133,961 research outputs found
Serum sex steroids and steroidogenesis-related enzyme expression in skeletal muscle during experimental weight gain in men
No full textAbstract not availableK. Sato, D. Samocha-Bonet, D.J. Handelsman, S. Fujita, G.A. Wittert, L.K. Heilbron
Raised circulating fetuin-a after 28-day overfeeding in healthy humans
Get PDFAbstract not availableDorit Samocha-Bonet, Charmaine S. Tam, Lesley V. Campbell and Leonie Kaye Heilbron
Skeletal muscle extracellular matrix remodeling after short-term overfeeding in healthy humans
No full textAbstract not availableCharmaine S Tam, Rima Chaudhuri, Amy T Hutchison, Dorit Samocha-Bonet, Leonie K Heilbron
Does skeletal muscle oxidative stress initiate insulin resistance in genetically predisposed individuals?
No full textReactive oxygen species (ROS) are postulated to be a common trigger of insulin resistance. For example, treatment of adipocytes with either tumor-necrosis factor-alpha or dexamethasone increases ROS before impairing glucose uptake. Similarly, treatment with mitochondria-specific antioxidants preserves insulin sensitivity in animal models of insulin resistance. However, it remains unclear whether ROS contribute to insulin resistance in humans. First-degree relatives (FDRs) of type 2 diabetes subjects are at increased risk of developing insulin resistance and type 2 diabetes. Here we review the documented metabolic impairments in FDRs that could contribute to insulin resistance via increased oxidative stress. We propose that lipotoxic intermediates and lipid peroxides in skeletal muscle interfere with insulin signaling and might cause insulin resistance in these 'at risk' individuals.Dorit Samocha-Bonet, Leonie K. Heilbronn, Dov Lichtenberg and Lesley V. Campbel
Serum S-adenosylmethionine, but not methionine, increases in response to overfeeding in humans
No full textBackground: Plasma concentration of the methyl donor S-adenosylmethionine (SAM) is linearly associated with body mass index (BMI) and fat mass. As SAM is a high-energy compound and a sensor of cellular nutrient status, we hypothesized that SAM would increase with overfeeding. Methods: Forty normal to overweight men and women were overfed by 1250 kcal per day for 28 days. Results: Serum SAM increased from 106 to 130 nmol/l (P=0.006). In stratified analysis, only those with weight gain above the median (high-weight gainers; average weight gain 3.9±0.3 kg) had increased SAM (+42%, P=0.001), whereas low-weight gainers (weight gain 1.5±0.2 kg) did not (Pinteraction=0.018). Overfeeding did not alter serum concentrations of the SAM precursor, methionine or the products, S-adenosyl-homocysteine and homocysteine. The SAM/SAH (S-adenosylhomocysteine) ratio was unchanged in the total population, but increased in high-weight gainers (+52%, P=0.006, Pinteraction =0.005). Change in SAM correlated positively with change in weight (r=0.33, P=0.041) and fat mass (r=0.44, P=0.009), but not with change in protein intake or plasma methionine, glucose, insulin or low-density lipoprotein (LDL)-cholesterol. Conclusion: Overfeeding raised serum SAM in proportion to the fat mass gained. The increase in SAM may help stabilize methionine levels, and denotes a responsiveness of SAM to nutrient state in humans. The role of SAM in human energy metabolism deserves further attention.A K Elshorbagy, F Jernerén, D Samocha-Bonet, H Refsum and L K Heilbron
Obesity is associated with activated and insulin resistant immune cells
No full textBackgroundObesity and type 2 diabetes mellitus are characterized by insulin resistance and 'low-grade inflammation'; however, the pathophysiological link is poorly understood. To determine the relative contribution of obesity and insulin resistance to systemic 'inflammation', this study comprehensively characterized circulating immune cells in different grades of obesity.MethodsImmune cell phenotypes and activation status were analysed by flow cytometry cross-sectionally in morbidly obese (n = 16, body mass index (BMI) 42.2 ± 5.4 kg/m2), overweight (n = 13, BMI 27.4 ± 1.6 kg/m2) and normal weight (n = 12, BMI 22.5 ± 1.9 kg/m2) subjects.ResultsObese, but not overweight subjects, had increased activation marker expression on neutrophils, monocytes, T-lymphocytes and polarization of T helper cells towards a pro-inflammatory type 1-phenotype (Th1). Th1 numbers correlated positively with the degree of insulin resistance (homeostasis model assessment, p ConclusionsThese results show that morbid obesity is characterized by circulating immune cells that are activated and insulin resistant, with the T-cell balance polarized towards a pro-inflammatory Th1 phenotype. The loss of insulin-induced suppression of inflammatory phenotypes in circulating immune cells could contribute to the systemic and adipose tissue inflammation found in morbid obesity.A. Viardot, L.K. Heilbronn, D. Samocha-Bonet, F. Mackay, L.V. Campbell and K. Samara
Dietary acid load, metabolic acidosis and insulin resistance - Lessons from cross-sectional and overfeeding studies in humans
No full textAbstract not availableRebecca S. Williams, Leonie K. Heilbronn, Daniel L. Chen, Adelle C.F. Coster,
Jerry R. Greenfield, Dorit Samocha-Bone
Effects of intraduodenal glutamine on incretin hormone and insulin release, the glycemic response to an intraduodenal glucose infusion, and antropyloroduodenal motility in health and type 2 diabetes
Get PDFOBJECTIVE Glutamine reduces postprandial glycemia when given before oral glucose. We evaluated whether this is mediated by stimulation of insulin and/or slowing of gastric emptying. RESEARCH DESIGN AND METHODS Ten healthy subjects were studied during intraduodenal (ID) infusion of glutamine (7.5 or 15 g) or saline over 30 min, followed by glucose (75 g over 100 min), while recording antropyloroduodenal pressures. Ten patients with type 2 diabetes mellitus (T2DM) were also studied with 15 g glutamine or saline. RESULTS ID glutamine stimulated glucagon-like peptide 1 (GLP-1; healthy: P < 0.05; T2DM: P < 0.05), glucose-dependent insulinotropic polypeptide (GIP; P = 0.098; P < 0.05), glucagon (P < 0.01; P < 0.001), insulin (P = 0.05; P < 0.01), and phasic pyloric pressures (P < 0.05; P < 0.05), but did not lower blood glucose (P = 0.077; P = 0.5). CONCLUSIONS Glutamine does not lower glycemia after ID glucose, despite stimulating GLP-1, GIP, and insulin, probably due to increased glucagon. Its capacity for pyloric stimulation suggests that delayed gastric emptying is a major mechanism for lowering glycemia when glutamine is given before oral glucose.Jessica Chang, Tongzhi Wu, Jerry R. Greenfield, Dorit Samocha-Bonet, Michael Horowitz, and Christopher K. Rayne
CAJA 165 - LEGAJO V - SIGNATURA 01
No full textInforme de la Comisión de Ciencias sobre el líquido inventado por D. Tomás Bonet para hacer crecer el pelo.Bonet, T. (1865). Informe de la Comisión de Ciencias sobre el líquido inventado por D. Tomás Bonet para hacer crecer el pelo. Real Sociedad Económica de Amigos del País de Valencia. https://riunet.upv.es/handle/10251/23220Importación Masiv
Metabolically protective cytokines adiponectin and fibroblast growth factor-21 are increased by acute overfeeding in healthy humans
Get PDFContext: Circulating levels of metabolically protective and adverse cytokines are altered in obese humans and rodent models. However, it is not clear whether these cytokines are altered rapidly in response to over-nutrition, or as a later consequence of the obese state. Methods: Forty sedentary healthy individuals were examined prior to and at 3 and 28 days of high fat overfeeding (+1250 kCal/day, 45% fat). Insulin sensitivity (hyperinsulinaemic-euglycaemic clamp), adiposity, serum levels of adiponectin and fibroblast growth factor-21 (FGF21), fatty acid binding protein-4 (FABP4), lipocalin-2 and plasminogen activator factor-1 (PAI1) were assessed. Statistics were performed by repeated measures ANOVA. Results: Overfeeding increased weight, body fat and liver fat, fasting glucose, insulin and reduced insulin sensitivity by clamp (all P <0.05). Metabolically protective cytokines, adiponectin and FGF21 were increased at day 3 of overfeeding (P ≤0.001) and adiponectin was also elevated at day 28 (P=0.001). FABP4, lipocalin-2 and PAI-1 were not changed by overfeeding at either time point. Conclusion: Metabolically protective cytokines, adiponectin and FGF-21, were increased by over nutrition and weight gain in healthy humans, despite increases in insulin resistance. We speculate that this was in attempt to maintain glucose homeostasis in a state of nutritional excess. PAI-I, FABP4 and lipocalin 2 were not altered by overfeeding suggesting that changes in these cytokines may be a later consequence of the obese state.Leonie K. Heilbronn, Lesley V. Campbell, Aimin Xu, Dorit Samocha-Bone
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