The Experts below are selected from a list of 1482 Experts worldwide ranked by ideXlab platform
Ida Kinalska - One of the best experts on this subject based on the ideXlab platform.
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Insulin resistance in obese subjects with impaired glucose tolerance. Studies with hyperinsulinemic euglycemic Clamp Technique
Polskie Archiwum Medycyny Wewnetrznej, 2003Co-Authors: Marek Straczkowski, Stella Dzienis-straczkowska, Małgorzata Szelachowska, Irina Kowalska, Agnieszka Stępień, Ida KinalskaAbstract:Insulin resistance is a key factor in the pathogenesis of impaired glucose tolerance (IGT) and type 2 diabetes and is also associated with greater risk for cardiovascular disease. Insulin resistance is more common in obese individuals and is considered to be the link between obesity and IGT and diabetes. The aim of the present study was to assess insulin resistance in obese subjects with IGT. We examined 57 subjects with marked overweight or obesity (BMI > > 27.8 kg x m-2), 27 with IGT and 30 with normal glucose tolerance (NGT), assessed by an oral glucose tolerance test, according to WHO criteria. Thirty lean (BMI < 25 kg x m-2) healthy subjects served as a control group. Anthropometric and biochemical parameters were measured. Insulin sensitivity was evaluated with hyperinsulinemic euglycemic Clamp Technique. Subjects with IGT had higher levels of glucose, insulin, non-esterified fatty acids and glycated hemoglobin than obese with NGT, all those parameters were also higher in both obese groups in comparison to controls. We showed significant differences in insulin sensitivity between the studied groups, an index of the whole-body glucose uptake was decreased in both obese groups in comparison to controls, and it was also lower in IGT than in obese NGT group. We observed marked negative correlations between insulin sensitivity and estimated anthropometric and biochemical parameters. Our study indicates that insulin resistance is an important factor determining a deterioration of glucose tolerance in subjects with overweight and obesity.
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Assessment of insulin sensitivity during exercise training program in obese women. Comparison of simple indices with hyperinsulinemic euglycemic Clamp Technique
Polskie Archiwum Medycyny Wewnetrznej, 2003Co-Authors: Marek Straczkowski, Irina Kowalska, Angieszka Stepień, Jolanta Topolska, Ida KinalskaAbstract:Insulin resistance is a key element of metabolic syndrome, which includes disturbances of glucose tolerance, obesity, hypertension, coronary heart disease, dyslipidemia and many other defects. An important problem in scientific research is precise measurement of insulin sensitivity. The method considered ,,the gold standard" is glucose Clamp, however, it is difficult to apply this method in large studies. Therefore, simple indices of insulin resistance are proposed. It remains unclear whether those indices are able to reflect changes occurring during insulin-sensitizing intervention. The aim of the present study was to assess the use of indirect indices for the changes in insulin sensitivity during exercise training and to compare those indices with results derived from Clamp. Fourteen obese normoglycemic women participated in 12-week exercise training program, which included exercise performed on a bicycle ergometer, 5 days a week for 30 minutes. Insulin sensitivity (M/FFM value) before and after training was measured with hyperinsulinemic euglycemic Clamp Technique. Simple indices of insulin resistance were also assessed: fasting plasma insulin (INS), logarithm INS (log [INS]), homeostasis model assessment (HOMA), logarithm HOMA (log [HOMA]) and quantitative insulin sensitivity check index (QUICKI). Before training, all those indices were markedly related to M/FFM. After training, an increase in M/FFM was observed. None of the examined indices markedly changed after training. There was no corelations between changes of evaluated indices and in M/FFM during training, and no relationships of those parameters after training. Our study indicates that simple indices are not able to reflect changes occurring during insulin-sensitizing intervention.
Markku Laakso - One of the best experts on this subject based on the ideXlab platform.
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Brief Genetics Report Single Nucleotide Polymorphisms in the Peroxisome Proliferator–Activated Receptor Gene Are Associated With Skeletal Muscle Glucose Uptake
2016Co-Authors: Pirjo Nuutila, Teemu Kuulasmaa, Juhani Knuuti, Markku LaaksoAbstract:The peroxisome proliferator–activated receptors (PPARs) belong to a superfamily of nuclear receptors. It includes PPAR-, a key regulator of fatty acid oxidation and energy uncoupling, universally expressed in different tissues. The PPAR- gene (PPARD) maps to 6p21.2-p21.1 and has 11 exons and spans 35 kbp. We investigated the effects of single nucleotide polymorphisms (SNPs) of PPARD on whole-body, skeletal muscle, and subcutaneous adipose tissue glucose uptake in 129 healthy individuals using the Hyperinsulinemic-Euglycemic Clamp Technique combined with fluorine-18–labeled fluorodeoxyglucose ([18F]FDG) and positron emission tomography (PET). Three of six SNPs of PPARD and their haplogenotypes were signifi-cantly associated with whole-body insulin sensitivity. [18F]FDG-PET scanning indicated that SNPs of PPAR
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A major gene effect on fasting insulin and insulin sensitivity in familial combined hyperlipidemia.
Diabetes, 2001Co-Authors: Jussi Pihlajamäki, Melissa A. Austin, Karen L. Edwards, Markku LaaksoAbstract:The most common inherited dyslipidemia, familial combined hyperlipidemia (FCHL), is associated with insulin resistance. Whether insulin sensitivity in these families is inherited is not known. Therefore, we investigated the inheritance of insulin sensitivity in 352 nondiabetic family members from 37 families with FCHL, 105 of whom had undergone testing using the Hyperinsulinemic-Euglycemic Clamp Technique for the measurement of insulin sensitivity. First, complex segregation analysis of fasting insulin levels (both unadjusted and age-, age2-, and BMI-adjusted) was used for modeling of the variance in fasting insulin levels. In these analyses, Mendelian codominant inheritance ( P = 0.320 for unadjusted and P = 0.295 for adjusted insulin values) was not rejected over the most general model and fit the data significantly better than the sporadic model ( P < 0.001). Polygenic and environmental models were rejected ( P < 0.001). The Mendelian codominant model explained 44 and 45% of the variance in unadjusted and adjusted fasting insulin levels, respectively. The proposed genotypes of this locus, based on segregation analysis, were associated with directly measured insulin sensitivity in 105 FCHL family members who underwent the Hyperinsulinemic-Euglycemic Clamp ( P < 0.001). These results provide evidence for a major gene regulating insulin sensitivity in FCHL families. Possible pleiotropic effects of this insulin sensitivity locus on dyslipidemias in FCHL remain to be elucidated.
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Impaired insulin-stimulated glucose oxidation and free fatty acid suppression in patients with familial combined hyperlipidemia : A precursor defect for dyslipidemia?
Arteriosclerosis thrombosis and vascular biology, 1998Co-Authors: Leena Karjalainen, Jussi Pihlajamäki, Pauli Karhapää, Markku LaaksoAbstract:Abstract —Familial combined hyperlipidemia (FCHL) is characterized by hyperlipidemia and insulin resistance, but intracellular defect in insulin action is unknown. Therefore, we investigated insulin action by applying the hyperinsulinemic euglycemic Clamp Technique with indirect calorimetry in 58 FCHL family members (28 with FCHL; 30 without dyslipidemia; aged 49±12 years; body mass index [BMI], 25.2±4.0 kg/m 2 ) and in 72 healthy control subjects (aged 54±6 years; BMI, 26.3±3.1 kg/m 2 ). In the fasting state, FCHL patients had higher levels of total cholesterol, total triglycerides, and apolipoprotein B than control subjects ( P P =0.001) and higher rates of lipid oxidation (0.15±0.13 versus 0.01±0.25 mg/kg/min; P =0.024), as well as higher levels of serum-free fatty acids (FFA) (0.24±0.17 versus 0.06±0.06 mmol/L; P P P =0.408). In FCHL family members without dyslipidemia and in control subjects, FFAs during the Clamp correlated positively with levels of total triglycerides ( P P =0.008). We conclude that in patients with FCHL, and also in their first-degree relatives, insulin’s suppressive effect on FFA levels is impaired, which may precede dyslipidemia in FCHL.
Marek Straczkowski - One of the best experts on this subject based on the ideXlab platform.
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Insulin resistance in obese subjects with impaired glucose tolerance. Studies with hyperinsulinemic euglycemic Clamp Technique
Polskie Archiwum Medycyny Wewnetrznej, 2003Co-Authors: Marek Straczkowski, Stella Dzienis-straczkowska, Małgorzata Szelachowska, Irina Kowalska, Agnieszka Stępień, Ida KinalskaAbstract:Insulin resistance is a key factor in the pathogenesis of impaired glucose tolerance (IGT) and type 2 diabetes and is also associated with greater risk for cardiovascular disease. Insulin resistance is more common in obese individuals and is considered to be the link between obesity and IGT and diabetes. The aim of the present study was to assess insulin resistance in obese subjects with IGT. We examined 57 subjects with marked overweight or obesity (BMI > > 27.8 kg x m-2), 27 with IGT and 30 with normal glucose tolerance (NGT), assessed by an oral glucose tolerance test, according to WHO criteria. Thirty lean (BMI < 25 kg x m-2) healthy subjects served as a control group. Anthropometric and biochemical parameters were measured. Insulin sensitivity was evaluated with hyperinsulinemic euglycemic Clamp Technique. Subjects with IGT had higher levels of glucose, insulin, non-esterified fatty acids and glycated hemoglobin than obese with NGT, all those parameters were also higher in both obese groups in comparison to controls. We showed significant differences in insulin sensitivity between the studied groups, an index of the whole-body glucose uptake was decreased in both obese groups in comparison to controls, and it was also lower in IGT than in obese NGT group. We observed marked negative correlations between insulin sensitivity and estimated anthropometric and biochemical parameters. Our study indicates that insulin resistance is an important factor determining a deterioration of glucose tolerance in subjects with overweight and obesity.
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Assessment of insulin sensitivity during exercise training program in obese women. Comparison of simple indices with hyperinsulinemic euglycemic Clamp Technique
Polskie Archiwum Medycyny Wewnetrznej, 2003Co-Authors: Marek Straczkowski, Irina Kowalska, Angieszka Stepień, Jolanta Topolska, Ida KinalskaAbstract:Insulin resistance is a key element of metabolic syndrome, which includes disturbances of glucose tolerance, obesity, hypertension, coronary heart disease, dyslipidemia and many other defects. An important problem in scientific research is precise measurement of insulin sensitivity. The method considered ,,the gold standard" is glucose Clamp, however, it is difficult to apply this method in large studies. Therefore, simple indices of insulin resistance are proposed. It remains unclear whether those indices are able to reflect changes occurring during insulin-sensitizing intervention. The aim of the present study was to assess the use of indirect indices for the changes in insulin sensitivity during exercise training and to compare those indices with results derived from Clamp. Fourteen obese normoglycemic women participated in 12-week exercise training program, which included exercise performed on a bicycle ergometer, 5 days a week for 30 minutes. Insulin sensitivity (M/FFM value) before and after training was measured with hyperinsulinemic euglycemic Clamp Technique. Simple indices of insulin resistance were also assessed: fasting plasma insulin (INS), logarithm INS (log [INS]), homeostasis model assessment (HOMA), logarithm HOMA (log [HOMA]) and quantitative insulin sensitivity check index (QUICKI). Before training, all those indices were markedly related to M/FFM. After training, an increase in M/FFM was observed. None of the examined indices markedly changed after training. There was no corelations between changes of evaluated indices and in M/FFM during training, and no relationships of those parameters after training. Our study indicates that simple indices are not able to reflect changes occurring during insulin-sensitizing intervention.
Antti Viljanen - One of the best experts on this subject based on the ideXlab platform.
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Single Nucleotide Polymorphisms in the Peroxisome Proliferator–Activated Receptor δ Gene Are Associated With Skeletal Muscle Glucose Uptake
Diabetes, 2005Co-Authors: Markku Vänttinen, Pirjo Nuutila, Teemu Kuulasmaa, Jussi Pihlajamäki, Kirsti Hällsten, Kirsi A. Virtanen, Riikka Lautamäki, Pauliina Peltoniemi, Teemu Takala, Antti ViljanenAbstract:The peroxisome proliferator–activated receptors (PPARs) belong to a superfamily of nuclear receptors. It includes PPAR-δ, a key regulator of fatty acid oxidation and energy uncoupling, universally expressed in different tissues. The PPAR-δ gene (PPARD) maps to 6p21.2-p21.1 and has 11 exons and spans 35 kbp. We investigated the effects of single nucleotide polymorphisms (SNPs) of PPARD on whole-body, skeletal muscle, and subcutaneous adipose tissue glucose uptake in 129 healthy individuals using the Hyperinsulinemic-Euglycemic Clamp Technique combined with fluorine-18–labeled fluorodeoxyglucose ([18F]FDG) and positron emission tomography (PET). Three of six SNPs of PPARD and their haplogenotypes were significantly associated with whole-body insulin sensitivity. [18F]FDG-PET scanning indicated that SNPs of PPARD primarily affected insulin sensitivity by modifying glucose uptake in skeletal muscle but not in adipose tissue. Our results give evidence that SNPs of PPARD regulate insulin sensitivity particularly in skeletal muscle.
Jussi Pihlajamäki - One of the best experts on this subject based on the ideXlab platform.
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Single Nucleotide Polymorphisms in the Peroxisome Proliferator–Activated Receptor δ Gene Are Associated With Skeletal Muscle Glucose Uptake
Diabetes, 2005Co-Authors: Markku Vänttinen, Pirjo Nuutila, Teemu Kuulasmaa, Jussi Pihlajamäki, Kirsti Hällsten, Kirsi A. Virtanen, Riikka Lautamäki, Pauliina Peltoniemi, Teemu Takala, Antti ViljanenAbstract:The peroxisome proliferator–activated receptors (PPARs) belong to a superfamily of nuclear receptors. It includes PPAR-δ, a key regulator of fatty acid oxidation and energy uncoupling, universally expressed in different tissues. The PPAR-δ gene (PPARD) maps to 6p21.2-p21.1 and has 11 exons and spans 35 kbp. We investigated the effects of single nucleotide polymorphisms (SNPs) of PPARD on whole-body, skeletal muscle, and subcutaneous adipose tissue glucose uptake in 129 healthy individuals using the Hyperinsulinemic-Euglycemic Clamp Technique combined with fluorine-18–labeled fluorodeoxyglucose ([18F]FDG) and positron emission tomography (PET). Three of six SNPs of PPARD and their haplogenotypes were significantly associated with whole-body insulin sensitivity. [18F]FDG-PET scanning indicated that SNPs of PPARD primarily affected insulin sensitivity by modifying glucose uptake in skeletal muscle but not in adipose tissue. Our results give evidence that SNPs of PPARD regulate insulin sensitivity particularly in skeletal muscle.
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A major gene effect on fasting insulin and insulin sensitivity in familial combined hyperlipidemia.
Diabetes, 2001Co-Authors: Jussi Pihlajamäki, Melissa A. Austin, Karen L. Edwards, Markku LaaksoAbstract:The most common inherited dyslipidemia, familial combined hyperlipidemia (FCHL), is associated with insulin resistance. Whether insulin sensitivity in these families is inherited is not known. Therefore, we investigated the inheritance of insulin sensitivity in 352 nondiabetic family members from 37 families with FCHL, 105 of whom had undergone testing using the Hyperinsulinemic-Euglycemic Clamp Technique for the measurement of insulin sensitivity. First, complex segregation analysis of fasting insulin levels (both unadjusted and age-, age2-, and BMI-adjusted) was used for modeling of the variance in fasting insulin levels. In these analyses, Mendelian codominant inheritance ( P = 0.320 for unadjusted and P = 0.295 for adjusted insulin values) was not rejected over the most general model and fit the data significantly better than the sporadic model ( P < 0.001). Polygenic and environmental models were rejected ( P < 0.001). The Mendelian codominant model explained 44 and 45% of the variance in unadjusted and adjusted fasting insulin levels, respectively. The proposed genotypes of this locus, based on segregation analysis, were associated with directly measured insulin sensitivity in 105 FCHL family members who underwent the Hyperinsulinemic-Euglycemic Clamp ( P < 0.001). These results provide evidence for a major gene regulating insulin sensitivity in FCHL families. Possible pleiotropic effects of this insulin sensitivity locus on dyslipidemias in FCHL remain to be elucidated.
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Impaired insulin-stimulated glucose oxidation and free fatty acid suppression in patients with familial combined hyperlipidemia : A precursor defect for dyslipidemia?
Arteriosclerosis thrombosis and vascular biology, 1998Co-Authors: Leena Karjalainen, Jussi Pihlajamäki, Pauli Karhapää, Markku LaaksoAbstract:Abstract —Familial combined hyperlipidemia (FCHL) is characterized by hyperlipidemia and insulin resistance, but intracellular defect in insulin action is unknown. Therefore, we investigated insulin action by applying the hyperinsulinemic euglycemic Clamp Technique with indirect calorimetry in 58 FCHL family members (28 with FCHL; 30 without dyslipidemia; aged 49±12 years; body mass index [BMI], 25.2±4.0 kg/m 2 ) and in 72 healthy control subjects (aged 54±6 years; BMI, 26.3±3.1 kg/m 2 ). In the fasting state, FCHL patients had higher levels of total cholesterol, total triglycerides, and apolipoprotein B than control subjects ( P P =0.001) and higher rates of lipid oxidation (0.15±0.13 versus 0.01±0.25 mg/kg/min; P =0.024), as well as higher levels of serum-free fatty acids (FFA) (0.24±0.17 versus 0.06±0.06 mmol/L; P P P =0.408). In FCHL family members without dyslipidemia and in control subjects, FFAs during the Clamp correlated positively with levels of total triglycerides ( P P =0.008). We conclude that in patients with FCHL, and also in their first-degree relatives, insulin’s suppressive effect on FFA levels is impaired, which may precede dyslipidemia in FCHL.