scholarly journals Metabolic Syndrome and Insulin Resistance in Normal Glucose Tolerant Brazilian Adolescents With Family History of Type 2 Diabetes

Diabetes Care ◽  
2005 ◽  
Vol 28 (3) ◽  
pp. 716-718 ◽  
Author(s):  
R. C.Q. da Silva ◽  
W. L. Miranda ◽  
A. R. Chacra ◽  
S. A. Dib
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Family History ◽  
Normal Glucose Tolerant ◽  
Normal Glucose ◽  
Glucose Tolerant ◽  
History Of

scholarly journals Prevalence of insulin resistance in obese adolescents

2013 ◽  
Vol 53 (3) ◽  
pp. 167 ◽  
Author(s):  
Aman B. Pulungan ◽  
Ardita Puspitadewi ◽  
Rini Sekartini
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Type 2 Diabetes Mellitus ◽  
Family History ◽  
Model Assessment ◽  
Obese Adolescents ◽  
History Of

Background Childhood obesity is a global health problem, withthe prevalence is differed in each country and affected by manyfactors, such as lifestyle and physical activity. Insulin resistance(IR) as a basic mechanism of several metabolic diseases in obesity,is related with metabolic syndrome (MetS) along with its longterm complications, such as type 2 diabetes mellitus (T2DM).Several factors are known to be associated with IR, and thepresence of acanthosis nigricans (AN) has an important meaningin predicting IR.Objectives To assess the prevalence of IR, MetS in obeseadolescents and its potentially associated factors, such as gender,signs of AN, and family history of metabolic diseases.Methods A cross-sectional study was performed in obeseadolescents, aged 12-15 years, over a two-month period. Fastingblood glucose, insulin, and lipid profiles were measured. Obesitywas defined using body mass index (BMI). Insulin resistancewas quantified by the homeostasis model assessment for IR(HOMA-IR) . Metabolic syndrome was defined according to theInternational Diabetes Federation (IDF) 2007 criteria.Results Of92 obese adolescents, IR was found in 38% of subjects,with females predominating (57.2%). Signs of AN were seen in71. 4% of subj ects and a positive family history of metabolic diseaseswas found in 82.8% of subjects, including family history of obesity,type 2 diabetes mellitus (T2DM), and hypertension. Less than10% of subjects were considered to be in a prediabetic state, andnone had T2DM. No statistical significance was found betweengender, family history, or signs of AN and IR (P>0.05). Metabolicsyndromes was found in 19.6% of subjects, with the fo llowingprevalences for each component: 34.8% for hypertension, 78.3%for central obesity, 8.7% for impaired fasting glucose (IFG), 22.8%for low levels of HDL, and 2 1. 7% for high triglyceride levels. Astrong correlation was found between IR and IFG with OR= 5 .69(95%CI 1.079 ~ 29.993, P= D.04).Conclusion We find a high prevalence ofIRin obese adolescents,and IR increases the risk of prediabetes. Thus, prevention strategies are needed to overcome the long term impact of obesity on health.

scholarly journals Serum Matrix Metalloproteinase 9 and Macrophage Migration Inhibitory Factor (MIF) Are Increased in Young Healthy Nonobese Subjects with Positive Family History of Type 2 Diabetes

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Agnieszka Nikołajuk ◽  
Natalia Matulewicz ◽  
Magdalena Stefanowicz ◽  
Monika Karczewska-Kupczewska
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Family History ◽  
Macrophage Migration Inhibitory Factor ◽  
Positive Family History ◽  
Macrophage Migration ◽  
History Of

Insulin resistance increases the risk for cardiovascular disease (CVD) even in the absence of classic risk factors, such as hyperglycemia, hypertension, dyslipidemia, and obesity. Low-grade chronic inflammatory state is associated both with insulin resistance and atherosclerosis. An increased circulating level of proinflammatory proatherogenic factors and biomarkers of endothelial activation was observed in diabetes and CVD. The aim of our study was to assess serum proatherogenic and proinflammatory factors in young healthy nonobese subjects with positive family history of type 2 diabetes. We studied 74 young healthy nonobese subjects with normal glucose tolerance (age < 35 years, BMI < 30 kg/m2), 29 with positive family history of type 2 diabetes (relatives, 25 males and 4 females) and 45 subjects without family history of diabetes (control group, 39 males and 6 females). Hyperinsulinemic-euglycemic clamp was performed, and serum concentrations of monocyte chemoattractant protein-1 (MCP-1), interleukin 18 (IL-18), macrophage inhibitory cytokine 1 (MIC-1), macrophage migration inhibitory factor (MIF), matrix metalloproteinase (MMP-9), and soluble forms of adhesion molecules were measured. Relatives had markedly lower insulin sensitivity (p=0.019) and higher serum MMP-9 (p<0.001) and MIF (p=0.006), but not other chemokines and biomarkers of endothelial function. Insulin sensitivity correlated negatively with serum MMP-9 (r=−0.23, p=0.045). Our data show that young healthy subjects with positive family history of type 2 diabetes already demonstrate an increase in some nonclassical cardiovascular risk factors.

scholarly journals Adipocytokine Levels in Genetically High Risk for Type 2 Diabetes in the Indian Population: A Cross-Sectional Study

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
K. Subhash Chandra Bose ◽  
Shachin K. Gupta ◽  
Prerna Vyas
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Regression Analysis ◽  
Family History ◽  
High Risk ◽  
Diabetes Group ◽  
Family History Of Diabetes ◽  
Group Iii ◽  
History Of

Introduction. In view of the noteworthy role of adipocytokines in the onset of insulin resistance and diabetes in gene-knockout-rat-model-cell-line studies we aimed to study the influence of genetic predisposition for diabetes on adipocytokine levels and their role in building insulin-resistance-like environment well before the onset of diabetes; thus a hypothesis can be drawn on their role in developing diabetes in high risk population.Methods. Ages between 18 and 22 years were selected and divided into three groups. Group I(n=81): control group with no family history of diabetes. Group II(n=157): with one of their parents with history of type 2 diabetes. Group III(n=47): with both parents having history of type 2 diabetes. In all the groups we estimated fasting plasma glucose, insulin and adipocytokines like adiponectin, leptin, TNF-α, and IL-6.Results. Of all adipocytokines we observed significantly lower levels of adiponectin (8.7±1 μg/mL in group III and9.5±1.3 μg/mL group II) when compared to control (11.0±1.2 μg/mL;P<0.01)and it has strong correlation with family history of diabetes with Pearson’s coefficient of −0.502. Linear regression analysis showed significant negative association with HOMA-IR(P<0.01)and logistic regression analysis showed highest association with parental diabetes (P<0.01; OR .260, 95% CI .260–.468).Conclusion. Genetic predisposition for diabetes may influence adiponectin gene expression leading to decrease in its plasma concentration, which might play a key role in developing diabetes in near future.

Discordant effects of a chronic physiological increase in plasma FFA on insulin signaling in healthy subjects with or without a family history of type 2 diabetes

2004 ◽  
Vol 287 (3) ◽  
pp. E537-E546 ◽  
Author(s):  
Sangeeta R. Kashyap ◽  
Renata Belfort ◽  
Rachele Berria ◽  
Swangjit Suraamornkul ◽  
Thongchai Pratipranawatr ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Family History ◽  
Insulin Receptor ◽  
Insulin Signaling ◽  
Insulin Action ◽  
Low Dose ◽  
History Of ◽  
Plasma Ffa

Muscle insulin resistance develops when plasma free fatty acids (FFAs) are acutely increased to supraphysiological levels (∼1,500–4,000 μmol/l). However, plasma FFA levels >1,000 μmol/l are rarely observed in humans under usual living conditions, and it is unknown whether insulin action may be impaired during a sustained but physiological FFA increase to levels seen in obesity and type 2 diabetes mellitus (T2DM) (∼600–800 μmol/l). It is also unclear whether normal glucose-tolerant subjects with a strong family history of T2DM (FH+) would respond to a low-dose lipid infusion as individuals without any family history of T2DM (CON). To examine these questions, we studied 7 FH+ and 10 CON subjects in whom we infused saline (SAL) or low-dose Liposyn (LIP) for 4 days. On day 4, a euglycemic insulin clamp with [3-3H]glucose and indirect calorimetry was performed to assess glucose turnover, combined with vastus lateralis muscle biopsies to examine insulin signaling. LIP increased plasma FFA ∼1.5-fold, to levels seen in T2DM. Compared with CON, FH+ were markedly insulin resistant and had severely impaired insulin signaling in response to insulin stimulation. LIP in CON reduced insulin-stimulated glucose disposal (Rd) by 25%, insulin-stimulated insulin receptor tyrosine phosphorylation by 17%, phosphatidylinositol 3-kinase activity associated with insulin receptor substrate-1 by 20%, and insulin-stimulated glycogen synthase fractional velocity over baseline (44 vs. 15%; all P < 0.05). In contrast to CON, a physiological elevation in plasma FFA in FH+ led to no further deterioration in Rd or to any additional impairment of insulin signaling. In conclusion, a 4-day physiological increase in plasma FFA to levels seen in obesity and T2DM impairs insulin action/insulin signaling in CON but does not worsen insulin resistance in FH+. Whether this lack of additional deterioration in insulin signaling in FH+ is due to already well-established lipotoxicity, or to other molecular mechanisms related to insulin resistance that are nearly maximally expressed early in life, remains to be determined.

scholarly journals Chemerin Is a Novel Adipokine Associated with Obesity and Metabolic Syndrome

Endocrinology ◽  
2007 ◽  
Vol 148 (10) ◽  
pp. 4687-4694 ◽  
Author(s):  
Kiymet Bozaoglu ◽  
Kristy Bolton ◽  
Janine McMillan ◽  
Paul Zimmet ◽  
Jeremy Jowett ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Signal Sequence ◽  
Normal Glucose Tolerant ◽  
Normal Glucose ◽  
Glucose Tolerant ◽  
Membrane Bound ◽  
Key Aspects ◽  
First Time

Soluble protein hormones are key regulators of a number of metabolic processes, including food intake and insulin sensitivity. We have used a signal sequence trap to identify genes that encode secreted or membrane-bound proteins in Psammomys obesus, an animal model of obesity and type 2 diabetes (T2D). Using this signal sequence trap, we identified the chemokine chemerin as being a novel adipokine. Gene expression of chemerin and its receptor, chemokine-like receptor 1 (CMKLR1), was significantly higher in adipose tissue of obese and type 2 diabetic P. obesus compared with lean, normoglycemic P. obesus. Fractionation of P. obesus adipose tissue confirmed that chemerin was predominantly expressed in adipocytes, whereas CMKLR1 was expressed in both adipocytes and stromal-vascular cells of adipose tissue. In 3T3-L1 adipocytes, chemerin was markedly induced during differentiation, whereas CMKLR1 was down-regulated during differentiation. Serum chemerin levels were measured by ELISA in human plasma samples from 114 subjects with T2D and 142 normal glucose tolerant controls. Plasma chemerin levels were not significantly different between subjects with T2D and normal controls. However, in normal glucose tolerant subjects, plasma chemerin levels were significantly associated with body mass index, circulating triglycerides, and blood pressure. Here we report, for the first time, that chemerin is an adipokine, and circulating levels of chemerin are associated with several key aspects of metabolic syndrome.

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