Nutritional characterization of the extrusion-processed micronutrient-fortified corn snacks enriched with protein and dietary fiber.

The current study focused on developing protein- and dietary fiber-enriched, micronutrient-fortified corn snacks using extrusion technology. Corn, soybean, and chickpea flour were used to develop micronutrient-fortified (Fe, Zn, I, and vitamin A, and C) extruded snacks, followed by an exploration of their nutritional traits. Soybean and chickpea were supplemented discretely (20-40/100 g) or in a combination of both (10:10, 15:15, and 20:20/100 g). According to the results, the relative proportion of the raw material composition was reflected in corn snacks' proximate composition and mineral and vitamin levels. Corn snacks with 40/100 g soy flour showed the best nutrient profile, with a maximum percent increase in protein (171.9%) and fiber (106%), as compared to the snacks developed using chickpea and/or mixed supplementation with soy and chickpea. Total dietary fiber (18.44 ± 0.34%), soluble dietary fiber (10.65 ± 0.13%), and insoluble dietary fiber (7.76 ± 0.38%) were also found to be highest in the soy-supplemented snacks (40/100 g). It was discovered that 100 g of corn snacks could provide 115-127% of the RDA for iron, 77-82% of the RDA for zinc, 90-100% of the RDA for vitamin A, and 45-50% of the RDA for vitamin C. The results for the effect of extrusion processing on amino acids showed a 2.55-45.1% reduction in essential amino acids, with cysteine and valine showing the greatest decrease and leucine and tryptophan remaining relatively stable during extrusion.

Effect of cooking on the nutritive quality, sensory properties and safety of lamb meat: Current challenges and future prospects.

Lamb meat is cooked using different methods which help to impart good taste, flavour and aroma and they also improve the nutritional quality and ensure food safety. However traditional methods also induce some potential health hazards i.e. formation of polyaromatic hydrocarbons, heterocyclic aromatic amines and acrylamides. These harmful compounds are produced through protein aggregation (protein increased with loss of water), lipid degradation (lipid breakdown due to cooking), oxidation (radicals formation due to heat and oxygen combination), and the Maillard reaction (reaction between sugars and amino acids). This review focuses on: 1) the use of modern cooking technologies to reduce the generation of hazardous compounds by a) applying low temperature cooking with minimum contact with the meat; b) faster cooking, with the added benefits of minimum nutritional losses and less energy consumption 2) the adoption of natural plant sources as extracts to: a) inhibit lipid oxidation; b) improve the stability of meat products to limit the generation of hazardous compounds.

Taurine Promotes Neuritic Growth of Dorsal Root Ganglion Cells Exposed to High Glucose in Vitro.

Diabetic neuropathy (DN) is the most common chronic complication of DM and its major pathological changes show axonal dysfunction, atrophy and loss. However, there are few reports that taurine promotes neurite growth of dorsal root ganglion (DRG) cells. In current study, DRG neurons were exposed to high glucose (HG) with or without taurine. The neurite outgrowth of DRG neurons was observed by fluorescent immunohistochemistry method. Expression of Gap-43, Akt, phosphorylated Akt, mTOR and phosphorylated mTOR was determined by Western blot assay. Our results showed that HG significantly decreased the neurite outgrowth and expression of Gap-43 in DRG neurons. Moreover, phosphorylated levels of Akt and mTOR were downregulated in DRG neurons exposed to HG. On the contrary, taurine supplementation significantly reversed the decreased neurite outgrowth and Gap-43 expression, and the downregulated phosphorylated levels of Akt and mTOR. However, the protective effects of taurine were blocked in the presence of PI3K antagonists LY294002 or Akt antagonists Perifosine. These results indicate that taurine promotes neurite outgrowth of DRG neurons exposed to HG via activating Akt/mTOR signal pathway.