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The influence of diet with reduction in calorie intake on metabolic syndrome parameters in obese subjects with impaired glucose tolerance  [PDF]
Polovina Sne?ana,Mici? Dragan
Medicinski Pregled , 2010, DOI: 10.2298/mpns1008465p
Abstract: Introduction. Current therapy of metabolic syndrome includes the assessment of cardiovascular risk together with control of high blood pressure, hyperlipidaemia and prevention of type 2 diabetes with adequate diet and increase in physical activity. Aim of the study. To investigate the influence of medical nutritive therapy in obese people with impaired glucose tolerance risk factor for Type 2 Diabetes mellitus and potential consecutive lowering of cardio-metabolic risk. Material and methods. The 55 obese (body mass index greater than 30 kg/m2) subjects were divided into two groups, the study group A (n=35), and the control group B (n=20). Group A was on diet for a period of 12 weeks (1200-1500kcal/day diet with 55-65% carbohydrates, 15-18% proteins and 22-23% predominantly unsaturated fats, and 20-40g fibers/day.). Before and after 12 weeks the following parameters were determined: waist circumference, blood pressure, fasting plasma glucose, Index HOMA-IR, HDL cholesterol and triglycerides. Results. After 12 weeks on low calorie diet in Group A there was a decrease in the waist circumference (p=0.001); systolyc blood pressure (p=0.001); diastolic blood pressure (p= 0.01); fasting blood glucose (p=0.001); Index HOMA IR (p<0.001); triglycerides (p<0.001) and increase in HDL cholesterol (p<0.05). Conclusion. These results suggest that implementation of low callorie-high fibers diet with balanced nutritive elements have a positive effect on visceral obesity, fasting glucose, lipid profile, and hypertension in obese people with impaired glucose tolerance and lead to consecutive lowering of cardiometabolic risk.
Adipokine Pattern in Subjects with Impaired Fasting Glucose and Impaired Glucose Tolerance in Comparison to Normal Glucose Tolerance and Diabetes  [PDF]
Anke T?njes,Mathias Fasshauer,Jürgen Kratzsch,Michael Stumvoll,Matthias Blüher
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0013911
Abstract: Altered adipokine serum concentrations early reflect impaired adipose tissue function in obese patients with type 2 diabetes (T2D). It is not entirely clear whether these adipokine alterations are already present in prediabetic states and so far there is no comprehensive adipokine panel available. Therefore, the aim of this study was to assess distinct adipokine profiles in patients with normal glucose tolerance (NGT), impaired fasting glucose (IFG), impaired glucose tolerance (IGT) or T2D.
Prevalence of impaired glucose tolerance and insulin resistance among obese children and adolescents
Robabeh Ghergherechi, Ali Tabrizi
Therapeutics and Clinical Risk Management , 2010, DOI: http://dx.doi.org/10.2147/TCRM.S12033
Abstract: evalence of impaired glucose tolerance and insulin resistance among obese children and adolescents Original Research (4461) Total Article Views Authors: Robabeh Ghergherechi, Ali Tabrizi Published Date July 2010 Volume 2010:6 Pages 345 - 349 DOI: http://dx.doi.org/10.2147/TCRM.S12033 Robabeh Ghergherechi1, Ali Tabrizi2 1Department of Pediatrics Endocrinology, Tabriz University of Medical Sciences, Tabriz, Iran; 2Students’ Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran Purpose: Obesity is one of the most important nutritional disorders in the world which has an obvious relationship with the incidence of metabolic diseases. Obesity prevalence has increased among children and adolescents during recent decades, leading to a rise in Type 2 diabetes mellitus (DM II) prevalence in these two age brackets. Hence, the aim of this study was to assess impaired glucose tolerance and insulin resistance, and gather metabolic findings in obese children and adolescents. Methods and materials: We studied 110 obese children and adolescents (body mass index > 95th percentile for age and gender) 4–18 years of age referred to the endocrine clinic of the Children’s Hospital at Tabriz University in a descriptive cross-sectional study. -Fasting glucose, insulin, and lipid profile in all subjects were determined. Oral glucose tolerance test after eating 75 g/kg glucose was performed. Homeostatic model assessment was used to -estimate insulin resistance. Results: Impaired glucose tolerance and insulin resistance prevalence in 68 obese adolescents was 14.7% and 31.8%, respectively. Impaired glucose tolerance and insulin resistance was not seen in 23.8% of 42 obese children. No case of DM II was seen. There was a significant statistical difference in glucose (P = 0.003) and insulin (P < 0.001) level at minute 120 in individuals with impaired glucose tolerance compared to obese children and adolescents without impaired glucose tolerance. Rate of insulin resistance in patients with impaired glucose tolerance was greater and had a significant statistical difference (P = 0.03). Conclusion: Obesity has a close relationship with increased risk of impaired glucose tolerance and insulin resistance in children and adolescents. Oral glucose tolerance test, unlike fasting glucose test, is a benefit test to predict impaired glucose tolerance. With prompt identification and treatment of obese children with impaired glucose tolerance, we can prevent it from progression towards DM II.
Prevalence of impaired glucose tolerance and insulin resistance among obese children and adolescents  [cached]
Robabeh Ghergherechi,Ali Tabrizi
Therapeutics and Clinical Risk Management , 2010,
Abstract: Robabeh Ghergherechi1, Ali Tabrizi21Department of Pediatrics Endocrinology, Tabriz University of Medical Sciences, Tabriz, Iran; 2Students’ Research Committee, Tabriz University of Medical Sciences, Tabriz, IranPurpose: Obesity is one of the most important nutritional disorders in the world which has an obvious relationship with the incidence of metabolic diseases. Obesity prevalence has increased among children and adolescents during recent decades, leading to a rise in Type 2 diabetes mellitus (DM II) prevalence in these two age brackets. Hence, the aim of this study was to assess impaired glucose tolerance and insulin resistance, and gather metabolic findings in obese children and adolescents.Methods and materials: We studied 110 obese children and adolescents (body mass index > 95th percentile for age and gender) 4–18 years of age referred to the endocrine clinic of the Children’s Hospital at Tabriz University in a descriptive cross-sectional study. -Fasting glucose, insulin, and lipid profile in all subjects were determined. Oral glucose tolerance test after eating 75 g/kg glucose was performed. Homeostatic model assessment was used to -estimate insulin resistance.Results: Impaired glucose tolerance and insulin resistance prevalence in 68 obese adolescents was 14.7% and 31.8%, respectively. Impaired glucose tolerance and insulin resistance was not seen in 23.8% of 42 obese children. No case of DM II was seen. There was a significant statistical difference in glucose (P = 0.003) and insulin (P < 0.001) level at minute 120 in individuals with impaired glucose tolerance compared to obese children and adolescents without impaired glucose tolerance. Rate of insulin resistance in patients with impaired glucose tolerance was greater and had a significant statistical difference (P = 0.03).Conclusion: Obesity has a close relationship with increased risk of impaired glucose tolerance and insulin resistance in children and adolescents. Oral glucose tolerance test, unlike fasting glucose test, is a benefit test to predict impaired glucose tolerance. With prompt identification and treatment of obese children with impaired glucose tolerance, we can prevent it from progression towards DM II.Keywords: impaired glucose tolerance, insulin resistance, obesity
Risk factors for impaired glucose tolerance in obese children and adolescents  [cached]
Michaela Kleber,Gideon de Sousa,Sophie Papcke,Thomas Reinehr
World Journal of Diabetes , 2010,
Abstract: AIM: To investigate which obese children have an increased risk for impaired glucose tolerance (IGT), a risk factor for later diabetes.METHODS: We studied 169 European untreated obese children and adolescents with normal glucose tolerance at baseline. Waist circumference, fasting glucose, lipids, blood pressure, pubertal stage, 2 h glucose in oral glucose tolerance test (oGTT), and HbA1c were determined at baseline and 1 year later.RESULTS: One year after baseline, 19 (11.2%) children demonstrated IGT, 4 (2.4%) children had impaired fasting glucose, no (0%) child suffered from diabetes, and 146 (86%) children still showed normal glucose tolerance. At baseline, the children with IGT and with normal glucose tolerance in a one-year follow-up did not differ significantly in respect of any analyzed parameter, apart from pubertal stage. The children developing IGT entered puberty significantly more frequently (37% vs 3%, P < 0.001). One year after baseline, the children with IGT demonstrated significantly increased waist circumference, blood pressure values, insulin and triglyceride concentrations, and insulin resistance index HOMA. The children remaining in the normal glucose tolerance status 1 year after baseline did not demonstrate any significant changes.CONCLUSION: During the study period of 1 year, more than 10% of the obese children with normal glucose tolerance converted to IGT. Repeated screening with oGTT seems meaningful in obese children entering puberty or demonstrating increased insulin resistance, waist circumference, blood pressure, or triglyceride concentrations.
Altered or Impaired Immune Response to Hepatitis B Vaccine in WNIN/GR-Ob Rat: An Obese Rat Model with Impaired Glucose Tolerance  [PDF]
Prathibha Bandaru,Hemalatha Rajkumar,Giridharan Nappanveettil
ISRN Endocrinology , 2011, DOI: 10.5402/2011/980105
Abstract: Obesity is shown to increase the incidence and severity of infectious diseases and individuals seem to exhibit poor antibody response to vaccination due to several inherent immune defects. With the increasing prevalence of impaired glucose tolerance (IGT) seen in obese individuals, the present study was aimed to investigate the basal immune response and immune response upon Hepatitis B vaccination (HBV) in an obese rat model WNIN/GR-Ob with impaired glucose tolerance (IGT). Decreased proportions of splenic CD4+ T helper cells and CD3+ T cells were observed in obese animals compared to lean animals. Upon HBV, obese animals showed reduced cell-mediated immunity and humoral immunity in terms of splenic lymphocyte proliferative response to Concanavalin A (Con A) and Hepatitis B surface antigen (HBsAg) and HBsAg-specific IgG response. Innate immunity as assessed in terms of Tumor Necrosis Factor α (TNF α) and Nitric oxide (NO) production by peritoneal macrophages upon HBV was low and unchanged, respectively, in obese animals. Thus long-term immunological memory is impaired or altered upon HBV. 1. Introduction Obesity is often associated with increased risk of degenerative diseases like type 2 diabetes, cardiovascular disease (CVD), and cancer [1]. However, clinically a positive correlation between body weight index and incidence of nosocomial infections was also observed [2]. Increased infections were reported in genetically obese and diet-induced obese rodent models. For example, Zucker obese rats showed an increased susceptibility to Candida albicans infections [3], while Ob/Ob mice displayed impaired immune response to Listeria monocytogenes and Candida albicans [4]. In diet-induced obese (DIO) rodent models, a poor response to Porphyromonas gingivalis infection were observed and infection with influenza virus seemed to cause high mortality rate in mice [5, 6]. In obese individuals reduction in lymphocyte numbers and reduced responsiveness to mitogen were observed [7, 8]. Defects in specific immunity such as reduced lymphocyte numbers in spleen, thymus, and peripheral blood have been reported in Ob/Ob and db/db mice and fa/fa Zucker rats [9]. Diminished responsiveness to mitogen as well as cytotoxic activity was also seen in these animals [9]. Same was true in DIO models where reduced lymphocyte response and altered cytokine secretion were observed [10]. Poor antibody response was reported in obese individuals and overweight children’s against vaccination [11–13]. Furthermore, reduced lymphocyte function upon HBV was observed in WNIN/Ob obese rat [14]. In
Effects of Growth Hormone and Pioglitazone in Viscerally Obese Adults with Impaired Glucose Tolerance: A Factorial Clinical Trial  [PDF]
Hamdee Attallah, Anne L Friedlander, Matilde Nino-Murcia, Andrew R Hoffman
PLOS ONE , 2007, DOI: 10.1371/journal.pctr.0020021
Abstract: Objective Recombinant human growth hormone (GH) and pioglitazone (PIO) in abdominally obese adults with impaired glucose tolerance were evaluated under the hypothesis that the combination attenuates GH-induced increases in glucose concentrations, reduces visceral adipose tissue (VAT), and improves insulin sensitivity over time. Design Randomized, double-blind, placebo-controlled, 2 × 2 factorial design. Setting Veterans Affairs Palo Alto Health Care System, Palo Alto, California, United States. Participants 62 abdominally obese adults aged 40–75 with impaired glucose tolerance. Interventions GH (8 μg/kg/d, or placebo) and pioglitazone (30 mg/d, or placebo) for 40 wk. Outcome Measures Baseline and after 40 wk of treatment, VAT content was quantified by CT scan, glucose tolerance was assessed using a 75-g oral glucose tolerance test, and insulin sensitivity was measured using steady-state plasma glucose levels obtained during insulin suppression test. Results Baseline: body mass index (BMI), plasma glucose, and visceral fat content were similar. 40 wk: visceral fat area declined 23.9 ± 7.4 cm2 in GH group, mean difference from placebo: ?28.1 cm2 (95% CI ?49.9 to ?6.3 cm2; p = 0.02). Insulin resistance declined 52 ± 11.8 mg/dl with PIO, mean difference from placebo of ?58.8 mg/dl (95% CI ?99.7 to ?18.0 mg/dl; p = 0.01). VAT and SSPG declined with GH and PIO combined, mean differences from placebo of ?31.4 cm2 (95% CI ?56.5 cm2 to ?6.3 cm2; p = 0.02) and ?55.3 mg/dl (95% CI ?103.9 to ?6.7 mg/dl; p = 0.02), respectively. Fasting plasma glucose increased transiently in GH group. No significant changes in BMI were observed. Conclusions Addition of PIO to GH attenuated the short-term diabetogenic effect of GH; the drug combination reduced VAT and insulin resistance over time. GH plus PIO may have added benefit on body composition and insulin sensitivity in the metabolic syndrome. Trial Registration ClinicalTrials.gov NCT00352287
Allele Summation of Diabetes Risk Genes Predicts Impaired Glucose Tolerance in Female and Obese Individuals  [PDF]
Katarzyna Linder, Robert Wagner, Erifili Hatziagelaki, Caroline Ketterer, Martin Heni, Fausto Machicao, Norbert Stefan, Harald Staiger, Hans-Ulrich H?ring, Andreas Fritsche
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0038224
Abstract: Introduction Single nucleotide polymorphisms (SNPs) in approximately 40 genes have been associated with an increased risk for type 2 diabetes (T2D) in genome-wide association studies. It is not known whether a similar genetic impact on the risk of prediabetes (impaired glucose tolerance [IGT] or impaired fasting glycemia [IFG]) exists. Methods In our cohort of 1442 non-diabetic subjects of European origin (normal glucose tolerance [NGT] n = 1046, isolated IFG n = 142, isolated IGT n = 140, IFG+IGT n = 114), an impact on glucose homeostasis has been shown for 9 SNPs in previous studies in this specific cohort. We analyzed these SNPs (within or in the vicinity of the genes TCF7L2, KCNJ11, HHEX, SLC30A8, WFS1, KCNQ1, MTNR1B, FTO, PPARG) for association with prediabetes. Results The genetic risk load was significantly associated with the risk for IGT (p = 0.0006) in a model including gender, age, BMI and insulin sensitivity. To further evaluate potential confounding effects, we stratified the population on gender, BMI and insulin sensitivity. The association of the risk score with IGT was present in female participants (p = 0.008), but not in male participants. The risk score was significantly associated with IGT (p = 0.008) in subjects with a body mass index higher than 30 kg/m2 but not in non-obese individuals. Furthermore, only in insulin resistant subjects a significant association between the genetic load and the risk for IGT (p = 0.01) was found. Discussion We found that T2D genetic risk alleles cause an increased risk for IGT. This effect was not present in male, lean and insulin sensitive subjects, suggesting a protective role of beneficial environmental factors on the genetic risk.
Inflammatory Markers in Middle-Aged Obese Subjects: Does Obstructive Sleep Apnea Syndrome Play a Role?  [PDF]
Paschalis Steiropoulos,Nikolaos Papanas,Evangelia Nena,Maria Antoniadou,Evangelia Serasli,Sophia Papoti,Olga Hatzizisi,Georgios Kyriazis,Argyris Tzouvelekis,Efstratios Maltezos,Venetia Tsara,Demosthenes Bouros
Mediators of Inflammation , 2010, DOI: 10.1155/2010/675320
Abstract: Background. Obstructive Sleep Apnea Syndrome (OSAS) is associated with inflammation, but obesity may be a confounding factor. Thus, the aim of this study was to explore differences in serum levels of inflammation markers between obese individuals with or without OSAS. Methods. Healthy individuals ( ) from an outpatient obesity clinic were examined by polysomnography and blood analysis, for measurement of TNF- , IL-6, CRP, and fibrinogen levels. According to Apnea-Hypopnea Index (AHI), participants were divided into two BMI-matched groups: controls (AHI?<?15/h, ) and OSAS patients (AHI? ?15/h, ). Results. OSAS patients had significantly higher TNF- levels ( ) while no other difference in the examined inflammation markers was recorded between groups. Overall, TNF- levels were correlated with neck circumference ( ), AHI ( ), and Oxygen Desaturation Index ( ). Conclusions. Obese OSAS patients have elevated TNF- levels compared to BMI-matched controls, suggesting a role of OSAS in promoting inflammation, possibly mediated by TNF-a. 1. Introduction Obstructive Sleep Apnea Syndrome (OSAS) is a common disorder, known to affect about 4% of middle-aged men and 2% of middle-aged women [1]. Patients exhibit repetitive episodes of partial or complete obstruction of the upper airway during sleep, ultimately leading to increased respiratory effort, oxyhemoglobin desaturation, sleep fragmentation, and excessive daytime sleepiness. Increasing evidence suggests that OSAS is associated with hypertension and other cardiovascular diseases, metabolic derangement, and impaired glucose tolerance [2]. Obesity is not only a well-established risk factor for OSAS [1, 3–6] but also a proinflammatory state [7]. In contrast to earlier theories which considered the adipose tissue as a sole energy depot, current data demonstrate that it is an active endocrine organ, releasing a number of bioactive mediators (adipokines) that modulate blood pressure, lipid- and glucose-metabolism, atherosclerosis, and inflammation [7–9]. Indeed, macrophages of the adipose tissue secrete proinflammatory cytokines such as Tumor Necrosis Factor- (TNF- ) and Interleukin-6 (IL-6) [7, 10]. Similarly, inflammation is one of the postulated links between OSAS and increased cardiovascular morbidity [2]. Indeed, the proinflammatory transcription factor NF- B is upregulated in OSAS. This is mediated by the alterations between hypoxia and reoxygenation, along with sleep deprivation. NF- B plays a key role in inflammatory responses, regulating the expression of inflammatory genes [11]. So far, previous studies, as
The Effect of Chronic Candesartan Therapy on the Metabolic Profile and Renal Tissue Cytokine Levels in the Obese Zucker Rat
Carolyn M. Ecelbarger,Arjun Rash,Rajesh K. Sinha,Swasti Tiwari
Mediators of Inflammation , 2010, DOI: 10.1155/2010/841343
Abstract: The effect of candesartan, an angiotensin-II type-1 receptor antagonist, on the metabolic profile and renal inflammation is unclear. We evaluated this relationship by feeding male lean (LZ) and obese (OZ) Zucker rats chow or chow with candesartan (23.5 mg/kg?diet) for 14 weeks (=6–8/treatment/body type). Candesartan reduced serum triglycerides, plasma creatinine, urine albumin, and renal cortical collagen and glycogen deposition in the OZ. An ELISA-based cytokine array revealed that candesartan normalized elevated renal interleukin (IL) 1- and monocyte chemoattractant protein-1 (MCP-1) levels in OZ. Nonetheless, candesartan impaired glucose tolerance, and did not lower blood insulin or glucose levels. Moreover, renal IL-1, -2, -4, -6 and -10 tumor necrosis factor-, interferon-, were significantly reduced in OZ relative to LZ, and increased by candesartan. Furthermore, candesartan increased growth-regulated oncogene, transforming growth factor-1 and IL-18 in OZ kidneys to a level higher than LZ or untreated OZ. Candesartan did not affect renal cytokine levels in LZ. Overall, candesartan attenuated renal disease and improved renal function in OZ, despite mixed effects on metabolic factors and cytokines. Reduced plasma triglycerides and/or renal MCP-1 and IL-1 may have had a role in this protection. However, these effects were clearly independent of any improvement in glucose tolerance.
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