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Adiponectin Gene Variant rs266729 Interacts with Different Macronutrient Distribution of Two Different Hypocaloric Diets.
de Luis, DA, Primo, D, Izaola, O, Aller, R
Lifestyle genomics. 2020;(1):20-27
Abstract
BACKGROUND The role of ADIPOQ gene variants in weight loss after different dietary fat amounts remains unclear. OBJECTIVE Our aim was to analyze the effects of ADIPOQ gene polymorphism rs266729 on metabolic changes after two different amounts of dietary fat in two hypocaloric diets. DESIGN A population of 283 obese patients was recruited in a randomized clinical trial with two diets: Diet HF (high-fat diet: 38% carbohydrates, 24% proteins, and 38% fats) versus Diet LF (low-fat diet: 53% carbohydrates, 20% proteins, and 27% fats). Before and after 3 months, an anthropometric evaluation, an assessment of nutritional intake, and a biochemical analysis were carried out. The variant of the ADIPOQgene was assessed by real-time PCR. RESULTS Weight loss was similar with both diets in both genotypes (CC vs. CG+GG). After dietary intervention with Diet HF, only subjects with CC genotype showed a significant improvement in insulin levels (-3.3 ± 0.6 vs. -1.8 ± 0.9 mU/L; p = 0.03) and the homeostasis model assessment for insulin resistance (HOMA-IR) (-1.3 ± 0.1 vs. -0.8 ± 0.2 units; p = 0.02). After Diet LF, subjects with CC genotype showed a significant improvement in total cholesterol levels (CC vs. CG+GG) (-15.3 ± 1.4 vs. -6.4 ± 1.3 mg/dL; p = 0.01), LDL cholesterol (-14.6 ± 1.8 vs. -6.4 ± 1.3 mg/dL; p = 0.01), insulin levels (-4.6 ± 1.0 vs. -1.6 ± 0.5 mU/L; p = 0.01), and HOMA-IR (-1.6 ± 0.1 vs. -1.0 ± 0.2 units; p = 0.02). Only subjects with CC genotype showed a significant increase of adiponectin levels after both diets (CC vs. CG+GG): Diet HF (10.6 ± 2.0 vs. 1.8 ± 1.0 ng/dL; p = 0.01) and Diet LF (16.1 ± 2.8 vs. 1.3 ± 1.0 ng/dL: p = 0.03). CONCLUSION CC genotype of ADIPOQgene variantrs266729 was associated with a better metabolic response after both diets. Additionally, Diet LF produced a significant improvement in lipid profile in noncarriers of allele G.
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Changes in Lipoinflammation Markers in People with Obesity after a Concurrent Training Program: A Comparison between Men and Women.
González-Jurado, JA, Suárez-Carmona, W, López, S, Sánchez-Oliver, AJ
International journal of environmental research and public health. 2020;(17)
Abstract
Obesity is related to low-grade systemic inflammation. This state of inflammation is characterized by the alteration in adipokine regulation, which may lead to a situation of cardiometabolic risk. The aim of this study was to evaluate the effects of a concurrent training program on markers of lipoinflammation in adult people with obesity, comparing the response to the training between men and women. A quasi-experimental, quantitative, and longitudinal study with a pre-post intervention was conducted. An 8-week concurrent training program was carried out, in which 26 individuals with obesity participated (mean ± SD; age = 46.38 ± 4.66) (BMI = 36.05 ± 4.99) (12 men and 14 women). Before and after the intervention period, blood samples were taken by percutaneous puncture. The blood levels of adiponectin and leptin were evaluated. Significant differences were obtained in the adiponectin-leptin ratio (A/L ratio) of the entire sample (p = 0.009, ES = 0.53), which indicates a decrease in the risk of cardiovascular diseases and lipoinflammation. There were no significant differences in the improvements observed after the training in A/L ratio between women (A/L change = +63.5%) and men (A/L change= +59.2%). It can be concluded that the combination of aerobic exercise and resistance training induced an improvement in markers of lipoinflammation and cardiometabolic risk in the individuals with obesity evaluated in this study.
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Homeostatic model assessment of adiponectin (HOMA-Adiponectin) as a surrogate measure of insulin resistance in adolescents: Comparison with the hyperglycaemic clamp and homeostatic model assessment of insulin resistance.
da Silva, CC, Zambon, MP, Vasques, ACJ, Camilo, DF, De Bernardi Rodrigues, AM, Antonio, MÂRGM, Dâmaso, AR, Tufik, S, de Mello, MT, Campos, RMDS, et al
PloS one. 2019;(3):e0214081
Abstract
BACKGROUND Studies on adults have reported inverse association between the homeostatic model assessment (HOMA) of adiponectin (HOMA-Adiponectin) and the insulin resistance assessed by the glucose clamp technique. To our knowledge, in the pediatric population this association has not been previously investigated. OBJECTIVES To evaluate the association between the HOMA-Adiponectin and the insulin resistance assessed by the glucose clamp technique in adolescents, and to compare the accuracy of HOMA-Adiponectin and HOMA-insulin resistance (HOMA-IR) for identifying insulin resistance. METHODS This was a cross-sectional study of 56 adolescents (aged 10-18 years). Insulin resistance was assessed using the HOMA-IR, HOMA-Adiponectin and the hyperglycaemic clamp technique. The clamp-derived insulin sensitivity index, HOMA-Adiponectin, and HOMA-IR were log-transformed to get closer to a normal distribution before analysis. RESULTS In the multivariable linear regression analysis controlling for sex and Tanner stage, HOMA-Adiponectin was inversely associated with the clamp-derived insulin sensitivity index (unstandardized coefficient [B] = -0.441; P < 0.001). After additional adjustment for waist circumference-to-height ratio, this association remained significant (B = -0.349; P = < 0.001). Similar results were observed when HOMA-IR replaced HOMA-Adiponectin in the model (B = -1.049 and B = -0.968 after additional adjustment for waist circumference-to-height ratio); all P < 0.001. The area under the receiver operating characteristic curve for predicting insulin resistance was 0.712 (P = 0.02) for HOMA-Adiponectin and 0.859 (P < 0.0001) HOMA-IR. CONCLUSIONS The HOMA-Adiponectin was independently associated with insulin resistance and exhibited a good discriminatory power for predicting it. However, it did not show superiority over HOMA-IR in the diagnostic accuracy.
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Effects of canagliflozin versus glimepiride on adipokines and inflammatory biomarkers in type 2 diabetes.
Garvey, WT, Van Gaal, L, Leiter, LA, Vijapurkar, U, List, J, Cuddihy, R, Ren, J, Davies, MJ
Metabolism: clinical and experimental. 2018;:32-37
Abstract
OBJECTIVE Type 2 diabetes and obesity are pro-inflammatory states associated with increased risk of cardiovascular disease. Canagliflozin, an SGLT2 inhibitor, demonstrated superiority in lowering HbA1c versus glimepiride with less hypoglycemia and greater weight reduction via loss of fat mass in a 52-week trial of type 2 diabetes patients. This post hoc, exploratory analysis assessed the effects of canagliflozin versus glimepiride on select adipokines, inflammatory biomarkers, and chemokines. METHODS Changes from baseline to Week 52 in serum leptin, adiponectin, IL-6, TNFα, CRP, PAI-1, VCAM-1, and MCP-1 were measured in a randomly selected subset of type 2 diabetes patients on metformin receiving canagliflozin 300 mg (n = 100) or glimepiride (n = 100) in the overall study. Correlations between change in biomarkers and change in select metabolic and anthropometric variables were assessed. RESULTS At Week 52, canagliflozin decreased median serum leptin by 25% (95% CI: -34%, -15%) and increased median serum adiponectin by 17% (95% CI: 11%, 23%) compared with glimepiride. There was a 22% reduction in median serum IL-6 (95% CI: -34%, -10%) and a 7% increase in median serum TNFα (95% CI: 1%, 12%) with canagliflozin versus glimepiride. No between-group differences were observed with the other biomarkers. The decrease in serum leptin with canagliflozin was correlated with change in weight (r ≥ 0.3) only; the increase in adiponectin and decrease in IL-6 with canagliflozin occurred independently of changes in HbA1c, weight, or lipids. CONCLUSIONS These results indicate that canagliflozin may improve adipose tissue function and induce changes in serum leptin, adiponectin, and IL-6 that favorably impact insulin sensitivity and cardiovascular disease risk.
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Circulating cytokines as determinants of weight loss-induced improvements in insulin sensitivity.
Weiss, EP, Reeds, DN, Ezekiel, UR, Albert, SG, Villareal, DT
Endocrine. 2017;(1):153-164
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Dietary calorie restriction and exercise promote weight loss and may have additive effects for improving insulin sensitivity, independent of weight loss. It is not known if these effects are attributable to changes in circulating cytokines. We evaluated the hypothesis that modest, matched weight loss induced by calorie restriction and exercise have additive effects on circulating cytokines and these changes correlate with improvements in insulin sensitivity. Overweight and sedentary women and men (n = 52, 45-65 years) were randomized to undergo 7 % weight loss by using 3-6 months of calorie restriction, exercise, or a combination of both calorie restriction and exercise. Concentrations of cytokines and hormones were measured in fasting and oral glucose tolerance test blood samples. Insulin sensitivity was estimated based on oral glucose tolerance test for glucose and insulin. With all groups combined, fasting leptin (p < 0.0001) and high molecular weight adiponectin (p = 0.04) decreased and pentraxin-3 increased (p < 0.0001), in a manner that correlated with improvements in insulin sensitivity (all p ≤ 0.0002). These changes, combined with decreases in glucose-dependent insulinotropic polypeptide from the oral glucose tolerance test, explained 63 % of the variance (p < 0.0001) in insulin sensitivity improvements. Exercise and calorie restriction had additive effects on leptin, with a similar trend for high molecular weight adiponectin. Monocyte chemoattractant protein-1 and C-reactive protein concentrations did not change. Calorie restriction and exercise had opposite effects on soluble tumor necrosis factor receptor-1. Modest weight loss in overweight adults decreases serum leptin and high molecular weight adiponectin, and increases pentraxin-3 concentrations in a manner that correlates with increased insulin sensitivity. Exercise has additive effects to those induced by calorie restriction for reductions in leptin and possibly adiponectin. These changes may contribute to the additive effects of calorie restriction and exercise for improving insulin sensitivity.
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Homeostasis Model Assessment-Adiponectin: the role of different types of physical exercise in obese adolescents.
da Silveira Campos, RM, Landi Masquio, DC, Campos Corgosinho, F, de Lima Sanches, P, de Piano, A, Carnier, J, Leão da Silva, P, Grotti Clemente, AP, de Castro Ferreira Vicente, SE, Oyama, LM, et al
The Journal of sports medicine and physical fitness. 2017;(6):831-838
Abstract
BACKGROUND Homeostasis Model Assessment-Adiponectin (HOMA-AD) is suggesting a new biomarker of insulin resistance in obese population. In this way, the purpose of this study was to investigate the effects of different kinds of exercise in the sensitive index predictor of insulin resistance. METHODS A total of 148 obese adolescents were enrolled in the program. They aged 15-19 y, with Body Mass Index (BMI) ≥P95th and were submitted to 1 year of interdisciplinary weight loss therapy, randomized in two groups, aerobic training (AT) (N.=51) and aerobic plus resistance training (N.=97). Blood samples were collected to analyze adiponectin, glucose and insulin concentrations. The insulin resistance was measured by HOMA-AD and Homeostasis Model Assessment Insulin Resistance Index (HOMA-IR). RESULTS Both kinds of exercise training promoted a decrease in body mass, body mass index, fat mass, visceral and subcutaneous fat. However, only aerobic plus resistance training was effective to reduce HOMA-AD, insulin and glucose concentration; and increase insulin sensibility and adiponectin concentration. CONCLUSIONS The aerobic plus resistance training was more effective than AT alone to improve the HOMA-AD, suggesting clinical application on obesity, diabetes, atherosclerosis and metabolic syndrome control in the pediatric population.
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Adiponectin protects against incident hypertension independent of body fat distribution: observations from the Dallas Heart Study.
Peri-Okonny, PA, Ayers, C, Maalouf, N, Das, SR, de Lemos, JA, Berry, JD, Turer, AT, Neeland, IJ, Scherer, PE, Vongpatanasin, W
Diabetes/metabolism research and reviews. 2017;(2)
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BACKGROUND Excess adipose tissue has been implicated in the pathogenesis of insulin resistance and atherosclerosis and is a key risk factor for blood pressure (BP) elevation. However, circulating levels of adiponectin, a protein produced by adipose tissue and widely implicated in the pathogenesis of insulin resistance and atherosclerosis, are inversely proportional to adiposity. The relationship between adiponectin and incident hypertension has not been determined in the general US population. METHODS Normotensive participants (n = 1233) enrolled in the Dallas Heart Study, a multiethnic, probability-based population sample of Dallas County adults were followed for median of 7 years. Retroperitoneal, intraperitoneal, visceral, and subcutaneous adipose tissue were measured at baseline by magnetic resonance imaging. Liver fat content was measured by 1 H-magnetic resonance spectroscopy. Relative risk regression was used to determine the association of adiponectin with incident hypertension after adjustment for age, race, sex, BMI, smoking, diabetes, baseline systolic BP, total cholesterol, and regional fat depot. RESULTS Of the 1233 study participants (median age 40 years, 40% black, and 56% women), 391 (32%) had developed hypertension over a median follow-up of 7 years. Adiponectin levels were associated with reduced risk of incident hypertension (RR 0.81, 95% CI [0.68-0.96]) in the fully adjusted model, which included liver fat. Similar results were observed after adjustment for subcutaneous or visceral fat depots when tested individually or simultaneously in the model. CONCLUSION Our study suggested a protective role of adiponectin against incident hypertension independent of body fat distribution.
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Change in adiponectin explains most of the change in HDL particles induced by lifestyle intervention but not metformin treatment in the Diabetes Prevention Program.
Goldberg, RB, Temprosa, M, Mele, L, Orchard, T, Mather, K, Bray, G, Horton, E, Kitabchi, A, Krakoff, J, Marcovina, S, et al
Metabolism: clinical and experimental. 2016;(5):764-775
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OBJECTIVE In addition to slowing diabetes development among participants in the Diabetes Prevention Program (DPP), intensive lifestyle change and metformin raised HDL-cholesterol (HDL-C) compared to placebo treatment. We investigated the lifestyle and metabolic determinants as well as effects of biomarkers of inflammation, endothelial dysfunction and coagulation and their changes resulting from lifestyle and metformin interventions on the increase in HDL-C in the DPP. METHODS The effects of a 1year period of intensive lifestyle change aimed at achieving 7% weight loss or metformin 850mg twice daily versus placebo on HDL-C were assessed in 3070 participants with impaired glucose tolerance, and on HDL particle concentration (HDL-P) and size in a subgroup of 1645 individuals. Treatment-associated changes in lifestyle and metabolic factors as well as in novel biomarkers were investigated for their associations with change in HDL-C using multiple regression analysis. RESULTS After adjusting for BMI, insulin resistance, glycemia, dietary saturated fat, alcohol intake, physical activity and nine different biomarkers, only adiponectin accounted for the effect of intensive lifestyle change on HDL-C via an increase in large HDL-P. By contrast baseline and change in BMI and tissue plasminogen activator levels attenuated the effect of metformin on HDL-C, with adiponectin having no specific effect. CONCLUSION While both lifestyle and metformin interventions used to prevent diabetes increase HDL-C, the mechanisms involved differ between the two treatments and may have consequences for future risk of cardiovascular disease.
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Adiponectin, C-reactive protein, fibrinogen and tissue plasminogen activator antigen levels among glucose-intolerant women with and without histories of gestational diabetes.
Kim, C, Christophi, CA, Goldberg, RB, Perreault, L, Dabelea, D, Marcovina, SM, Pi-Sunyer, X, Barrett-Connor, E
Diabetic medicine : a journal of the British Diabetic Association. 2016;(1):32-8
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AIM: To examine concentrations of biomarkers (adiponectin, C-reactive protein, fibrinogen and tissue plasminogen-activator antigen) associated with glucose homeostasis and diabetes risk by history of gestational diabetes (GDM). METHODS We conducted a secondary analysis of the Diabetes Prevention Program, a randomized trial of lifestyle intervention or metformin for diabetes prevention. At baseline, participants were overweight and had impaired glucose tolerance. Biomarkers at baseline and 1 year after enrolment were compared between parous women with (n = 350) and without histories of GDM (n = 1466). Cox proportional hazard models evaluated whether history of GDM was associated with diabetes risk, after adjustment for baseline biomarker levels as well as for change in biomarker levels, demographic factors and anthropometrics. RESULTS At baseline, women with histories of GDM had lower adiponectin (7.5 μg/ml vs. 8.7 μg/ml; p < 0.0001) and greater log C-reactive protein (-0.90 mg/l vs. -0.78 mg/l, p = 0.04) levels than women without histories of GDM, but these associations did not persist after adjustment for demographic factors. Fibrinogen and tissue plasminogen-activator antigen were similar between women with and without histories of GDM. Women with and without histories of GDM had a similar pattern of changes in biomarkers within randomization arm. Adjustment for age, race/ethnicity, baseline weight, change in weight, baseline biomarker level and change in biomarker level did not significantly alter the association between history of GDM, and diabetes risk. CONCLUSIONS Among women with impaired glucose tolerance, biomarkers in women with and without histories of GDM are similar and respond similarly to lifestyle changes and metformin. Adjustment for biomarker levels did not explain the higher risk of diabetes observed in women with histories of GDM.
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Postprandial adiponectin and gelatinase response to a high-fat versus an isoenergetic low-fat meal in lean, healthy men.
Kennedy, A, Spiers, JP, Crowley, V, Williams, E, Lithander, FE
Nutrition (Burbank, Los Angeles County, Calif.). 2015;(6):863-70
Abstract
OBJECTIVE Evidence suggests that an acute systemic inflammatory response is invoked after consumption of a high-energy meal. Postprandial regulation of adiponectin, an adipose tissue-derived, anti-inflammatory hormone, and the gelatinases, matrix metalloproteinase (MMP)-2 and MMP-9, endopeptidases implicated in a diverse range of inflammatory processes, remain inconclusive. The aim of this study was to assess the postprandial effect of a high-energy (1212 kcal) meal on plasma adiponectin, MMP-2 and MMP-9 activity, glucose, insulin, triacylglycerols, total cholesterol, high-density lipoprotein cholesterol, and the differential effects on these parameters depending on whether the test meal was high fat (HF; 46 g fat, 1210 kcal) or isoenergetic and low fat (LF; 15 g fat, 1214 kcal energy). METHODS Test meals were consumed by 17 lean, healthy men on two separate occasions with blood samples collected by venipuncture at baseline (0 h) and 1 and 3 h after consumption of each test meal. RESULTS At baseline, no significant difference was seen in the parameters between the two groups, except for MMP-2, MMP-9, and total cholesterol. Over the 3-h postprandial period, no significant differential effect of the HF versus the LF test meal was observed on adiponectin, MMP-2, MMP-9, or on metabolic markers other than triacylglycerol, which increased significantly in response to the HF test meal (time × treatment, P = 0.002). When analyzed independent of time, MMP-2 (treatment, P = 0.006), MMP-9 (treatment, P = 0.022), and glucose (treatment, P = 0.026) were lower after consumption of the HF meal compared with the LF test meal. When analyzed independent of treatment, adiponectin increased over the 3-h postprandial period (time, P = 0.031), but there was no change in MMP-2 or MMP-9 (time, P = 0.503 and P = 0.525, respectively). Over the 3-h postprandial period, insulin (time, P < 0.001) and total cholesterol (time, P = 0.002) increased, whereas glucose (time, P < 0.001) and high-density lipoprotein cholesterol (time, P < 0.001) decreased. CONCLUSION No differential effects of a HF versus a LF isoenergetic meal were seen on postprandial adiponectin or the gelatinases. Adiponectin increased in response to a high-energy meal independent of treatment, and the gelatinases were lower in response to the HF versus the LF isoenergetic meal, independent of time point. Given the considerable amount of time that humans spend in the postprandial state, additional research is necessary to further understand inflammatory changes in this state.