdehyde, glutathione peroxidase and adipokine concentration (leptin, adiponectin, interleukin (IL)-1β, IL-6, TNFα, plasminogen activator inhibitor (PAI)-1, monocyte chemotactic protein (MCP)-1). Adipokine secretion rates from visceral and subcutaneous adipose tissue explants were also determined.Obese rats had higher body weight, systolic blood pressure and fasting blood lipids, glucose, insulin, leptin and IL-1β in comparison to lean rats, and these measures were not reduced by consumption of wheat bran or barley based diets. Serum ORAC tended to be higher in obese rats fed wheat bran and barley in comparison to control (p = 0.06). Obese rats had higher plasma malondialdehyde (p < 0.01) and lower plasma glutathione peroxidase concentration (p < 0.01) but these levels were not affected by diet type. PAI-1 was elevated in the plasma of obese rats, and the wheat bran diet in comparison to the control group reduced PAI-1 to levels seen in the lean rats (p < 0.05). These changes in circulating PAI-1 levels could not be explained by PAI-1 secretion rates from visceral or subcutaneous adipose tissue.A 3-month dietary intervention was sufficient for Zucker obese rats to develop oxidative stress and systemic inflammation. Cereal-based diets with moderate and high antioxidant capacity elicited modest improvements in indices of oxidative stress and inflammation.Oxidative stress commonly develops in obesity and has been identified as the unifying mechanism underlying the development of obesity-related co-morbidities. In obesity, a variety of factors contribute to oxidative stress including; hyperglycemia, hyperleptinemia, increased tissue lipid levels, inadequate antioxidant
A Fasting Insulin–Raising Allele at IGF1 Locus Is Associated with Circulating Levels of IGF-1 and Insulin Sensitivity  [PDF]
Gaia Chiara Mannino, Annalisa Greco, Carlo De Lorenzo, Francesco Andreozzi, Maria A. Marini, Francesco Perticone, Giorgio Sesti
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0085483
Abstract: Background A meta-analysis of genome-wide data reported the discovery of the rs35767 polymorphism near IGF1 with genome-wide significant association with fasting insulin levels. However, it is unclear whether the effects of this polymorphism on fasting insulin are mediated by a reduced insulin sensitivity or impaired insulin clearance. We investigated the effects of the rs35767 polymorphism on circulating IGF-1 levels, insulin sensitivity, and insulin clearance. Methodology/Principal Findings Two samples of adult nondiabetic white Europeans were studied. In sample 1 (n=569), IGF-1 levels were lower in GG genotype carriers compared with A allele carriers (190±77 vs. 218±97 ng/ml, respectively; P=0.007 after adjusting for age, gender, and BMI). Insulin sensitivity assessed by euglycaemic-hyperinsulinemic clamp was lower in GG genotype carriers compared with A allele carriers (8.9±4.1 vs. 10.1±5.1 mg x Kg-1 free fat mass x min-1, respectively; P=0.03 after adjusting for age, gender, and BMI). The rs35767 polymorphism did not show significant association with insulin clearance. In sample 2 (n=859), IGF-1 levels were lower in GG genotype carriers compared with A allele carriers (155±60 vs. 164±63 ng/ml, respectively; P=0.02 after adjusting for age, gender, and BMI). Insulin sensitivity, as estimated by the HOMA index, was lower in GG genotype carriers compared with A allele carriers (2.8±2.2 vs. 2.5±1.3, respectively; P=0.03 after adjusting for age, gender, and BMI). Conclusion/Significance The rs35767 polymorphism near IGF1 was associated with circulating IGF-1 levels, and insulin sensitivity with carriers of the GG genotype exhibiting lower IGF-1 concentrations and insulin sensitivity as compared with subjects carrying the A allele.
The effect of metformin on fasting and postprandial insulin secretion in obese patients with diabetes mellitus type 2  [PDF]
Vukovi? Mira,Lap?evi? Mirjana,Kalezi? Nevena,Gvozdenovi? Branislav S.
Srpski Arhiv za Celokupno Lekarstvo , 2007, DOI: 10.2298/sarh0708447v
Abstract: Introduction The main causes of reduced glucose levels during metformin therapy appear to be an increase in insulin action in peripheral tissues and reduced hepatic glucose output due to inhibition gluconeogenesis. Objective The purpose of the study was to establish the effect of metformin on fasting and postprandial insulin secretion. Method The study carried out was double blind, controlled, comparative, randomized, multicentric, including two groups of out-patient department (OPD) patients. 43 patients were administered metformin (Tefor ICN Canada), and 46 patients were given placebo. Patients enrolled in the study were newly diagnosed with diabetes mellitus (DM) type 2, glycaemia < 12 mmol/l, and had the Body Mass Index (BMI) > 30 kg/m2. Before treatment, blood biochemistry was done: fasting and postprandial glycaemia, glycosylated haemoglobin (HbA1c) value, fasting and postprandial insulinaemia, blood lipids (total cholesterol, total triglycerides, HDL cholesterol, and LDL cholesterol), and gamma glutaryl transferase (GGT) level. BMI was also established. After 42 days of treatment, fasting and postprandial insulinaemia were tested again. Analysis of the effects of therapy, and identification of co-variants for fasting and postprandial insulinaemia, were done by ANOVA two way and ANCOVA method. Results It was shown that metformin accompanied by diet, as compared to placebo accompanied by diet, lowered the fasting insulinaemia value during six weeks of therapy in obese patients with DM type 2 (24.392 mU/l vs. 25.667 mU/l), interacting both with BMI pre-therapy, and interacting with fasting insulinaemia pre-therapy (p<0.001). A significant effect of the interaction of covariants BMI and GGT was defined. As for the effect of therapy on postprandial insulinaemia, it was found that there was a high statistical significance of the effect of BMI interacting with initial values for postprandial insulinaemia before therapy, and interacting with therapy (p<0.01). Adjusted mean values for postprandial insulinaemia after therapy in the placebo group were lower as compared to the metformin group (44.807 mU/l vs. 47.114 mU/l). Conclusion It can be concluded that, as compared to placebo, metformin is more efficient in reducing insulin resistance in obese patients with DM type 2. In addition, as compared to placebo, metformin maintains more efficient productive insulin secretion, indicating that metformin protects the pancreas from beta cell depletion.
Effect of Acute Maximal Exercise on Circulating Levels of Interleukin-12 during Ramadan Fasting  [cached]
Salma Abedelmalek,Nizar Souissi,Akimoto Takayuki,Sami Hadouk
Asian journal of Sports Medicine , 2011,
Abstract: Purpose:The purpose of this study was to examine the effects of Ramadan fasting on circulating levels of interleukin-12 (IL-12) after a brief maximal exercise.Methods:Nine subjects performed a Wingate test on three different occasions: (i) the first week of Ramadan (1WR), (ii) the fourth week of Ramadan (4WR), and (iii) three weeks after Ramadan (AR). Blood samples were taken before, immediately and 60 min after the exercise. Plasma concentrations of IL-12 were measured using enzyme-linked immunosorbent assay. Variance analysis revealed no significant effect of Ramadan on Ppeak and Pmean during the three testing periods.Results:Considering the effect of Ramadan on plasma concentrations of IL-12, analysis of the variance revealed a significant Ramadan effect (F(2, 16) = 66.27 ; P<0.001) as well as a significant time effect (F(2, 16)= 120.66; P<0.001). However, no significant (Ramadan time) of test interaction (F(4, 32) = 2.40; P>0.05). For all measures, IL-12 levels were lower during 1WR and 4WR in comparison with AR (P<0.05). Considering the exercise effects, IL-12 levels measured immediately after the exercise were significantly higher than those measured before and at 60 minutes after the exercise (P<0.001).Conclusions:These results suggest that an acute intense exercise-induced IL-12 response is modified by daytime fasting and modifications in sleep schedule during Ramadan.
Circulating Tryptase as a Marker for Subclinical Atherosclerosis in Obese Subjects  [PDF]
María Moreno, Josep Puig, Marta Serrano, José María Moreno-Navarrete, Francisco Ortega, Wifredo Ricart, Jose Manuel Fernandez-Real
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0097014
Abstract: Introduction Mast cells participate in atherogenesis by releasing cytokines to induce vascular cell protease expression. Tryptase is expressed highly in human atherosclerotic lesions and the inhibition of tryptase activity hampers its capacity to maintain cholesterol inside macrophague foam cells. We aimed to investigate the association between circulating tryptase levels and subclinical atherosclerosis through estimation of carotid intima-media thickness (c-IMT) as surrogate marker for increased cardiovascular risk in obese and non-obese subjects. Methods Circulating tryptase levels (ELISA) and metabolic parameters were analyzed in 228 subjects. Atherosclerosis (c-IMT>0.9 mm) was evaluated ultrasonographically. Results Significant positive associations were evident between circulating tryptase levels and BMI, fat mass, glycated haemoglobin, fasting insulin, HOMAIR, fasting triglycerides and ultrasensitive PCR (p<0.05 from linear-trend ANOVA). The positive association between tryptase levels and insulin resistance parameters, suggested a glucose homeostasis impairment in individuals with higher tryptase levels. The negative asociation between tryptase levels and HDL-cholesterol supports the proatherogenic role of this protease (p<0.0001). Circulating tryptase levels were strongly associated with c-IMT measurements (p<0.0001 from linear-trend ANOVA), and were higher in subjects with presence of carotid plaque (p<0.0001). Tryptase levels (beta = 0.015, p = 0.001) contributed independently to subclinical atherosclerosis variance after controlling for cardiovascular risk factors (BMI, blood pressure, LDL-cholesterol). Conclusions Circulating tryptase level is associated to obesity related parameters and has a close relation with various metabolic risk factors. Moreover, serum tryptase level was independently associated with c-IMT, suggesting its potential use as a surrogate marker for subclinical atherosclerosis in obese subjects.
Severely Obese Adolescents and Adults Exhibit a Different Association of Circulating Levels of Adipokines and Leukocyte Expression of the Related Receptors with Insulin Resistance  [PDF]
Antonello E. Rigamonti,Fiorenza Agosti,Alessandra De Col,Giancarlo Silvestri,Nicoletta Marazzi,Silvia Bini,Sara Bonomo,Marialuisa Giunta,Silvano G. Cella,Alessandro Sartorio
International Journal of Endocrinology , 2013, DOI: 10.1155/2013/565967
Abstract: Obese adults frequently exhibit a low-grade inflammation and insulin resistance, which have been hypothesized to be established early in childhood. Aim of this study was to evaluate the age-dependent relationships between inflammatory state and insulin resistance in obese adolescents and adults. Clinical and metabolic parameters, circulating adipokines (TNF-α, adiponectin, and leptin), ghrelin, their leukocyte receptors (TNFR1, ADIPOR2, OBRL and GHSR1a), and acute phase reactants (CRP and white blood cells) were assessed in lean and obese adolescents compared with the adult counterparts. Only obese adults had higher HOMA-IR, insulin, and triglycerides compared to the lean group. An inflammatory state was present in obese adolescents and adults, as demonstrated by the higher values of CRP and neutrophils. There were no group differences in circulating levels of TNF-α and leukocyte expression of TNFR1. Adiponectin concentrations and leukocyte expression of ADIPOR2 were higher in the lean groups than in the corresponding obese counterparts. For leptin and leukocyte expression of OBRL, the results were opposed. Circulating levels of ghrelin were higher in lean adolescents and adults than the related lean groups, while there was a higher leukocyte expression of GHSR1a in (only) lean adults than obese adults. When the analysis was performed in (lean or obese) adults, TNF-α, neutrophils, leptin, and GHSR1a were predictors of HOMA-IR. None of the considered independent variables accounted for the degree of insulin resistance in the adolescent group. In conclusion, a dissociation between the low-grade inflammation and insulin resistance is supposed to exist in the early phases of obesity. 1. Introduction Obesity is considered a low-grade chronic inflammatory disease that may contribute to the development of insulin resistance [1]. Obese adolescents and adults are at higher risk for developing type 2 diabetes (T2D), cardiovascular disease, nonalcoholic fatty liver disease (NAFLD), osteoarticular diseases, and several forms of cancer [2]. Recent clinical studies have suggested that mediators of low-grade chronic inflammation, such as adipokines, cytokines, ghrelin, and acute phase reactants, are involved in the development of these comorbid conditions [3, 4]. Tumor necrosis factor-α (TNF-α) is one of the main mediators of the inflammatory response in obesity and is expressed by infiltrating macrophages and adipocytes in the hypertrophic adipose tissue [5]. TNF-α receptors 1 (TNFR1) and 2 (TNFR2) are the two main transducers of the TNF-α signals in most cells and
New adipokines vaspin and omentin. Circulating levels and gene expression in adipose tissue from morbidly obese women
Teresa Auguet, Yunuen Quintero, David Riesco, Beatriz Morancho, Ximena Terra, Anna Crescenti, Montserrat Broch, Carmen Aguilar, Montserrat Olona, José Porras, Mercè Hernandez, Fátima Sabench, Daniel del Castillo, Cristóbal Richart
BMC Medical Genetics , 2011, DOI: 10.1186/1471-2350-12-60
Abstract: We analysed vaspin and omentin circulating levels in 71 women of European descent (40 morbidly obese [BMI ≥ 40 kg/m2] and 31 lean [BMI ≤ 25]). We assessed vaspin and omentin gene expression in paired samples of visceral and subcutaneous abdominal adipose tissue from 46 women: 40 morbidly obese and 6 lean. We determined serum vaspin and plasma omentin levels with an Enzyme-Linked Immunosorbent Assay and adipose tissue mRNA expression by real time RT-PCR.Serum vaspin levels in the morbidly obese were not significantly different from those in controls. They correlated inversely with levels of lipocalin 2 and interleukin 6. Vaspin mRNA expression was significantly higher in the morbidly obese, in both subcutaneous and visceral adipose tissue.Plasma omentin levels were significantly lower in the morbidly obese and they correlated inversely with glucidic metabolism parameters. Omentin circulating levels, then, correlated inversely with the metabolic syndrome (MS). Omentin expression in visceral adipose tissue was significantly lower in morbidly obese women than in controls.The present study indicates that vaspin may have a compensatory role in the underlying inflammation of obesity. Decreased omentin circulating levels have a close association with MS in morbidly obese women.The incidence of obesity is rising rapidly in industrialized and developing countries. Increased abdominal visceral fat is associated with insulin resistance, type 2 diabetes, and coronary heart disease [1]. Reduction of visceral fat mass by omentectomy has significant positive and long-term effects on glucose metabolism, insulin sensitivity, and metabolic profiles in obese subjects [2]. In the last decade, numerous studies have revealed that adipose tissue secretes a variety of bioactive substances that could explain the epidemiologic relationship between visceral fat mass and increased metabolic risk. These substances, termed adipokines, include leptin [3], adiponectin [4], resistin [5], lipocalin 2
Leptin, insulin and thyroid hormones in a cohort of Egyptian obese Down syndrome children: a comparative study  [cached]
Yahia Sohier,EL-farahaty Reham M,El-Hawary Amany K,El-hussiny Mona A
BMC Endocrine Disorders , 2012, DOI: 10.1186/1472-6823-12-22
Abstract: Background Obesity is a major worldwide health problem. It is commonly observed in Down syndrome individuals than in the general population. The reason for increased risk of obesity in DS is unclear. The current study was designed to clarify differences in some obesity- related hormones in a group of prepubertal Down syndrome children. Methods Thirty six Egyptian children with Down syndrome were enrolled in this study, divided according to their body mass index (BMI) into 23 obese and13 non obese. Another group of 43 non Down children were recruited, they were divided according to their BMI into 20 patients having simple obesity and 23 non obese, as control groups. Fasting blood samples were collected for estimation of fasting blood glucose (FBG), insulin, leptin, free thyroxin (FT4), thyroid stimulating hormones (TSH) and creatine kinase (CK). Insulin resistance was assessed by Homeostasis Model Assessment method (HOMA-IR). The ratio of leptin to BMI (LEP/BMI) was used as an index of leptin resistance. Results Median values of FBG, insulin, and HOMA-IR were significantly higher in Down versus non Down groups, while median values of leptin and leptin resistance were non-significantly different among Down versus non Down groups. Median TSH values were non- significantly different between obese Down and obese non Down. Although the median values of TSH and FT4 were within normal range in Down groups, four cases of subclinical hypothyroidism were encountered. Leptin levels were correlated with insulin and IR but not with TSH in Down groups. Conclusion Increased circulating leptin, a marker of leptin resistance in obese children with Down syndrome seems to be similar to that in children with simple obesity. Elevated FBG and insulin in obese Down children highlights the presence of early IR. Associated myopathy evidenced by mildly elevated CK levels could be an added factor for obesity in such group of patients.
Oral but Not Intravenous Glucose Acutely Decreases Circulating Interleukin-6 Concentrations in Overweight Individuals  [PDF]
Patrick J. Manning, Wayne H. F. Sutherland, Sheila M. Williams, Sylvia A. de Jong, Gavin P. Hendry
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0066395
Abstract: Background Plasma interleukin-6 (IL-6) concentrations decrease acutely 1 h after ingestion of a glucose load or mixed meals and this may be mediated by an anti-inflammatory effect of insulin. The aim of the present study was to compare the effect of higher versus lower insulin levels on plasma IL-6 concentrations following oral compared with intravenous glucose administration in overweight/obese subjects. Methods and Findings Fifteen subjects (12 women and 3 men) with BMI >28 kg/m2 were given an oral glucose load (75g) followed a week later by an intravenous infusion of glucose aimed at matching plasma glucose concentrations during the oral glucose load. A week later, they drank a volume of water equivalent to the volume consumed with the oral glucose load. Plasma glucose, insulin, nonesterified fatty acids, and IL-6 concentrations and blood hematocrit were measured at 30 minute intervals for 2 h following each intervention. Plasma IL-6 decreased (13–20%) significantly (P = 0.009) at 30 min to 90 min following the oral glucose load and did not change significantly following the other two interventions. The incremental area under the curve for plasma IL-6 concentrations following oral intake of glucose was significantly lower compared with concentrations following intravenous glucose (P = 0.005) and water control (P = 0.02). Circulating insulin concentrations were significantly (P<0.001) and 2.8 fold higher following oral compared with intravenous glucose administration. Conclusions These data show that plasma IL-6 concentrations did not decrease during isoglycemic, intravenous glucose administration suggesting that the markedly higher circulating insulin levels and/or gut-related factors may mediate the acute decrease in plasma IL-6 after oral glucose intake in overweight/obese subjects. Trial Registration Australian New Zealand Clinical Trials Registry ACTRN12612000491864
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