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Antonio P Tataranni - One of the best experts on this subject based on the ideXlab platform.
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plasma adiponectin concentrations in children relationships with obesity and Insulinemia
The Journal of Clinical Endocrinology and Metabolism, 2002Co-Authors: Norbert Stefan, Tohru Funahashi, Yuji Matsuzawa, Joy C Bunt, Arline D Salbe, Antonio P TataranniAbstract:Adiponectin, a novel adipokine with anti-inflammatory and insulin-sensitizing properties, has been found to have independent negative associations with obesity and hyperInsulinemia/insulin resistance in adults. We measured fasting plasma adiponectin and insulin concentrations and body composition (dual-energy x-ray absorptiometry or doubly labeled water) in 30 5-yr-old (11 boys and 19 girls) and 53 10-yr-old (17 boys and 36 girls) Pima Indian children. A subgroup of 20 children (5 boys and 15 girls) had all measurements at both 5 and 10 yr of age. Cross-sectionally, plasma adiponectin concentrations were negatively correlated with percentage body fat and fasting plasma insulin concentrations at both 5 yr (r = -0.35, P = 0.06, r = -0.42, P = 0.02) and 10 yr (r = -0.46, P = 0.001, r = -0.38, P = 0.005) of age. At age 10 yr, percentage body fat (P = 0.03) but not fasting plasma insulin (P = 0.59) was independently associated with fasting plasma adiponectin concentrations. Longitudinally, plasma adiponectin concentrations decreased with increasing adiposity. In summary, these results confirm our previously reported findings in adults of an inverse relationship between plasma adiponectin concentrations and adiposity in children. Longitudinal analyses indicated that hypoadiponectinemia is a consequence of the development of obesity in childhood. We did not find evidence that adiponectin is an early mediator of obesity-induced insulin resistance, a preliminary observation that needs to be confirmed in studies using a more direct measurement of insulin action than the one used in this investigation.
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hypoadiponectinemia in obesity and type 2 diabetes close association with insulin resistance and hyperInsulinemia
The Journal of Clinical Endocrinology and Metabolism, 2001Co-Authors: Christian Weyer, Tohru Funahashi, Richard E Pratley, Sachiyo Tanaka, Kikuko Hotta, Yuji Matsuzawa, Antonio P TataranniAbstract:Plasma concentrations of adiponectin, a novel adipose-specific protein with putative antiatherogenic and antiinflammatory effects, were found to be decreased in Japanese individuals with obesity, type 2 diabetes, and cardiovascular disease, conditions commonly associated with insulin resistance and hyperInsulinemia. To further characterize the relationship between adiponectinemia and adiposity, insulin sensitivity, Insulinemia, and glucose tolerance, we measured plasma adiponectin concentrations, body composition (dual-energy x-ray absorptiometry), insulin sensitivity (M, hyperinsulinemic clamp), and glucose tolerance (75-g oral glucose tolerance test) in 23 Caucasians and 121 Pima Indians, a population with a high propensity for obesity and type 2 diabetes. Plasma adiponectin concentration was negatively correlated with percent body fat (r = −0.43), waist-to-thigh ratio (r = −0.46), fasting plasma insulin concentration (r = −0.63), and 2-h glucose concentration (r = −0.38), and positively correlated with...
M Szurkowska - One of the best experts on this subject based on the ideXlab platform.
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Insulinemia a marker of early diagnosis and control of efficacy of treatment of type ii diabetes
Polskie Archiwum Medycyny Wewnetrznej-polish Archives of Internal Medicine, 2001Co-Authors: Z Szybinski, M SzurkowskaAbstract:: Metabolic Syndrome X defined by Reaven is caused by peripheral insuline receptor resistance, leads to hyperInsulinemia regarded as a cause of secondary dyslipidemia, hypertension, hemostatic disturbances, atherosclerosis and insulin as a growth factor takes part in carcinogenesis. Depending on a contribution of the primary risk factors of type 2 Diabetes Mellitus (2-DM) mainly genetic factors and obesity--an independent cause of insulin receptor resistance--glucose intolerance and 2-DM may overlap the Syndrome X. The aims of these studies were to determine in cross-sectional investigation a plasma insulin concentration in subjects aged over 35 years and to assess the clinical usefulness of Insulinemia in early diagnosis of diabetes type 2. Investigations were carried out in Krakow town's district with 200,000 inhabitants, out of those 3060 randomly selected subjects (1720 females and 1340 males aged over 35 years) took part in the Polish Multicenter Study on Diabetes Epidemiology (PMSDE) with protocol and methods previously presented. Glucose concentration was determine by enzymatic method, insuline in plasma by IRMA method using ready kits produced by the Swierk-Poland. Logistic multiple regression model was used to estimate the effect of risk factors on the development of glucose intolerance, Chi square test, Fisher test and Mann-Whitney test were used for statistical analysis by means of statistical package BMPD. Fasting Insulinemia in persons with normal glucose tolerance and body weight (BMI 30 increased by 50 and 100% responsively and in 2-nd h in OGTT by five-times. In the persons with glucose intolerance and new-diagnosed 2-DM Insulinemia increased 2-3 fold depending on BMI, and gender. In the subgroup with 2-DM and BMI > 30, Insulinemia in 2 h-OGTT treated values 152 (SD = 90) in women and 112 (SD = 83.4) microU/ml in men. Obesity and Insulinemia in 2 h-OGTT in multiple analysis have been identified as a strong predictors and risk factors of impaired glucose intolerance (IGT) 2-DM fasting Insulinemia may be useful as an indicator of the peripheric insulin receptor resistance. The results lead to the conclusions that determination of the plasma insulin concentration may be useful in early diagnosis of IGT and diabetes type 2, and should be monitored in the course of non-pharmacological and pharmacological treatment 2-DM. One of the main goals in the course of treatment of obesity and early phases of the 2-DM should be normalization or at least reduction of hyperInsulinemia. Insulinemia may be regarded also as an important criterion for selection of the oral antidiabetic drugs.
J. C. Brand-miller - One of the best experts on this subject based on the ideXlab platform.
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Algorithms to Improve the Prediction of Postprandial Insulinaemia in Response to Common Foods
Nutrients, 2016Co-Authors: Peter Petocz, Stephen Colagiuri, J. C. Brand-millerAbstract:Dietary patterns that induce excessive insulin secretion may contribute to worsening insulin resistance and beta-cell dysfunction. Our aim was to generate mathematical algorithms to improve the prediction of postprandial glycaemia and insulinaemia for foods of known nutrient composition, glycemic index (GI) and glycemic load (GL). We used an expanded database of food insulin index (FII) values generated by testing 1000 kJ portions of 147 common foods relative to a reference food in lean, young, healthy volunteers. Simple and multiple linear regression analyses were applied to validate previously generated equations for predicting insulinaemia, and develop improved predictive models. Large differences in insulinaemic responses within and between food groups were evident. GL, GI and available carbohydrate content were the strongest predictors of the FII, explaining 55%, 51% and 47% of variation respectively. Fat, protein and sugar were significant but relatively weak predictors, accounting for only 31%, 7% and 13% of the variation respectively. Nutritional composition alone explained only 50% of variability. The best algorithm included a measure of glycemic response, sugar and protein content and explained 78% of variation. Knowledge of the GI or glycaemic response to 1000 kJ portions together with nutrient composition therefore provides a good approximation for ranking of foods according to their “insulin demand”.
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Effects of human milk and formula on postprandial glycaemia and insulinaemia
European Journal of Clinical Nutrition, 2015Co-Authors: C. J. Wright, F S Atkinson, N Ramalingam, Anette E Buyken, J. C. Brand-millerAbstract:Background/Objectives:Consumption of formula in place of human milk may produce differences in postprandial glycaemia and insulinaemia that contribute to metabolic programming in the first year of life. The objective of the current study was to determine glycaemic and insulinaemic responses to human milk compared with a typical commercial formula, and then compare 11 other formulas.Subjects/Methods:On separate mornings in random order, 10 healthy breastfeeding mothers consumed 25 g available carbohydrate portions of their own milk, a formula and reference food (25 g glucose on two occasions). In the second study, 10 different healthy subjects consumed 25 g available carbohydrate portions of 11 different commercial formulas and three reference foods (25 g glucose on three occasions). Fingerpick blood samples were taken at regular intervals over 2 h, and the glycaemic index (GI) and insulin index determined according to a standardised protocol.Results:There were no significant differences in postprandial glycaemia or insulinaemia after human milk vs a typical formula ( P =0.3). Both produced a low GI (mean±s.e.m.: 38±7 vs 34±7, respectively) and high insulin index (87±14 vs 94±16). The GI and insulin indices of the other formulas ranged from 18±3 to 67±6 and 53±9 to 209±33, respectively.Conclusions:Human milk and a typical formula elicit similar postprandial glycaemic and insulinaemic responses, but there is a wide range of responses to other formulas.
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Effects of human milk and formula on postprandial glycaemia and insulinaemia
European Journal of Clinical Nutrition, 2015Co-Authors: C. J. Wright, N Ramalingam, Fiona Atkinson, Anette E Buyken, J. C. Brand-millerAbstract:Consumption of formula in place of human milk may produce differences in postprandial glycaemia and insulinaemia that contribute to metabolic programming in the first year of life. The objective of the current study was to determine glycaemic and insulinaemic responses to human milk compared with a typical commercial formula, and then compare 11 other formulas. On separate mornings in random order, 10 healthy breastfeeding mothers consumed 25 g available carbohydrate portions of their own milk, a formula and reference food (25 g glucose on two occasions). In the second study, 10 different healthy subjects consumed 25 g available carbohydrate portions of 11 different commercial formulas and three reference foods (25 g glucose on three occasions). Fingerpick blood samples were taken at regular intervals over 2 h, and the glycaemic index (GI) and insulin index determined according to a standardised protocol. There were no significant differences in postprandial glycaemia or insulinaemia after human milk vs a typical formula (P=0.3). Both produced a low GI (mean±s.e.m.: 38±7 vs 34±7, respectively) and high insulin index (87±14 vs 94±16). The GI and insulin indices of the other formulas ranged from 18±3 to 67±6 and 53±9 to 209±33, respectively. Human milk and a typical formula elicit similar postprandial glycaemic and insulinaemic responses, but there is a wide range of responses to other formulas.
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Optimal dietary approaches for prevention of type 2 diabetes: a life-course perspective
Diabetologia, 2010Co-Authors: Anette E Buyken, P. Mitchell, A. Ceriello, J. C. Brand-millerAbstract:In recent years, several alternative dietary approaches, including high-protein and low-glycaemic-load diets, have produced faster rates of weight loss than traditional low-fat, high-carbohydrate diets. These diets share an under-recognised unifying mechanism: the reduction of postprandial glycaemia and insulinaemia. Similarly, some food patterns and specific foods (potatoes, white bread, soft drinks) characterised by hyperglycaemia are associated with higher risk of adiposity and type 2 diabetes. Profound compensatory hyperinsulinaemia, exacerbated by overweight, occurs during critical periods of physiological insulin resistance such as pregnancy and puberty. The dramatic rise in gestational diabetes and type 2 diabetes in the young may therefore be traced to food patterns that exaggerate postprandial glycaemia and insulinaemia. The dietary strategy with the strongest evidence of being able to prevent type 2 diabetes is not the accepted low-fat, high-carbohydrate diet, but alternative dietary approaches that reduce postprandial glycaemia and insulinaemia without adversely affecting other risk factors.
Eleuterio Ferrannini - One of the best experts on this subject based on the ideXlab platform.
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effect of pioglitazone on the metabolic and hormonal response to a mixed meal in type ii diabetes
Clinical Pharmacology & Therapeutics, 2007Co-Authors: Amalia Gastaldelli, A Casolaro, Maura Pettiti, Monica Nannipieri, Demetrio Ciociaro, Silvia Frascerra, E Buzzigoli, Simona Baldi, Andrea Mari, Eleuterio FerranniniAbstract:We explored the mechanisms by which a 4-month, placebo-controlled pioglitazone treatment (45 mg/day) improves glycemic control in type II diabetic patients (T2D, n=27) using physiological testing (6-h mixed meal) and a triple tracer technique ([6,6-2H2]glucose infusion, 2H2O and [6-3H]glucose ingestion) to measure endogenous glucose production (EGP), gluconeogenesis (GNG), insulin-mediated glucose clearance and β-cell glucose sensitivity (by c-peptide modeling). Compared to sex/age/weight-matched non-diabetic controls, T2D patients showed inappropriately (for prevailing Insulinemia) raised glucose production (1.05[0.53] vs 0.71[0.36]mmol min−1 kgffm−1 pM, P=0.03) because of enhanced GNG (73.1±2.4 vs 59.5±3.6%, P<0.01) persisting throughout the meal, reduced insulin-mediated glucose clearance (6[5] vs 12[13]ml min−1 kgffm−1 nM−1, P<0.005), and impaired β-cell glucose-sensitivity (27[38] vs 71[37]pmol min−1 m−2 mM−1, P=0.002). Compared to placebo, pioglitazone improved glucose overproduction (P=0.0001), GNG and glucose underutilization (P=0.05) despite lower Insulinemia. GNG improvement was quantitatively related to raised adiponectin. β-cell glucose sensitivity was unchanged. In mild-to-moderate T2D, pioglitazone monotherapy decreased fasting and post-prandial glycemia, principally via inhibition of gluconeogenesis, improved hepatic and peripheral insulin resistance. Clinical Pharmacology & Therapeutics (2007) 81, 205–212. doi:10.1038/sj.clpt.6100034
Daniel J West - One of the best experts on this subject based on the ideXlab platform.
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comparison of appetite responses to high and low glycemic index postexercise meals under matched Insulinemia and fiber in type 1 diabetes
The American Journal of Clinical Nutrition, 2015Co-Authors: Matthew Campbell, Javier T Gonzalez, Penny L S Rumbold, Mark Walker, James Shaw, Emma J Stevenson, Daniel J WestAbstract:BACKGROUND: Patients with type 1 diabetes face heightened risk of hypoglycemia after exercise. Subsequent overfeeding, as a preventative measure against hypoglycemia, negates the energy deficit after exercise. Patients are also required to reduce the insulin dose administered with postexercise foods to further combat hypoglycemia. However, the insulin dose is dictated solely by the carbohydrate content, even though postprandial glycemia is vastly influenced by glycemic index (GI). With a need to control the postexercise energy balance, appetite responses after meals differing in GI are of particular interest. OBJECTIVES: We assessed the appetite response to low-glycemic index (LGI) and high-glycemic index (HGI) postexercise meals in type 1 diabetes patients. This assessment also offered us the opportunity to evaluate the influence of GI on appetite responses independently of Insulinemia, which confounds findings in individuals without diabetes. DESIGN: Ten physically active men with type 1 diabetes completed 2 trials in a randomized crossover design. After 45 min of treadmill exercise at 70% of the peak oxygen uptake, participants consumed an LGI (GI ∼37) or HGI (GI ∼92) meal with a matched macronutrient composition, negligible fiber content, and standardized insulin-dose administration. The postprandial appetite response was determined for 180 min postmeal. During this time, circulating glucose, insulin, glucagon, and glucagon-like peptide-1 (GLP-1) concentrations and subjective appetite ratings were determined. RESULTS: The HGI meal produced an ∼60% greater postprandial glucose area under the curve (AUC) than did the LGI meal (P = 0.008). Insulin, glucagon, and GLP-1 did not significantly differ between trials (P > 0.05). The fullness AUC was ∼25% greater after the HGI meal than after the LGI meal (P < 0.001), whereas hunger sensations were ∼9% lower after the HGI meal than after the LGI meal (P = 0.001). CONCLUSION: Under conditions of matched Insulinemia and fiber, an HGI postexercise meal suppresses feelings of hunger and augments postprandial fullness sensations more so than an otherwise equivalent LGI meal in type 1 diabetes patients.
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Comparison of appetite responses to high– and low–glycemic index postexercise meals under matched Insulinemia and fiber in type 1 diabetes
The American Journal of Clinical Nutrition, 2014Co-Authors: Matthew Campbell, Javier T Gonzalez, Penny L S Rumbold, Mark Walker, James Shaw, Emma J Stevenson, Daniel J WestAbstract:BACKGROUND: Patients with type 1 diabetes face heightened risk of hypoglycemia after exercise. Subsequent overfeeding, as a preventative measure against hypoglycemia, negates the energy deficit after exercise. Patients are also required to reduce the insulin dose administered with postexercise foods to further combat hypoglycemia. However, the insulin dose is dictated solely by the carbohydrate content, even though postprandial glycemia is vastly influenced by glycemic index (GI). With a need to control the postexercise energy balance, appetite responses after meals differing in GI are of particular interest. OBJECTIVES: We assessed the appetite response to low-glycemic index (LGI) and high-glycemic index (HGI) postexercise meals in type 1 diabetes patients. This assessment also offered us the opportunity to evaluate the influence of GI on appetite responses independently of Insulinemia, which confounds findings in individuals without diabetes. DESIGN: Ten physically active men with type 1 diabetes completed 2 trials in a randomized crossover design. After 45 min of treadmill exercise at 70% of the peak oxygen uptake, participants consumed an LGI (GI ∼37) or HGI (GI ∼92) meal with a matched macronutrient composition, negligible fiber content, and standardized insulin-dose administration. The postprandial appetite response was determined for 180 min postmeal. During this time, circulating glucose, insulin, glucagon, and glucagon-like peptide-1 (GLP-1) concentrations and subjective appetite ratings were determined. RESULTS: The HGI meal produced an ∼60% greater postprandial glucose area under the curve (AUC) than did the LGI meal (P = 0.008). Insulin, glucagon, and GLP-1 did not significantly differ between trials (P > 0.05). The fullness AUC was ∼25% greater after the HGI meal than after the LGI meal (P < 0.001), whereas hunger sensations were ∼9% lower after the HGI meal than after the LGI meal (P = 0.001). CONCLUSION: Under conditions of matched Insulinemia and fiber, an HGI postexercise meal suppresses feelings of hunger and augments postprandial fullness sensations more so than an otherwise equivalent LGI meal in type 1 diabetes patients.
