An increase in plasma adiponectin multimeric complexes follows hypocaloric diet-induced weight loss in obese and overweight pre-menopausal women

2007 ◽  
Vol 112 (11) ◽  
pp. 557-565 ◽  
Author(s):  
Jan Polak ◽  
Zuzana Kovacova ◽  
Martin Jacek ◽  
Eva Klimcakova ◽  
Michaela Kovacikova ◽  
...  
Keyword(s):  
Weight Loss ◽  
Insulin Sensitivity ◽  
Hypocaloric Diet ◽  
Whole Body ◽  
Diabetic Patients ◽  
Model Assessment ◽  
Obese Women ◽  
Type 2 Diabetic Patients ◽  
Plasma Adiponectin ◽  
Insulin Resistant

Adiponectin is involved in the regulation of glucose and fatty acid metabolism, influences whole-body insulin sensitivity and protects arterial walls against the development of atherosclerosis. Plasma adiponectin is decreased in obese, insulin-resistant and Type 2 diabetic patients. Adiponectin circulates in plasma as high-, medium- and low-molecular-weight (‘mass’) forms (HMW, MMW and LMW respectively). The HMW form is believed to be closely associated with insulin sensitivity. The aim of the present study was to investigate whether diet-induced changes in body weight and insulin sensitivity were associated with changes in the quantity of adiponectin multimeric complexes. A total of 20 overweight or obese women (age, 39.4±9.5 years; body mass index, 32.2±6.4 kg/m2) underwent 12 weeks of low caloric diet (600 kcal/day less than energy requirements; where 1 kcal≈4.184 kJ). Plasma samples were drawn before and after the study for biochemical analysis and Western blot detection of adiponectin multimeric complexes. The hypocaloric diet resulted in a weight reduction (89.8±16.4 kg compared with 83.1±15.6 kg; P<0.001) and an improvement in whole-body insulin sensitivity, as measured by HOMA (homoeostasis model assessment index; 1.9±0.8 compared with 1.5±0.7; P=0.013). Increases in the quantities of the HMW, MMW and LMW forms by 5.5, 8.5 and 18.1% respectively, were observed (P<0.05 for all of the forms). Total plasma adiponectin was increased by 36% with borderline significance (P=0.08). No correlations between changes in adiponectin complexes and changes in indices of insulin sensitivity were observed. In conclusion, diet-induced weight loss improved insulin sensitivity as well as increased the amount of HMW, MMW and LMW adiponectin complexes in plasma.

scholarly journals Total adiponectin and adiponectin multimeric complexes in relation to weight loss-induced improvements in insulin sensitivity in obese women: the NUGENOB study.

2008 ◽  
Vol 158 (4) ◽  
pp. 533-541 ◽  
Author(s):  
J Polak ◽  
Z Kovacova ◽  
C Holst ◽  
C Verdich ◽  
A Astrup ◽  
...  
Keyword(s):  
Weight Loss ◽  
Insulin Sensitivity ◽  
Resistance Index ◽  
Diabetic Patients ◽  
Model Assessment ◽  
Obese Women ◽  
Total Plasma ◽  
Type 2 Diabetic Patients ◽  
Plasma Adiponectin ◽  
Induced Changes

AimAdiponectin increases insulin sensitivity, protects arterial walls against atherosclerosis, and regulates glucose metabolism, and is decreased in obese, insulin resistant, and type 2 diabetic patients. Adiponectin circulates in plasma as high, medium, and low molecular weight forms (HMW, MMW, and LMW). The HMW form was suggested to be closely associated with insulin sensitivity. This study investigated whether diet-induced changes in insulin sensitivity were associated with changes in adiponectin multimeric complexes.SubjectsTwenty obese women with highest and twenty obese women with lowest diet induced changes in insulin sensitivity (responders and non-responders respectively), matched for weight loss (body mass index (BMI)=34.5 (s.d.2.9) resp. 36.5 kg/m2(s.d.4.0) for responders and non-responders), were selected from 292 women who underwent a 10-week low-caloric diet (LCD; 600 kcal/d less than energy requirements). Plasma HMW, MMW, and LMW forms of adiponectin were quantified using Western blot method.ResultsLCD induced comparable weight reduction in responders and non-responders by 8.2 and 7.6 kg. Homeostasis model assessment insulin resistance index decreased by 48.1% in responders and remained unchanged in non-responders. Total plasma adiponectin and the quantity of HMW and MMW remained unchanged in both groups, while LMW increased by 16.3% in non-responders. No differences between both groups were observed at baseline and after the study. Total plasma adiponectin, MMW, and LMW were negatively associated with fasting insulin levels at baseline.ConclusionNo differences in total plasma adiponectin, HMW, MMW, and LMW forms were observed between responders and non-responders following 10-week LCD, suggesting that adiponectin is not a major determinant of weight loss-induced improvements in insulin sensitivity.

scholarly journals Evaluation of insulin sensitivity with a new lipid-based index in non-diabetic postmenopausal overweight and obese women before and after a weight loss intervention

2009 ◽  
Vol 161 (1) ◽  
pp. 51-56 ◽  
Author(s):  
Barbara Antuna-Puente ◽  
Emmanuel Disse ◽  
May Faraj ◽  
Marie-Eve Lavoie ◽  
Martine Laville ◽  
...  
Keyword(s):  
Weight Loss ◽  
Insulin Sensitivity ◽  
Weight Loss Program ◽  
Model Assessment ◽  
Weight Loss Intervention ◽  
Obese Women ◽  
Insulin Resistant ◽  
Significant Difference ◽  
Before And After ◽  
Post Menopausal

ObjectiveTo evaluate the validity of a new lipid-based index (Disse index) in assessing insulin sensitivity (IS) compared with the hyperinsulinemic-euglycemic (HIEG) clamp in overweight and obese, non-diabetic, postmenopausal women, before and after a weight loss intervention.Research design and methodsAssociation between Disse index and the HIEG clamp was evaluated in 86 non-diabetic postmenopausal overweight and obese women before and after weight loss. Percentage changes (%Δ) were calculated for several fasting indices and compared with %Δ of HIEG clamp.ResultsWe observed a strong correlation between Disse index and HIEG clamp (r=0.69, P<0.001). This association was higher than those of homeostasis model assessment (HOMA), quantitative insulin sensitivity check index (QUICKI), and McAuley indices while no significant difference was observed with Revised-QUICKI. Percent change of Disse index (pre- versus post-weight loss program) was significantly correlated with %Δ of HIEG clamp (r=0.34, P<0.01). This correlation was similar to those observed for the other indices tested.ConclusionsWe validated the reliability of Disse index in assessing IS in non-diabetic post-menopausal overweight and obese women, before and after weight loss intervention. Disse index may be useful not only for insulin resistant diagnostics in this type of population, but also for the IS follow-up after a weight-loss program and weight stabilization. The presence of lipid elements in this fasting index improves the estimation of IS in overweight and obese non-diabetic post-menopausal women and could add more information about peripheral IS.

Effect of 10 days of bedrest on metabolic and vascular insulin action: a study in individuals at risk for type 2 diabetes

2010 ◽  
Vol 108 (4) ◽  
pp. 830-837 ◽  
Author(s):  
Mette P. Sonne ◽  
Amra C. Alibegovic ◽  
Lise Højbjerre ◽  
Allan Vaag ◽  
Bente Stallknecht ◽  
...  
Keyword(s):  
Physical Activity ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
High Sensitivity ◽  
Whole Body ◽  
Diabetic Patients ◽  
Activity Levels ◽  
Type 2 Diabetic Patients ◽  
Increased Risk

Physical inactivity is a known risk factor for type 2 diabetes. We studied whole body and forearm insulin sensitivity in subjects at increased risk for type 2 diabetes [persons with low birth weight (LBW group; n = 20) and first-degree relatives to type 2 diabetic patients (FDR group; n = 13)] as well as a control (CON) group ( n = 20) matched for body mass index, age, and physical activity levels before and after 10 days of bedrest. Subjects were studied by hyperinsulinemic isoglycemic clamp combined with arterial and deep venous catheterization of the forearm. Forearm blood flow (FBF) was measured by venous occlusion plethysmography. All groups responded with a decrease in whole body insulin sensitivity in response to bedrest [CON group: 6.8 ± 0.5 to 4.3 ± 0.3 mg·min−1·kg−1( P < 0.0001), LBW group: 6.2 ± 0.5 to 4.3 ± 0.3 mg·min−1·kg−1( P < 0.0001), and FDR group: 4.3 ± 0.7 to 3.1 ± 0.3 mg·min−1·kg−1( P = 0.068)]. The percent decrease was significantly greater in the CON group compared with the FDR group (CON group: 34 ± 4%, LBW group: 27 ± 4%, and FDR group: 10 ± 13%). Forearm insulin-stimulated glucose clearance decreased significantly in the CON and LBW groups in response to bedrest; in the FDR group, clearance was very low before bedrest and no change was observed. Before bedrest, the CON and LBW groups demonstrated a significant increase in FBF during hyperinsulinemia; after bedrest, an increase in FBF was observed only in the CON group. In conclusion, bedrest induced a pronounced reduction in whole body, skeletal muscle, and vascular insulin sensitivity in the CON and LBW groups. The changes were most pronounced in the CON group. In the FDR group, insulin resistance was already present before bedrest, but even this group displayed a high sensitivity to changes in daily physical activity.

Decreased whole body lipolysis as a mechanism of the lipid-lowering effect of pioglitazone in type 2 diabetic patients

2009 ◽  
Vol 297 (1) ◽  
pp. E225-E230 ◽  
Author(s):  
Amalia Gastaldelli ◽  
Arturo Casolaro ◽  
Demetrio Ciociaro ◽  
Silvia Frascerra ◽  
Monica Nannipieri ◽  
...  
Keyword(s):  
Lipid Lowering ◽  
Whole Body ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Mixed Meal ◽  
Plasma Triglycerides ◽  
Insulin Resistant ◽  
Type 2 Diabetic ◽  
Lipid Lowering Effect

Pioglitazone has been shown to reduce fasting triglyceride levels. The mechanisms of this effect have not been fully elucidated, but decreased lipolysis may contribute to blunt the hypertriglyceridemic response to a meal. To test this hypothesis, we studied 27 type 2 diabetes mellitus (T2DM) patients and 7 sex-, age-, and body mass index-matched nondiabetic controls. Patients were randomized to pioglitazone (45 mg/day) or placebo for 16 wk. Whole body lipolysis was measured [as the [2H5]glycerol rate of appearance (Ra)] in the fasting state and for 6 h following a mixed meal. Compared with controls, T2DM had higher postprandial profiles of plasma triglycerides, free fatty acid (FFA), and β-hydroxybutyrate, and a decreased suppression of glycerol Ra ( P < 0.04) despite higher insulin levels [268 (156) vs. 190 (123) pmol/l, median (interquartile range)]. Following pioglitazone, triglycerides and FFA were reduced ( P = 0.05 and P < 0.04, respectively), and glycerol Ra was more suppressed [−40 (137) vs. +7 (202) μmol/min of placebo, P < 0.05] despite a greater fall in insulin [−85 (176) vs. −20 (58) pmol/l, P = 0.05]. We conclude that, in well-controlled T2DM patients, whole body lipolysis is insulin resistant, and pioglitazone improves the insulin sensitivity of lipolysis.

scholarly journals Cross-Talk between PPARγand Insulin Signaling and Modulation of Insulin Sensitivity

PPAR Research ◽  
2009 ◽  
Vol 2009 ◽  
pp. 1-12 ◽  
Author(s):  
Anna Leonardini ◽  
Luigi Laviola ◽  
Sebastio Perrini ◽  
Annalisa Natalicchio ◽  
Francesco Giorgino
Keyword(s):  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Insulin Signaling ◽  
Energy Homeostasis ◽  
Whole Body ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Beneficial Effects ◽  
Major Mediator

PPARγactivation in type 2 diabetic patients results in a marked improvement in insulin and glucose parameters, resulting from an improvement of whole-body insulin sensitivity. Adipose tissue is the major mediator of PPARγaction on insulin sensitivity. PPARγactivation in mature adipocytes induces the expression of a number of genes involved in the insulin signaling cascade, thereby improving insulin sensitivity. PPARγis the master regulator of adipogenesis, thereby stimulating the production of small insulin-sensitive adipocytes. In addition to its importance in adipogenesis, PPARγplays an important role in regulating lipid, metabolism in mature adipocytes by increasing fatty acid trapping. Finally, adipose tissue produces several cytokines that regulate energy homeostasis, lipid and glucose metabolism. Disturbances in the production of these factors may contribute to metabolic abnormalities, and PPARγactivation is also associated with beneficial effects on expression and secretion of a whole range of cytokines.

PPARγ-mediated insulin sensitization: the importance of fat versus muscle

2005 ◽  
Vol 288 (2) ◽  
pp. E287-E291 ◽  
Author(s):  
Ulrich Kintscher ◽  
Ronald E. Law
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Nuclear Hormone Receptor ◽  
Whole Body ◽  
Diabetic Patients ◽  
Peroxisome Proliferator ◽  
Type 2 Diabetic Patients ◽  
Peroxisome Proliferator Activated Receptor ◽  
Peripheral Tissues

Peroxisome proliferator-activated receptor-γ (PPARγ) is a nuclear hormone receptor that functions as a transcriptional regulator in a variety of tissues. PPARγ activation, e.g., through binding of the synthetic glitazones or thiazolidinediones (TZD), results in a marked improvement in type 2 diabetic patients of insulin and glucose parameters resulting from an improvement of whole body insulin sensitivity. The role of different metabolic tissues (fat, skeletal muscle, liver) in mediating PPARγ function in glucose and insulin homeostasis is still unclear. Recently, the function of PPARγ in adipose tissue and skeletal muscle has been intensively characterized by using targeted deletion of PPARγ in those tissues. In those studies, adipose PPARγ has been identified as an essential mediator for the maintainance of whole body insulin sensitivity. Two major mechanisms have been described. 1) Adipose PPARγ protects nonadipose tissue against excessive lipid overload and maintains normal organ function (liver, skeletal muscle); and 2) adipose PPARγ guarantees a balanced and adequate production of secretion from adipose tissue of adipocytokines such as adiponectin and leptin, which are important mediators of insulin action in peripheral tissues. In contrast to studies in adipose-specific PPARγ-deficient mice, the data in muscle-specific PPARγ−/− mice demonstrate that whole body insulin sensitivity is, at least in part, relying on an intact PPARγ system in skeletal muscle. Finally, these early and elegant studies using tissue-specific PPARγ knockout mouse models pinpoint adipose tissue as the major target of TZD-mediated improvement of hyperlipidemia and insulin sensitization.

scholarly journals GLP-1 analogues as a new treatment option for hypothalamic obesity in adults: report of nine cases

2013 ◽  
Vol 168 (5) ◽  
pp. 699-706 ◽  
Author(s):  
Flavius Zoicas ◽  
Michael Droste ◽  
Bernhard Mayr ◽  
Michael Buchfelder ◽  
Christof Schöfl
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Nausea And Vomiting ◽  
Diabetic Patients ◽  
Model Assessment ◽  
Obese Patients ◽  
Type 2 Diabetic Patients ◽  
Hypothalamic Obesity ◽  
Metabolic Alterations

BackgroundPatients with hypothalamic pathology often develop morbid obesity, causing severe metabolic alterations resulting in increased morbidity and mortality. Glucagon-like peptide-1 (GLP-1) analogues improve glycaemic control in type 2 diabetic patients and cause weight loss in obese patients by yet unknown mechanisms. Here we tested whether GLP-1 analogues were also effective in the treatment of obesity and associated metabolic alterations in patients with hypothalamic disease.MethodsNine patients (eight with type 2 diabetes mellitus) with moderate to severe hypothalamic obesity were treated with GLP-1 analogues for up to 51 months. Body weight, homeostasis model assessment - insulin resistance (HOMA-IR), HbA1c and lipids were assessed.ResultsEight patients experienced substantial weight loss (−13.1±5.1 kg (range −9 to −22)). Insulin resistance (HOMA-IR −3.2±3.5 (range −9.1 to 0.8)) and HbA1c values (−1.3±1.4% (range −4.5 to 0.0)) improved under treatment (24.3±18.9 months (range 6 to 51)). Five patients reported increased satiation in response to the treatment. Two of the eight patients complained about nausea and vomiting and one of them abandoned therapy because of sustained gastrointestinal discomfort after 6 months. One patient suffered from intolerable nausea and vomiting and discontinued treatment within 2 weeks.ConclusionGLP-1 analogues can cause substantial and sustained weight loss in obese patients with hypothalamic disease. This offers a new approach for medical treatment of moderate to severe hypothalamic obesity and associated metabolic alterations.

Plasma adiponectin concentrations do not increase in association with moderate weight loss in insulin-resistant, obese women

Metabolism ◽  
2004 ◽  
Vol 53 (3) ◽  
pp. 280-283 ◽  
Author(s):  
Fahim Abbasi ◽  
Cindy Lamendola ◽  
Tracey McLaughlin ◽  
John Hayden ◽  
Gerald M Reaven ◽  
...  
Keyword(s):  
Weight Loss ◽  
Obese Women ◽  
Plasma Adiponectin ◽  
Insulin Resistant
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