An exploratory study of pre-extrusion flavouring: investigation with vitamins, amino acids, essential oils, natural aromas and seasonings

Expanded corn snacks are obtained through thermoplastic extrusion and then a lipid vehicle (oil or hydrogenated vegetable fat) is sprinkled on the product, giving the desired flavour. However, this second step called post-extrusion flavouring increases the lipid content and the caloric value of the snack, reasons why these products are highly criticized. Thus, the study of pre-extrusion flavourings is an interesting way of finding corn snacks with better nutritive value. Therefore, we aimed to explore pre-extrusion flavouring using different substances, investigating the odour and flavour on the extrudates and the impact of such substances on their expansion ratio, density, and colour. To do this, vitamins, amino acids, essential oils, natural aromas and seasonings were added to corn grits and extruded. The addition of different substances, especially the essential oils, natural aromas and seasonings, produced odour and flavour in the extrudates, as well as having little negative impact on their physical properties of the extrudates, no impact or even a small positive impact. Therefore, this study provides a range of possibilities to be explored, using pre-extrusion flavouring as a way of reducing the use of lipids and improving the nutritive value of expanded snacks.

Polychlorinated Biphenyl 153 in Lipid Medium Modulates Differentiation of Human Adipocytes

Emerging evidence indicates that polychlorinated biphenyls (PCBs) are involved in the development of diabetes mellitus in the obese. The purpose of this study was to determine mechanisms by which PCB 153 (2,2′,4,4′,5,5′-hexachloro-biphenyl) could influence diet-induced obesity and insulin resistance during adipogenesis. Lineage of h-ADMSCs was differentiated either as control (differentiation medium only), or with lipid vehicle modeling high fat nutrition (NuTRIflex) or lipid free vehicle (dimethylsulfoxide) for 28 days with or without PCB 153 daily co-exposure (in three concentrations 0.1, 1, and 10 µM). Gene expression analyses were performed using RT-qPCR at days 4, 10, 21, 24, 28; protein levels Akt and phosphorylated Akt (Phospho-Akt) by Western blot at days 4, and 21. PCB 153 treatment of h-ADMSCs only in lipid vehicle was associated with down regulation of key master genes of adipogenesis: PPARγ, SREBP-1, PPARGC1B, and PLIN2 during the whole process of differentiation; and with increased Akt and decreased Phospho-Akt protein level at day 21. We have shown that PCB 153, in concentration 0.1 µM, has a potential in lipid rich environment to modulate differentiation of adipocytes. Because European and U.S. adults have been exposed to PCB 153, this particular nutrient-toxicant interaction potentially impacts human obesity and insulin sensitivity.

Intravenous Emulsified Halogenated Anesthetics Produce Acute and Delayed Preconditioning against Myocardial Infarction in Rabbits

Background Preconditioning against myocardial infarction by volatile anesthetics is well known. The authors tested the hypothesis that new emulsified formulations of halogenated anesthetics administered intravenously reduce myocardial infarct size when administered either 1 or 24 h before prolonged ischemia and reperfusion. Methods Pentobarbital-anesthetized rabbits (n = 39) were instrumented for measurement of hemodynamics and randomly assigned to receive intravenous saline (control), lipid vehicle, or infusions (3.5 ml . kg . h for 30 min) of emulsified isoflurane (6.9%), enflurane (7.1%), or sevoflurane (7.5%). Infusions were discontinued 30 min before a 30-min coronary occlusion and 3 h of reperfusion. In three additional groups, conscious rabbits (n = 21) received saline, lipid vehicle, or emulsified sevoflurane (7.5%) infusions (3.5 ml . kg . h for 30 min) 24 h before ischemia and reperfusion. Infarct size was determined using triphenyltetrazolium staining. Results Lipid vehicle produced transient increases in heart rate, whereas emulsified volatile anesthetics had no effect on hemodynamics before coronary occlusion. Lipid vehicle did not affect infarct size (38 +/- 2% of the area at risk; mean +/- SEM) as compared with saline control (41 +/- 4%). In contrast, emulsified isoflurane, enflurane, and sevoflurane reduced infarct size (20 +/- 3%, 20 +/- 3%, and 21 +/- 2% of the area at risk, respectively; P < 0.05). Administration of lipid vehicle or emulsified sevoflurane did not produce sedation or respiratory depression in conscious rabbits. Emulsified sevoflurane (18 +/- 2%) but not lipid vehicle (44 +/- 2%) reduced infarct size as compared with control in delayed preconditioning experiments. Conclusions Intravenous emulsified halogenated anesthetics produce acute and delayed preconditioning against myocardial infarction.

Modulation of gastric distension-induced sensations by small intestinal receptors

Duodenal lipid exacerbates gastrointestinal sensations during gastric distension. Using luminal application of the local anesthetic benzocaine, we investigated the role of intestinal receptors in the induction of these sensations. Nine healthy subjects were studied on five occasions, during which isotonic saline or 20% lipid (2 kcal/min), combined with (duodenal or jejunal) 0.75% benzocaine or vehicle at 2.5 ml/min, was infused intraduodenally before and during gastric distension. Intragastric pressures and volumes, gastrointestinal sensations, and plasma CCK levels were determined. Duodenal lipid combined with vehicle increased gastric volume (in ml: saline, −10 ± 18; lipid/vehicle, 237 ± 30) and plasma CCK [mean levels (pmol/l): saline, 2.0 ± 0.2; lipid/vehicle, 8.0 ± 1.6] and, during distensions, induced nausea (scores: saline, 3 ± 2: lipid/vehicle, 58 ± 19) and decreased pressures at which fullness and discomfort occurred. Duodenal but not jejunal benzocaine attenuated the effect of lipid on gastric volume, plasma CCK, and nausea during distension (135 ± 38 and 216 ± 40 ml, 4.6 ± 0.6 pmol/l and not assessed, and 37 ± 12 and 64 ± 21 for lipid + duodenal benzocaine and lipid + jejunal benzocaine, respectively) and on pressures for sensations. In conclusion, intestinal receptors modulate gastrointestinal sensations associated with duodenal lipid and gastric distension. There is also the potential for local neural mechanisms to regulate CCK release and thereby reduce afferent activation indirectly.