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Showing 4 results for Metabolic Syndrome
Lipid Profile and Leptin Levels in Patients with Metabolic Syndrome
R Esmaeili, T Hassanzadeh,
Volume 8, Issue 3 (8-2014)
Abstract
Abstract Background and Objective: Metabolic syndrome called a cluster of several metabolic disorders is associated with increased risk of cardiovascular diseases. Genetic differences in leptin receptor gene are related with the concentration and activity of leptin in that these discrepancies can influence lipid levels. We aimed to determine the association between the leptin receptor gene polymorphism on serum lipid profile and leptin activity in metabolic syndrome patients. Material and Methods: This case-control study was conducted on 200 patients with metabolic syndrome and 200 healthy individuals. Polymerase Chain Reaction (PCR) and Restriction Fragment Length Polymorphisms (RFLP) were used to determine genotypic distribution and allelic frequencies of polymorphisms, respectively. The plasma leptin activity was measured by a kit in a fluorescence spectrometer, and Lipid concentration by routine biochemical and enzymatic assays. Results: Two groups had significant differences in all measured factors such as lipid profiles, fast blood sugar, waist circumference, blood pressure and leptin concentration (P< 0.05). Conclusion: Given that the two groups had significant differences in blood and body measurements, no role of K656N polymorphism was observed. Overall, Lys656Asn (K656N) polymorphism of leptin receptor gene is not associated with serum lipid profile and leptin activity with metabolic syndrome. Keywords: Metabolic Syndrome, Leptin Receptor Gene, PolymorphismK656N
The Effects of Aerobic Training on Serum Level of Liver Enzymes and Metabolic Syndrome Risk Factors in Young Inactive Women
Fatemeh Islami ,
Volume 9, Issue 5 (11-2015)
Abstract

Abstract

       Background and Objectives: Nonalcoholic fatty liver disease is the most common chronic liver disorder and is also currently considered as the hepatic manifestation of metabolic syndrome. Regular exercise training may decrease fatty liver disease complications, although its impact is not yet clear. This study aimed to evaluate the effects of six weeks of aerobic training on liver enzymes and other factors contributing to metabolic syndrome in young inactive women.

       Methods: In this quasi-experimental study, 37 inactive overweight women were randomly divided into an experimental and a control group. The experimental one participated in a controlled aerobic training program (5-minute interval walking) at 65-90% maximum heart rate for 6 weeks, 45-90 minutes per session and 4 sessions per week. Blood samples were taken following 12 hours of fasting, both before and after the training program.

       Results: The levels of aspartate aminotransferase and alkaline phosphatase decreased in both groups. Alanine aminotransferase level, weight and waist circumference were significantly decreased in the experimental group following the 6-week exercise training (P<0.05). High-density lipoprotein concentration was significantly increased in both groups. Gamma-glutamyl transferase level was decreased in the experimental group, but increased in the control group. The results showed no significant difference in the basic profile of participants, liver enzymes concentration and lipid profile between the experimental and control group.

        Conclusion: Six weeks of aerobic training may help prevent hepatic damage through decreasing serum levels of liver enzymes, anthropometric factors and some metabolic syndrome factors associated with nonalcoholic fatty liver disease.

        Keywords: Fatty liver, Aerobic training, Metabolic syndrome, Liver enzyme.


Engineering a DYRK1B R102C mutation: insights into metabolic syndrome pathogenesis through lentiviral gene delivery
Afrooz Daneshparvar , Iman Jamhiri , Vahid Razban, Jafar Fallahi , Nasrin Hamidizadeh , Behnam Moghtaderi , Mehdi Dianatpour ,
Volume 18, Issue 5 (9-2024)
Abstract
Background: A rare heterozygous DYRK1B mutation (R102C) recently linked to a familial form of metabolic syndrome prompted this study to introduce the R102C mutation into the mouse DYRK1B gene, utilizing recombinant lentiviruses for long-term gene expression.
Methods: In the present fundamental study, the DYRK1B R102C mutation was generated via Overlap Extension-PCR (OE-PCR) and inserted into the LeGO-iG2 transfer vector with a GFP marker. Recombinant lentiviruses were produced by co-transfection of the transfer vector carrying DYRK1B R102C, psPAX2 (Packaging vector), and pMD2 (Envelope vector) into HEK-293T cells.
Results: The accuracy of the intended mutation was confirmed through OE-PCR and sequencing. Expression of DYRK1B and successful gene transfer were visualized using a fluorescence microscope to detect the GFP marker. Lentiviral titer was quantified using flow cytometry, with an infection efficiency of 108 TU/ml in HEK-293T cells.
Conclusion: DYRK1B plays a crucial role in the pathogenesis of metabolic syndrome, central obesity, early-onset coronary artery disease, hypertension, type 2 diabetes, and adipogenesis, suggesting its potential as a target for therapeutic interventions. Lentiviruses carrying the DYRK1B R102C mutation offer significant advantages for both in vitro and in vivo research on metabolic syndrome. This study showcases the successful application of recombinant lentiviral vectors for gene transfer into eukaryotic cells.
 

Evaluation of serum adiponectin and leptin levels in type 2 diabetic patients: The potential role in predicting metabolic syndrome
Sharabeh Hezarkhani , Khosro Ghojoghi , Sara Hosseinzadeh , Naser Behnampour , Farshid Fathabadi , Zahra Hesari , Hamid Reza Joshaghani ,
Volume 18, Issue 6 (11-2024)
Abstract
Background: Leptin and adiponectin, two members of the adipokine family, play roles in increasing lipid metabolism and inhibiting lipogenesis. Reduced levels of these cytokines are associated with obesity and insulin resistance. This study aimed to determine the serum levels of leptin and adiponectin in type-2 diabetic patients with and without metabolic syndrome compared to a control group.
Methods: Three groups of individuals participated in this study: 47 type-2 diabetic patients with metabolic syndrome (DM+MetS), 25 type-2 diabetic patients without metabolic syndrome (DM-MetS), and 40 individuals with no history of diabetes or metabolic syndrome (Control group). Fasting blood samples were collected, and serum levels of fasting blood sugar, cholesterol, triglycerides, HDL-cholesterol, and LDL-cholesterol were measured using the enzymatic method. Blood pressure, height, and weight were recorded using stadiometers, while leptin and adiponectin levels were determined via enzyme-linked immunosorbent assay.
Results: A significant difference was observed between the DM+MetS group and the DM-MetS group in serum leptin (p = 0.004) and adiponectin (p < 0.001) levels. In patients with type-2 diabetes and metabolic syndrome, serum leptin (p = 0.530) and adiponectin (p < 0.001) levels were lower compared to the control group.
Conclusion: A decrease in the serum levels of key adipokines, such as leptin and adiponectin, in type-2 diabetic patients may serve as a predictor of metabolic syndrome.
 

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