There are 6 clinical trials
Obesity is a worldwide epidemic with increasing prevalence, specially severe obesity (Body Mass Index (BMI) ≥ 35 kg/m2). It is a multifactorial disease that involves genetic and environmental factors that lead to increased mortality from cardiovascular disease, diabetes, cancer, among others and impairs life quality. Most research on severe obesity focuses on surgical alternatives and their results, thus this clinical trial aims to evaluate the effect of a non-pharmacological approach based on nutritional intervention and supplementation with a functional food, the olive oil. It will analyze the effectiveness of interventions on: weight loss, improvements on body composition and inflammatory profile (TNF-alfa, interleucins 1, 6 and 10, adiponectin), insulin resistance and serum lipids control, changing eating habits and physical activity practice, modification on bone mineral density and sarcopenia, and reduction of cardiovascular risk and other diseases. Also, it will be investigated the influence of polymorphisms (Pro12Ala of PPAR-γ gene, -174G>C of IL6 gene e Trp64Arg of ADRB3 gene) on nutritional intervention effectiveness with and without olive oil. This research looks for improving severely obese patient's care and contributing to effective results by reducing costs and risk treatment. The investigators believe that this informations will contribute significantly to the scientific field, expanding the knowledge about severe obesity.
Also, it will be investigated the influence of polymorphisms (Pro12Ala of PPAR-γ gene, -174G>C of IL6 gene e Trp64Arg of ADRB3 gene) on nutritional intervention effectiveness with and without olive oil. --- Pro12Ala ---
Polymorphism Pro12Ala of Peroxisome Proliferator-Activated Receptor Alfa (PPAR-alfa). --- Pro12Ala ---
Description: Measurements of weight, arm circumference and Body Mass Index (BMI) will be evaluated to assess anthropometric change.
Measure: Anthropometric measurements change Time: Baseline, week 12Description: Body fat mass (BFM), body fat percentage (%BF) and body mass density (BMD) will be evaluated to assess body composition change. BFM and %BF will be assessed using multifrequency bioelectrical impedance analysis (BIA) and dual energy X-ray absorptiometry (DXA) and BMD will be assessed using DXA.
Measure: Body composition change Time: Baseline, week 12Description: TNF-alfa, interleucin 6 (IL6), IL1, IL10, adiponectin, C-reactive protein (CRP)
Measure: Change in inflammation parameters Time: Baseline, week 12Description: Lipid profile (total cholesterol, LDL-c, HDL-c, VLDL-c), insulin resistance (HOMA-IR, glycated hemoglobin), fasting glycaemia, hemogram
Measure: Change in metabolic parameters Time: Baseline, week 12Description: Creatinine, urea and uric acid
Measure: Change in kidney function Time: Baseline, week 12Description: AST and ALT
Measure: Change in liver function Time: Baseline, week 12Description: TSH, T4 and parathyroid hormone
Measure: Change in thyroid function Time: Baseline, week 12Description: Vitamin D, vitamin B12 and folic acid
Measure: Change in vitamins Time: Baseline, week 12Description: Iron, calcium, sodium, potassium and zinc
Measure: Change in minerals Time: Baseline, week 12Description: Difference in responses between intervention groups for anthropometric measurements (weight, arm circumference and body mass index) and body composition variables (body fat mass and body fat percentage) according to this polymorphism
Measure: Polymorphism Pro12Ala of Peroxisome Proliferator-Activated Receptor Alfa (PPAR-alfa) Time: Baseline, week12Description: Difference in responses between intervention groups for anthropometric measurements (weight, arm circumference and body mass index) and body composition variables (body fat mass and body fat percentage) according to this polymorphism
Measure: PolymorphismTrp64Arg of Beta-3 Adrenergic Receptor (ADRB3) gene Time: Baseline, week12Description: Difference in responses between intervention groups for anthropometric measurements (weight, arm circumference and body mass index) and body composition variables (body fat mass and body fat percentage) according to this polymorphism
Measure: Polymorphism -174G>C of Interleukin 6 (IL6) gene. Time: Baseline, week12Description: Change in the following variables: bone density using DXA, falls and fractures and sun exposure
Measure: Change in bone health parameters Time: Baseline, week 12Description: It will be evaluated through changes in food consumption (food frequency questionnaire)
Measure: Adherence to nutritional intervention Time: Baseline, week 12Description: It will be evaluated through attendance to the clinic visits
Measure: Adherence to the health service Time: Baseline, week 12Postmenopausal women, stratified by a peroxisome proliferator-activated receptor gamma-2 (PPARG) polymorphism, were given the following treatments in a random order with a 5w wash-out period: a 400mg ibuprofen tablet or a placebo tablet; both treatments were followed after 30min by a single acute dose of 0.4g alcohol per kg bw. Serum estrogen levels were measured before and at three timepoints after alcohol intake. It is hypothesized that the acute decrease in estrogen sulphate and other markers of estrogens after alcohol intake is modulated by ibuprofen and by PPARG genotype.
cholesterol lowering medicine); 7. being allergic to alcohol and/or Ibuprofen 8. smoking Breast Cancer Breast Neoplasms In a pilot human intervention trial we aimed to determine the effect of the PPARG Pro12Ala polymorphism and the PPARγ stimulator, Ibuprofen, on sex-hormone levels following alcohol intake in postmenopausal women. --- Pro12Ala ---
Seven women with PPARG Pro12Ala and 18 PPARG wildtype women were included.The study was performed as a randomised, double-blinded, placebo controlled 2x24 h crossover study. --- Pro12Ala ---
Description: Plasma estrone sulfate concentration after acute ethanol intake by Ibuprofen intake and/or PPARG genotype
Measure: Serum estrone sulphate (pmol/l) Time: from 40 min before to 90 min after alcohol consumptionDescription: Plasma estrone decrease after acute ethanol intake by ibuprofen intake and/or PPARG genotype
Measure: Serum estrone (pmol/l) Time: from 40 min before to 90 min after alcohol consumptionDescription: Plasma SHBG concentration after acute ethanol ingestion by ibuprofen intake and/or PPARG genotype
Measure: Serum SHBG (nmol/l) Time: from 40 min before to 90 min after alcohol consumptionDescription: Plasma ethanol concentration after acute ethanol ingestion
Measure: Serum ethanol (g/l) Time: from 40 min before to 90 min after alcohol consumptionDescription: The plasma metabolome profile by time after alcohol intake
Measure: Serum metabolomics (relative metabolite intensity) Time: from 40 min before to 24h after alcohol intakeDescription: The urine metabolome profile by time after alcohol intake
Measure: Urine metabolomics (relative metabolite intensity) Time: from 40 min before to 24h after alcohol intakeInteractions between genes and environment, i.e. our inherited responses to environmental changes, may be crucial in the development of the common diseases. The investigators were the first to identify PPARG gene as risk gene for type 2 diabetes. The role of the Pro12Ala polymorphism in diabetes risk has also been verified in meta-analysis. However, this effect on seems to depend on intervention and age. In this study the effects of diets high with saturated fatty acids (SAFA) and polyunsaturated fatty acids (PUFA) are compared in subjects carrying either Pro12Pro or Ala12Ala genotype of the PPARG gene. Aim of the study: To test if subjects with Pro12Pro and Ala12Ala genotypes respond differentially to a diet supplemented with high saturated (SAFA) or polyunsaturated fat (PUFA). Hypotheses: 1. Specific: Subjects with the Ala12Ala genotype will be more sensitive to dietary modification, and therefore respond more favorably to PUFA diet 2. More general: Dietary instructions individually tailored according to the genotype would allow better treatment of obesity and diabetes
The role of the Pro12Ala polymorphism in diabetes risk has also been verified in meta-analysis. --- Pro12Ala ---
Inclusion Criteria: - BMI >20kg/m2 <29kg/m2 - Pro12Pro and Ala12Ala genotypes of PPARG Pro12Ala polymorphism - participation to METSIM-study (METabolic Syndrome in Men, currently >10000 men included from the population living in Kuopio, principal investigator Markku Laakso) - normoglycemia Exclusion Criteria: - type 2 diabetes - other chronic diseases Inclusion Criteria: - BMI >20kg/m2 <29kg/m2 - Pro12Pro and Ala12Ala genotypes of PPARG Pro12Ala polymorphism - participation to METSIM-study (METabolic Syndrome in Men, currently >10000 men included from the population living in Kuopio, principal investigator Markku Laakso) - normoglycemia Exclusion Criteria: - type 2 diabetes - other chronic diseases Insulin Sensitivity Hypersensitivity Insulin Resistance Obesity and type 2 diabetes are increasing in all western countries, including Finland. --- Pro12Ala ---
Inclusion Criteria: - BMI >20kg/m2 <29kg/m2 - Pro12Pro and Ala12Ala genotypes of PPARG Pro12Ala polymorphism - participation to METSIM-study (METabolic Syndrome in Men, currently >10000 men included from the population living in Kuopio, principal investigator Markku Laakso) - normoglycemia Exclusion Criteria: - type 2 diabetes - other chronic diseases Inclusion Criteria: - BMI >20kg/m2 <29kg/m2 - Pro12Pro and Ala12Ala genotypes of PPARG Pro12Ala polymorphism - participation to METSIM-study (METabolic Syndrome in Men, currently >10000 men included from the population living in Kuopio, principal investigator Markku Laakso) - normoglycemia Exclusion Criteria: - type 2 diabetes - other chronic diseases Insulin Sensitivity Hypersensitivity Insulin Resistance Obesity and type 2 diabetes are increasing in all western countries, including Finland. --- Pro12Ala --- --- Pro12Ala ---
The role of the Pro12Ala polymorphism in diabetes risk has also been verified in meta-analysis. --- Pro12Ala ---
Based on these findings the investigators created in collaboration with Johan Auwerx an Pro12Ala animal model that demonstrated a differential effect of dietary fat composition depending on the genotype. --- Pro12Ala ---
However, an important conclusive proof that subjects selected based on their Pro12Ala genotype would respond differently to specifically tailored diet modification is still needed. --- Pro12Ala ---
Description: insulin sensitivity measured by oral glucose tolerance test at the beginning of the first, randomised diet
Measure: insulin sensitivity Time: week 0Description: insulin sensitivty measured by oral glucose tolerance test after the first diet
Measure: insulin sensitivity Time: week 8Description: Insulin sensitivity measured by oral glucose tolerance test in the beginning of the second, randomised diet
Measure: insulin sensitivity Time: week 10Description: insulin sensitivity measured by oral glucose tolerance test after the second diet
Measure: insulin sensitivity Time: week 18Description: serum lipids, including serum lipidomics and fatty acid composition
Measure: serum lipids Time: week 8Description: serum lipids, including serum lipidomics and fatty acid composition
Measure: serum lipids Time: week 18Description: inflammation measured as serum cytokines and adipose tissue inflammation
Measure: inflammation Time: week 8Description: inflammation measured as serum cytokines and adipose tissue inflammation
Measure: inflammation Time: week 18Description: energy expenditure and the rates of substrate oxidation
Measure: energy expenditure Time: week 8Description: energy expenditure and the rates of substrate oxidation
Measure: energy expenditure Time: week 18Our aim was to assess the effects of a hypocaloric diet, including diet fruit jelly with microencapsulated fish oil or conjugated linoleic acid or placebo, on anthropometry, body composition, insulin resistance and lipid profile in women with metabolic syndrome and genotype Pro12Pro in the PPAR gamma 2 gene.
Hypocaloric Diet With or Without Microencapsulated Fish Oil or Conjugated Linoleic Acid on Oxidative Stress and Cardiovascular Risk Factors in Women With Metabolic Syndrome Genotyped for Polymorphisms in the Genes PPAR Gamma 2 (Pro12Ala) and Adiponectin (G276T). --- Pro12Ala ---
Description: Plasma malondialdehyde levels
Measure: Oxidative stress biomarker Time: Change from baseline at 12 weeksDescription: Homeostatic Model Assessment-Insulin Resistance index, adiponectin, glucose and insulin levels
Measure: Insulin resistance Time: Change from baseline at 12 weeksDescription: Total cholesterol, LDL-cholesterol, VLDL-cholesterol, HDL-cholesterol and triglycerides serum levels and EPA, DHA and total conjugated linoleic acid plasma levels
Measure: Lipid profile Time: Change from baseline at 12 weeksDescription: Body weight, body mass index and waist circumference
Measure: Anthropometric measures Time: Change from baseline at 12 weeksDescription: Fat-free mass and fat mass
Measure: Body composition measures Time: Change from baseline at 12 weeksDescription: Systolic blood pressure and diastolic blood pressure
Measure: Blood pressure Time: Change from baseline at 12 weeksThe study focuses on the influence of polymorphism in the FTO genes rs9939609 and PPARᵧ Pro12Ala, oxidative stress and systemic inflammation on changes in body composition and rest metabolism induced by HIIT and continuous aerobic programs in obese or overweight individuals.
Influence of Genetic and Physiological in Weight Loss The study focuses on the influence of polymorphism in the FTO genes rs9939609 and PPARᵧ Pro12Ala, oxidative stress and systemic inflammation on changes in body composition and rest metabolism induced by HIIT and continuous aerobic programs in obese or overweight individuals. --- Pro12Ala ---
Thus, the objective of the study is to analyze the influence of polymorphism in the genes FTO rs9939609 and PPARᵧ Pro12Ala, oxidative stress and systemic inflammation on changes in body composition and rest metabolism induced by continuous and continuous aerobic programs. --- Pro12Ala ---
Description: The procedure used for analysis is done using a Dual Energy Radiological Absortiometry (DEXA) equipment. The measurement of the body fat and fat free mass percentage measure is obtained by means of a full body scan using the LUNAR PRODIGY DF + 14.319 Radiation (Madison, WI) brand device, following manufacturer's protocols. The body mass is evaluated by means of a balance (Sanny®, São Bernardo do Campo - São Paulo, Brazil), with the volunteer barefoot and in orthostatic position using a Toledo scale sensitive to 100 g. The stature is evaluated by a stadiometer with a tape calibrated at 0.1 of the same mark. Waist circumference and other body perimeters are measured with a 0.1 cm Anthropometric Tape (Sanny®, São Bernardo do Campo - São Paulo, Brazil). Weight and height data are used to calculate BMI using the equation adopted by the WHO: BMI = (Weight / (Stature) 2).
Measure: Body Composition. The changes are being evaluated. Time: Before the intervention protocol and 48 hours immediately after the last exercise session.Description: The metabolic rate was measured using a gas spirometry analyzer. After having fasted from 8:00 pm the previous day, the volunteers were referred to the laboratory shortly after the awakening and were invited to remain seated in a thermoneutral environment for 30 minutes. For the next 30 minutes, VO2, VCO2, VE and RER were monitored until variations of no more than 10% occurred when five-minute intervals were compared. Once this steady state was obtained, these variables were recorded for five minutes. The calculation of the resting metabolic rate is done according to Macdonald (1990).
Measure: Metabolic Rate of Rest. The changes are being evaluated. Time: Before the intervention protocol and 48 hours immediately after the last exercise session.Description: Collections of 10 ml of blood from the antecubital vein will be performed early in the morning, with fasting from 10 to 12 hours. The collections will be done 24 hours before, in the 6th week and after the intervention period. They will remain seated for 10 minutes for subsequent collection. Five milliliters of blood will be placed in EDTA-containing test tubes, protected from light and gently homogenized by inversion. The other 5ml will be placed in tubes without anticoagulants. They will then be centrifuged at 3,000 rpm for 10 min. The plasma or serum will be separated, placed in eppendorf tubes and refrigerated at -20 ° C until analysis. All analyzes will be carried out using a commercial kit of the Labtest brand (Minas Gerais-Brazil). The analyzes will be carried out on serum samples using commercial Labtest kits (Minas Gerais, Brazil), following the manufacturer's recommendations and on a Labmax 240 premium automatic analyzer (Lagoa Santa-MG, Brazil).
Measure: Lipid and Glycemic Profile. The changes are being evaluated. Time: The collections will be done 24 hours before, in the 6th week and 48 hours after the end of the intervention.Description: 10 ml of blood will be collected in the beginning of the morning, with fasting of 10 to 12 hours, being done 24 hours before, in the 6th week and after the intervention period. Five milliliters of blood will be placed in test tubes containing EDTA and protected from light and the other 5ml will be placed in tubes without anticoagulants and centrifuged at 3,000 rpm for 10 min. The plasma or serum will be separated, placed in eppendorf tubes and refrigerated at -20 ° C until analyzed by a commercial kit of the Labtest brand (Minas Gerais, Brazil). For this, 250 μl of sample will be added to KCl and incubated in a water bath (37 ° / 60 minutes). The mixture will be precipitated with 35% AA perchloric acid and centrifuged at 14,000 rpm for 10 minutes at 4 ° C. The supernatant will be transferred to eppendorfs and 400μl of 0.6% thiobarbituric acid is added and incubated at 95-100 ° C for 30minutes. The material will be read in a spectrophotometer at a wavelength of 532nm.
Measure: Oxidative stress (Malondialdehyde). The changes are being evaluated. Time: The collections will be done 24 hours before, in the 6th week and 48 hours after the end of the intervention.Description: 10 ml of blood will be collected in the beginning of the morning, with fasting of 10 to 12 hours, being done 24 hours before, in the 6th week and after the intervention period. Five milliliters of blood will be placed in test tubes containing EDTA and protected from light and the other 5ml will be placed in tubes without anticoagulants and centrifuged at 3,000 rpm for 10 min. The plasma or serum will be separated, placed in eppendorf tubes and refrigerated at -20 ° C until analyzed by a commercial kit of the Labtest brand (Minas Gerais, Brazil). The evaluation of the total antioxidant capacity will be performed through DPPH. For analysis, 100 μl of plasma will be added to 3.9 ml of vortexed DPPH solution, set to stand for 30 minutes and then centrifuged at 10,000 rpm for 15 minutes at 20 ° C. The supernatant will be used for spectrophotometer reading at 515 nm wavelength, using distilled white water. The result will be expressed as a percentage of antioxidant activity.
Measure: Oxidative stress (Total antioxidant capacity). The changes are being evaluated. Time: The collections will be done 24 hours before, in the 6th week and 48 hours after the end of the intervention.Description: 10 ml of blood will be collected in the beginning of the morning, with fasting of 10 to 12 hours, being done 24 hours before, in the 6th week and after the intervention period. Five milliliters of blood will be placed in test tubes containing EDTA and protected from light and the other 5ml will be placed in tubes without anticoagulants and centrifuged at 3,000 rpm for 10 min. The plasma or serum will be separated, placed in eppendorf tubes and refrigerated at -20 ° C until analyzed by a commercial kit of the Labtest brand (Minas Gerais, Brazil). The concentration of hs-CRP will be quantified by immunoturbidimetry in serum samples. Calibration will use the Calibra Calibrator from Labtest (Calibra Plus PCR-ultra - Ref-345). Absorbance will be obtained on the Labmax 240 premium automatic analyzer at 540 nm wavelength. The concentrations of hs-CRP will be determined by the commercial kit (Labtest, Minas Gerais, Brazil) according to the manufacturer's instructions.
Measure: Systemic Inflammation (Plasma ultra-sensitive C-reactive protein). The changes are being evaluated. Time: The collections will be done 24 hours before, in the 6th week and 48 hours after the end of the intervention.Description: 10 ml of blood will be collected in the beginning of the morning, with fasting of 10 to 12 hours, being done 24 hours before, in the 6th week and after the intervention period. Five milliliters of blood will be placed in test tubes containing EDTA and protected from light and the other 5ml will be placed in tubes without anticoagulants and centrifuged at 3,000 rpm for 10 min. The plasma or serum will be separated, placed in eppendorf tubes and refrigerated at -20 ° C until analyzed by a commercial kit of the Labtest brand (Minas Gerais, Brazil). The A1GPA concentration will be quantified by immunoturbidimetry using the commercial kit (Labtest, Minas Gerais, Brazil) as per manufacturer's instructions. Calibration will use the Calibra Calibrator from Labtest (Calibra Plus Protein - Ref-346). The absorbance will be obtained in the Labmax 240 premium automatic analyzer (Lagoa Santa-MG, Brazil), at wavelength 340nm.
Measure: Systemic Inflammation (Analysis of alpha-1-glycoprotein acid). The changes are being evaluated. Time: The collections will be done 24 hours before, in the 6th week and 48 hours after the end of the intervention.Description: Oral cell samples were collected through a mouthwash for 60 seconds of 5 ml of 3% sucrose solution. The resulting contents of the mouthwash were transferred to a 15 ml tube, which immediately afterwards was placed in a solution of TNE (17 mM Tris-HCl pH 8.0, 50 mM NaCl and 7 mM EDTA), diluted to 66% alcohol and autoclaved distilled water.After this, the extraction and genotyping process followed the recommendations of Saiki et al. (1985)
Measure: DNA Extraction and Genotyping Time: The genetic collection will be made in the 6th week of the intervention.- The present study was undertaken to assess the efficacy and safety of two different insulin sensitizers (namely Pioglitazone and Metformin) among subjects with type 2 diabetes mellitus (T2DM) in Bangladesh. - A prospective, double-blind, single group, 'within-subject' designed clinical trial of 77 diagnosed T2DM patients out of 130 patients with glycosylated haemoglobin (HbA1c) ≥7.2±1.5%, aged 46±6.4 years and registered for diabetes treatment in Bangladesh Institute of Research and Rehabilitation in Diabetes Endocrine and Metabolic Disorders (BIRDEM) was carried out. - The study was conducted between November 2008 and September 2010. - Baseline data, included case history of the patients,anthropometric measurement, biomedical parameters psychosocial factors, were collected from each subject and then enrolled to receive treatment with 001 drug once daily for three months, then the patients were left for wash out with metformin 850mg once daily for one month; then they received 002 drug once daily for further three months. - Dietary chart was remained as before. - DNA was isolated by Chelex method using the primers and control DNA,restriction Digestion Enzyme Endonuclease Hae 111 for genotyping PPARγ-(Peroxisome Proliferator Activated Receptor gamma)Pro12Pro - (Proline12Proline)/Pro12Ala-(Proline12 Alanine))/Ala12Ala-(Alanine12Alanine). - The blinded drugs were decoded after analyzing results, 001 tablet was pioglitazone (30 mg once daily) and 002 tablets was metformin (850mg once daily). Bio-medical outcomes were measured to assess the efficacy of both the drugs each month. After finishing the treatment period the effects of two drugs were compared using SPSS.And the association between the pioglitazone drug effects and genetic polymorphism was also assessed. - The metformin effects was assessed also using the response rate of HbA1c <7.0% after 3 months treatment to the patients.
- DNA was isolated by Chelex method using the primers and control DNA,restriction Digestion Enzyme Endonuclease Hae 111 for genotyping PPARγ-(Peroxisome Proliferator Activated Receptor gamma)Pro12Pro - (Proline12Proline)/Pro12Ala-(Proline12 Alanine))/Ala12Ala-(Alanine12Alanine). - The blinded drugs were decoded after analyzing results, 001 tablet was pioglitazone (30 mg once daily) and 002 tablets was metformin (850mg once daily). --- Pro12Ala ---
We used a published document to select the primers for genotyping PPARγ Pro12Ala/Pro12Pro. --- Pro12Ala ---
The primers for the Pro12Ala SNP genotype, we amplified exon B using the reverse primer 5' CTG GAA GAC AAA CTA CAA GAG 3' and the forward primer 5' ACT CTG GGA GAT TCT CCT ATT GGC 3'. --- Pro12Ala ---
III.Control DNA: Professor Colin Palmer Laboratory, Biomedical Research Institute ,University of Dundee Medical School, University of Dundee, Scotland, UK sent six control samples of 3 types control DNA genotyped for PPARG SNP rs 1801282 (Pro12Ala). --- Pro12Ala ---
5) List of Abbreviations AEs Adverse Events ALT Alanine aminotransferase BMI Body Mass Index BMRC Bangladesh Medical Research Council BIRDEM Bangladesh Institute of Research and Rehabilitation in Diabetes,Endocrine and Metabolic Disorder BP Blood Pressure DNA Deoxynucleic Acid DBP Diastolic Blood Pressure DM Diabetes Mellitus EASD European Association for the Study of Diabetes EDTA Ethylene Diamine Tetra Acetic acid ELISA Enzyme Linked Immunosorbent Assay FBG/FSG Fasting Blood Glucose/Fasting Serum Glucose FSI Fasting Serum Insulin 2hBG 2 hours Blood Glucose HbA1c Glycosylated Haemoglobin HOMA percent B Homeostasis Model Assessment percentage of beta cell function HOMA percent S Homeostasis Model Assessment percentage of sensitivity HOMA IR Homeostasis Model Assessment Insulin Resistance HDL-C High Density Lipid Cholesterol IU/L International Unit/Litre LDL-C Low Density Lipid Cholesterol ml millilitre mm millimetre mg/dl milligram/ decilitre MLR Multiple Logistic Regression OPD Outdoor Patient Department OMIM Online Mendelian Inheritance in Man OR Odds Ratio PPARγ Peroxisome Proliferator Activated Receptor gamma Pro12Pro Proline12Proline Pro12Ala Proline 12 Alanine Ala12Ala Alanine12Alanine PCR Polymerase Chain Reaction QUICKI Quantitative Insulin sensitivity Check Index SD Standard Deviation SPSS Statistical Package for Social Science SBP Systolic Blood Pressure TC Total Cholesterol TG Triglyceride T2DM Type 2 Diabetes Mellitus TZD Thiazolidinedione µl Microliter WHO World Health Organization --- Pro12Ala ---
Description: Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin.
Measure: Comparison of Changes in Fasting Serum Glucose (FSG)With Pioglitazone and Metformin Time: 3 months for each drugDescription: Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin.
Measure: Comparison of Changes in Glycosylated Hemoglobin (HbA1c)With Pioglitazone and Metformin Time: 3 months for each drugDescription: Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin. Analysis 1: Homeostasis Model Assessment Insulin Resistance(HOMA IR) Analysis 2: Quantitative Insulin sensitivity Check Index(QUICKI)
Measure: Comparison of Changes in Insulin Levels (HOMA IR,QUICKI) With Pioglitazone and Metformin Time: 3 months for each drugDescription: Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin. Analysis 1: Homeostatic Model Assessment of Beta cell function(HOMA percent B) Analysis 2: Homeostatic Model Assessment of Insulin Sensitivity (Homa percent S)
Measure: Comparison of Changes in HOMA Percent B and HOMA Percent S With Pioglitazone and Metformin Time: 3 months for each drugDescription: Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin.
Measure: Comparison of Changes in Fasting Serum Insulin (FSI)With Pioglitazone and Metformin Time: 3 months for each drugDescription: Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin. Analysis 1:Total Cholesterol(TC) Analysis 2:Triglyceride(TG) Analysis 3:High Density Lipoprotein(HDL) Analysis 4:Low Density Lipoprotein(LDL)
Measure: Comparison of Changes in Lipid Profiles With Pioglitazone and Metformin Time: 3 months for each drug