Addition of pooled pumpkin seed to mixed meals reduced postprandial glycemia: a randomized placebo-controlled clinical trial.

We investigated if pumpkin and flaxseeds could improve postprandial glycemic, food intake, and appetitive responses. Herein, we hypothesize based on the literature that pumpkin seed has potential to lower postprandial glycemic effects. Therefore, we conducted a randomized, single-blind, placebo-controlled, crossover design study involving normoglycemic adults (food intake: n = 25; glycemia: n = 15). Three high-carbohydrate mixed meals presenting no seed (control [C]) or 65 g of the tested seeds (pumpkin seed [P] or flaxseed [F]) were consumed in 3 nonconsecutive days. Test meals had similar nutritional composition. Blood glucose was measured by capillary finger blood at 0 (immediately before), 15, 30, 45, 60, 90, and 120 minutes after the ingestion of each meal, and the incremental area under glycemic response curves (iAUC) were calculated. Appetitive responses were assessed, and dietary records were used to evaluate food intake on testing days. Glucose iAUC was significantly lower in P compared with C (reduction of ~35%, P = .025). There was no significant differences in glucose iAUC between F and C (P = .257). Glycemic response at each time point did not differ between C, P, and F (Pgroup × time = .238). Fiber consumption was higher in F (P = .009) than in C, but there were no differences in appetitive responses, energy, or macronutrient consumptions between dietary interventions. Acute consumption of 65 g of pumpkin seed markedly reduced postprandial glycemia. Pumpkin seed has potential as a hypoglycemic food, which now deserves to be confirmed in long-term studies.

Review of the mechanisms of probiotic actions in the prevention of colorectal cancer.

The purpose of this review is to discuss the potential mechanisms of probiotics action in colorectal cancer prevention. In this regard, the composition of the intestinal microbiota is considered as an important risk factor in the development of colorectal cancer, and probiotics are able to positively modulate the composition of this microbiota. Studies have shown that the regular consumption of probiotics could prevent the development of colorectal cancer. In this respect, in vitro and experimental studies suggest some potential mechanisms responsible for this anticarcinogenic action. The mechanisms include modification of the intestinal microbiota composition, changes in metabolic activity of the microbiota, binding and degradation of carcinogenic compounds present in the intestinal lumen, production of compounds with anticarcinogenic activity, immunomodulation, improvement of the intestinal barrier, changes in host physiology, inhibition of cell proliferation, and induction of apoptosis in cancer cells. In contrast, very few reports demonstrate adverse effects of probiotic oral supplementation. In light of the present evidence, more specific studies are needed on probiotic bacteria, especially regarding the identification of the bacterial strains with greater anticarcinogenic potential; the verification of the viability of these strains after passing through the gastrointestinal tract; the investigation of potential adverse effects in immunocompromised individuals; and finally establishing the dosage and frequency of use.