Carbohydrate Replacement of Rice or Potato with Lentils Reduces the Postprandial Glycemic Response in Healthy Adults in an Acute, Randomized, Crossover Trial.

Background: The postprandial blood glucose response (PBGR) following carbohydrate replacement of high-glycemic index (GI) foods with pulses, in a mixed meal, has not been accurately defined. Objective: We aimed to determine the extent to which PBGR and relative glycemic response (RGR) are lowered when half of the available carbohydrate (AC) from rice or potato is replaced with cooked lentils. Methods: Using a crossover design, 2 groups of 24 healthy adults randomly consumed 50 g AC from control white rice alone [mean ± SD body mass index (BMI, in kg/m2): 24.3 ± 0.5; mean ± SD age: 27.7 ± 1.2 y], instant potato alone (BMI: 24.0 ± 0.5; age: 27.4 ± 1.2 y), or the same starch source in a 50:50 AC combination with each of 3 types of commercially available lentils (large green, small green, split red). Fasting and postprandial blood samples were analyzed for glucose and insulin, and used to derive incremental area under the curve (iAUC), RGR, and maximum concentration (Cmax). Treatment effects were assessed with the use of repeated-measures ANOVA within the rice and potato treatments. Results: In comparison to rice alone, blood glucose iAUC and Cmax (P < 0.001) were lowered after consumption of rice with large green (P = 0.057), small green (P = 0.002), and split red (P = 0.006) lentils. Blood glucose iAUC and Cmax were also significantly lowered (P < 0.0001) after consumption of potato combined with each lentil, compared to potato alone. Plasma insulin iAUC and Cmax were significantly (P < 0.001) decreased when lentils were combined with potato, but not with rice. The RGRs of rice and potato were lowered by ∼20% and 35%, respectively, when half of their AC was replaced with lentils. Conclusions: Replacing half of the AC from high-GI foods with lentils significantly attenuates PBGR in healthy adults; this can contribute to defining a health claim for pulses and blood glucose lowering. This trial was registered at clinicaltrials.gov as NCT02426606.

Dendritic spine and dendritic field characteristics of layer V pyramidal neurons in the visual cortex of fragile-X knockout mice.

Fragile-X syndrome is a common form of mental retardation resulting from the inability to produce the fragile-X mental retardation protein. The specific function of this protein is unknown; however, it has been proposed to play a role in developmental synaptic plasticity. Examination of human brain autopsy material has shown that fragile-X patients exhibit abnormalities in dendritic spine structure and number, suggesting a failure of normal developmental dendritic spine maturation and pruning in this syndrome. Similar results using a knockout mouse model have previously been described; however, it was noted in retrospect that the mice used in that study may have carried a mutation for retinal degeneration, which may have affected cell morphology in the visual cortex of those animals. In this study, dendritic spines on layer V pyramidal cells of visual cortices, taken from fragile-X knockout and wild-type control mice without the retinal degeneration mutation and stained using the Golgi-Cox method, were investigated for comparison with the human condition. Quantitative analyses of the lengths, morphologies, and numbers of dendritic spines, as well as amount of dendritic arbor and dendritic branching complexity, were conducted. The fragile-X mice exhibited significantly more long dendritic spines and significantly fewer short dendritic spines than control mice. Similarly, fragile-X mice exhibited significantly more dendritic spines with an immature-like morphology and significantly fewer with a more mature type morphology. However, unlike the human condition, fragile-X mice did not exhibit statistically significant dendritic spine density differences from controls. Fragile-X mice also did not demonstrate any significant differences from controls in dendritic tree complexity or dendritic arbor. Long dendritic spines with immature morphologies are characteristic of early development or a lack of sensory experience. These results are similar to those found in the human condition and further support a role for the fragile-X mental retardation protein specifically in normal dendritic spine developmental processes. They also support the validity of these mice as a model of fragile-X syndrome.