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Background: The consumption of advanced glycation end products (AGEs) has increased because of modern food processing and has been linked to the development of type 2 diabetes in rodents. Objective: We determined whether changing dietary AGE intake could modulate insulin sensitivity and secretion in healthy, overweight individuals. Design: We performed a double-blind, randomized, crossover trial of diets in 20 participants [6 women and 14 men; mean ± SD body mass index (in kg/m²): 29.8 ± 3.7]. Isoenergetic- and macronutrient-matched diets that were high or low in AGE content were alternately consumed for 2 wk and separated by a 4-wk washout period. At the beginning and end of each dietary period, a hyperinsulinemiceuglycemic clamp and an intravenous glucose tolerance test were performed. Dietary, plasma and urinary AGEs N∈-(carboxymethyl) lysine (CML), N∈-(carboxyethyl)lysin (CEL), and methylglyoxal-derived hydroimadazolidine (MG-H1) were measured with the use of mass spectrometry. Results: Participants consumed less CML, CEL, and MG-H1 during the low-AGE dietary period than during the high-AGE period (all P < 0.05), which was confirmed by changes in urinary AGE excretion. There was an overall difference in insulin sensitivity of -22.1 mg ⋅ kg-1 ⋅ min-1 between diets (P = 0.001). Insulin sensitivity increased by 1.3 mg ⋅ kg-1 ⋅ min-1 after the low-AGE diet (P = 0.004), whereas it showed a tendency to decrease by 0.8 mg ⋅ kg-1 ⋅ min-1 after the high-AGE diet (P = 0.086). There was no difference in body weight or insulin secretion between diets (P = NS). Conclusions: A diet that is low in AGEs may reduce the risk of type 2 diabetes by increasing insulin sensitivity. Hence, a restriction in dietary AGE content may be an effective strategy to decrease diabetes and cardiovascular disease risks in overweight individuals. This trial was registered at clinicaltrials.gov as NCT00422253. [ABSTRACT FROM AUTHOR]

Background: Branched-chain amino acids (BCAAs), particularly leucine, act as nutrient signals regulating protein synthesis and degradation as well as glucose metabolism. In addition, leucine has been demonstrated in animal experiments to modulate eating and energy homeostasis. Objective: We aimed to characterize the effects of physiologic and supraphysiologic loads of intraduodenal leucine on eating, gut hormone and motor functions, and blood glucose in humans. Design: Twelve lean men were studied on 3 occasions in a randomized, double-blind order. Antropyloroduodenal motility, plasma ghrelin, cholecystokinin, glucagon-like peptide 1, peptide YY, insulin, glucagon, blood glucose, appetite perceptions, and gastrointestinal symptoms were measured during 90-min intraduodenal infusions of leucine at 0.15 kcal/min (total 3.3 g, 13.5 kcal), 0.45 kcal/min (total 9.9 g, 40.5 kcal), or saline (control). Ad libitum eating from a buffet lunch was quantified immediately after the infusions. Results: Leucine at 0.45 kcal/min inhibited eating (energy intake by w13%, P , 0.05), increased plasma cholecystokinin, slightly reduced blood glucose and increased plasma insulin, and decreased antral pressures (all P , 0.05). Leucine at 0.15 kcal/min had no effect on food intake, blood glucose, or antral pressures but also slightly increased plasma cholecystokinin (P , 0.05). Neither dose affected plasma ghrelin, glucagon, glucagon-like peptide 1 and peptide YY, or pyloric and duodenal pressures. Plasma leucine concentrations were related to the dose of intraduodenal leucine, with substantial increases during both 0.15 and 0.45 kcal/min. Conclusions: The effects of intraduodenal infusions of free leucine on eating are probably not primarily mediated by changes in gut motor and hormone functions, with perhaps the exception of cholecystokinin. Instead, increased plasma leucine concentrations may be a potential signal mediating the eating-inhibitory effect of leucine. The study was registered as a clinical trial with the Australia and New Zealand Clinical Trial Registry (www.anzctr.org.au) as ACTRN12613000899741. [ABSTRACT FROM AUTHOR]

Background: The Food Insulin Index (FII) is a novel classification of single foods based on insulin responses in healthy subjects relative to an isoenergetic reference food. Objective: Our aim was to compare day-long responses to 2 nutrientmatched diets predicted to have either high or low insulin demand in healthy controls and individuals with type 2 diabetes (T2DM). Design: Twenty adults (10 healthy adults and 10 adults with T2DM) were recruited. On separate mornings, subjects consumed either a high- or low-FII diet in random order. Diets consisted of 3 consecutive meals (breakfast, morning tea, and lunch), matched for macronutrients, fiber, and glycemic index (GI), but with 2-fold difference in insulin demand as predicted by the FII of the component foods. Postprandial glycemia and insulinemia were measured in capillary plasma at regular intervals over 8 h. Results: As predicted by their GI, there were no differences in glycemic responses between the 2 diets in either group (mean 6 SEM; healthy: 6.2 6 0.2 compared with 6.1 6 0.1 mmol/L $ min, P = 0.429; T2DM: 9.96 1.3 compared with 10.36 1.6 mmol/L $ min, P = 0.485). Compared with the high-FII diet, mean postprandial insulin response over 8 h was 53% lower with the low-FII diet in healthy subjects (mean 6 SEM; incremental AUCinsulin 31,900 6 4100 pmol/L $min compared with 68,100 6 11,400 pmol/L $ min, P = 0.003) and 41% lower in subjects with T2DM (mean 6 SEM; incremental AUCinsulin 11,000 6 1800 pmol/L $ min compared with 18,700 6 3100 pmol/L $ min, P = 0.018). Incremental AUCinsulin was statistically significantly different between diets when groups were combined (P = 0.001). Conclusions: The FII algorithm may be a useful tool for reducing postprandial hyperinsulinemia in T2DM, thereby potentially improving insulin resistance and b-cell function. This trial was registered at the Australian New Zealand Clinical Trials Registry as ACTRN12611000654954. [ABSTRACT FROM AUTHOR]

Background: Krill is an increasingly popular source of marine n-3 (ω-3) PUFA that is seen as a premium product. However, to our knowledge, the effect of krill-oil supplementation on insulin sensitivity in humans has not been reported. Objective: We assessed whether supplementation with a blend of krill and salmon (KS) oil [which is rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] affects insulin sensitivity in overweight men. Design: The design was a randomized, double-blind, controlled crossover trial. A total of 47 men with a mean ± SD age of 46.5 ± 5.1 y, who were overweight [body mass index (in kg/m²) from 25 to 30] but otherwise healthy, received 5 1-g capsules of KS oil or a control (canola oil) for 8 wk and crossed over to another treatment after an 8-wk washout period. The primary outcome was insulin sensitivity assessed by using the Matsuda method from an oral-glucose-tolerance test. Secondary outcomes included lipid profiles, inflammatory markers, 24-h ambulatory blood pressure, and carotid artery intimamedia thickness. Results: Unexpectedly, insulin sensitivity (per the Matsuda index) was 14% lower with the KS oil than with the control oil (P = 0.049). A mediation analysis showed that, after controlling for the likely positive effects of blood EPA and DHA (i.e., the omega-3 index), the reduction in insulin sensitivity after KS-oil supplementation was more marked [27% lower than with the control oil (P = 0.009)]. Conclusions: Supplementation with a blend of KS oil is associated with decreased insulin sensitivity. Thus, krill-oil supplementation in overweight adults could exacerbate risk of diabetes and cardiovascular disease. This trial was prospectively registered at the Australian New Zealand Clinical Trials Registry as ACTRN12611000602921. [ABSTRACT FROM AUTHOR]