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(1) Background: We examined the effect of the acute administration of olive oil (EVOO), linseed oil (GLO), soybean oil (SO), and palm oil (PO) on gastric motility and appetite in rats. (2) Methods: We assessed food intake, gastric retention (GR), and gene expression in all groups. (3) Results: Both EVOO and GLO were found to enhance the rate of stomach retention, leading to a decrease in hunger. On the other hand, the reduction in food intake caused by SO was accompanied by delayed effects on stomach retention. PO caused an alteration in the mRNA expression of NPY, POMC, and CART. Although PO increased stomach retention after 180 min, it did not affect food intake. It was subsequently verified that the absence of an autonomic reaction did not nullify the influence of EVOO in reducing food consumption. Moreover, in the absence of parasympathetic responses, animals that received PO exhibited a significant decrease in food consumption, probably mediated by lower NPY expression. (4) Conclusions: This study discovered that different oils induce various effects on parameters related to food consumption. Specifically, EVOO reduces food consumption primarily through its impact on the gastrointestinal tract, making it a recommended adjunct for weight loss. Conversely, the intake of PO limits food consumption in the absence of an autonomic reaction, but it is not advised due to its contribution to the development of cardiometabolic disorders.

Two experiments were conducted to determine the effects of phytate, phytase, fiber, and soybean oil on apparent total tract digestibility (ATTD) and standardized total tract digestibility (STTD) of Ca and on ATTD of P in fish meal fed to growing pigs. In Exp. 1, 40 growing pigs (initial average BW: 19.16 ± 2.04 kg) were randomly allotted to 1 of 5 diets with 8 pigs per treatment and placed in metabolism crates. Four diets were used in a 2 ´ 2 factorial design with 2 levels of phytate (0 or 0.7%) and 2 levels of microbial phytase (0 or 500 phytase units/kg). The diet containing no phytate was based on sucrose, cornstarch, fish meal, casein, and soybean oil, and the diet containing 0.7% phytate was based on corn, corn germ, fish meal, casein, and soybean oil. A Ca-free diet was used to determine basal endogenous losses of Ca. Feces were collected from d 6 to 13 after a 5-d adaptation period. Results indicated that the ATTD and STTD of Ca in fish meal and the ATTD of P increased ( < 0.001) if phytase was used and were greater ( < 0.05) in the diets based on corn and corn germ. Experiment 2 was conducted to determine the effects of fiber and soybean oil on the ATTD and STTD of Ca and the ATTD of P in fish meal. Fifty growing pigs (initial average BW: 19.36 ± 0.99 kg) were randomly allotted to 1 of 5 diets with 10 pigs per treatment. Two diets contained sucrose, cornstarch, fish meal, casein, and either 0 or 8% of a synthetic source of fiber. Two additional diets contained fish meal, casein, corn, and either 1 or 7% soybean oil. A Ca-free diet was also used. Pigs were housed individually in metabolism crates and fecal samples were collected. Results indicated that fiber increased ( < 0.001) the ATTD and STTD of Ca and the ATTD of P, but the ATTD and STTD of Ca or the ATTD of P were not affected by soybean oil. In agreement with the results of Exp. 1, the ATTD and STTD of Ca and the ATTD of P in the corn-based diet were greater ( < 0.05) than those in the cornstarch-based diet. In conclusion, phytase and fiber increased the ATTD and STTD of Ca and the ATTD of P in fish meal, but inclusion of soybean oil did not affect digestibility of Ca or P. The observation that values for the ATTD and STTD of Ca and ATTD of P are greater in corn-based diets than in cornstarch-based diets indicates that values for the digestibility of Ca and P obtained in cornstarch-based diets may not always be representative for the digestibility in practical corn-based diets.

Abstract Context Given the promising effects of prolonged treatment with beta2-agonist on insulin sensitivity in animals and nondiabetic individuals, the beta2-adrenergic receptor has been proposed as a target to counter peripheral insulin resistance. On the other hand, rodent studies also reveal that beta2-agonists acutely impair insulin action, posing a potential caveat for their use in treating insulin resistance. Objective To assess the impact of beta2-agonist on muscle insulin action and glucose metabolism and identify the underlying mechanism(s) in 10 insulin-resistant subjects. Methods and participants In a crossover design, we assessed the effect of beta2-agonist on insulin-stimulated muscle glucose uptake during a 3-hour hyperinsulinemic isoglycemic clamp with and without intralipid infusion in 10 insulin-resistant, overweight subjects. Two hours into the clamp, we infused beta2-agonist. We collected muscle biopsies before, 2 hours into, and by the end of the clamp and analyzed them using metabolomic and lipidomic techniques. Results We establish that beta2-agonist, independently from and additively to intralipid, impairs insulin-stimulated muscle glucose uptake via different mechanisms. In combination, beta2-agonist and intralipid nearly eliminates insulin-dependent muscle glucose uptake. Although both beta2-agonist and intralipid elevated muscle glucose-6-phosphate, only intralipid caused accumulation of downstream muscle glycolytic intermediates, whereas beta2-agonist attenuated incorporation of glucose into glycogen. Conclusion Our findings suggest that beta2-agonist inhibits glycogenesis, whereas intralipid inhibits glycolysis in skeletal muscle of insulin-resistant individuals. These results should be addressed in future treatment of insulin resistance with beta2-agonist.

The immunomodulatory effects of omega-3 and omega-6 fatty acids are a crucial subject of investigation for sustainable fish aquaculture, as fish oil is increasingly replaced by terrestrial vegetable oils in aquafeeds. Unlike previous research focusing on fish oil replacement with vegetable alternatives, our study explored how the omega-6 to omega-3 polyunsaturated fatty acid (PUFA) ratio in low-fish oil aquafeeds influences Atlantic salmon's antiviral and antibacterial immune responses. Atlantic salmon were fed aquafeeds rich in soy oil (high in omega-6) or linseed oil (high in omega-3) for 12 weeks and then challenged with bacterial (formalin-killed Aeromonas salmonicida ) or viral-like (polyriboinosinic polyribocytidylic acid) antigens. The head kidneys of salmon fed high dietary omega-3 levels exhibited a more anti-inflammatory fatty acid profile and a restrained induction of pro-inflammatory and neutrophil-related genes during the immune challenges. The high-omega-3 diet also promoted a higher expression of genes associated with the interferon-mediated signaling pathway, potentially enhancing antiviral immunity. This research highlights the capacity of vegetable oils with different omega-6 to omega-3 PUFA ratios to modulate specific components of fish immune responses, offering insights for future research on the intricate lipid nutrition-immunity interplay and the development of novel sustainable low-fish oil clinical aquaculture feeds.

ObjectiveFood intake normally stimulates release of satiety and insulin-stimulating intestinal hormones, such as glucagon-like peptide (GLP)-1. This response is blunted in obese insulin resistant subjects, but is rapidly restored following Roux-en-Y gastric bypass (RYGB) surgery. We hypothesised this to be a result of the metabolic changes taking place in the small intestinal mucosa following the anatomical rearrangement after RYGB surgery, and aimed at identifying such mechanisms.DesignJejunal mucosa biopsies from patients undergoing RYGB surgery were retrieved before and after very-low calorie diet, at time of surgery and 6 months postoperatively. Samples were analysed by global protein expression analysis and Western blotting. Biological functionality of these findings was explored in mice and enteroendocrine cells (EECs) primary mouse jejunal cell cultures.ResultsThe most prominent change found after RYGB was decreased jejunal expression of the rate-limiting ketogenic enzyme mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase (mHMGCS), corroborated by decreased ketone body levels. In mice, prolonged high-fat feeding induced the expression of mHMGCS and functional ketogenesis in jejunum. The effect of ketone bodies on gut peptide secretion in EECs showed a ∼40% inhibition of GLP-1 release compared with baseline.ConclusionIntestinal ketogenesis is induced by high-fat diet and inhibited by RYGB surgery. In cell culture, ketone bodies inhibited GLP-1 release from EECs. Thus, we suggest that this may be a mechanism by which RYGB can remove the inhibitory effect of ketone bodies on EECs, thereby restituting the responsiveness of EECs resulting in increased meal-stimulated levels of GLP-1 after surgery.

Two experiments investigated the effects of supplementing Ca salts of soybean oil (CSSO) during early gestation on reproductive function and pregnancy rates to AI in Bos taurus beef cows. In Exp. 1, 771 suckled, lactating, multiparous Angus cows were divided into 22 groups of approximately 35 cows per group and timed inseminated on day 0. After AI, groups were assigned randomly to receive (as-fed basis) 100 g of ground corn + 100 g of soybean meal per cow/d, in addition to 1) 100 g/cow daily of CSSO (n = 11) or 2) 87 g of prilled saturated fat + 13 g of limestone per cow/d (CON; n = 11). Groups were maintained in individual tall fescue-dominated pastures and offered treatments from day 0 to 21. Pregnancy status was determined between days 45 and 55 via transrectal ultrasonography. Cows receiving CSSO had greater (P = 0.01) pregnancy rates to timed AI compared with CON (60.2 vs. 51.7%; SEM = 4.2). In Exp. 2, 90 suckled, lactating, multiparous Angus × Hereford cows housed in 18 drylot pens (5 cows per pen) were assigned to the same timed AI program and treatments from Exp. 1 (9 pens per treatment) and received 20 kg/d (DM basis) of grass-alfalfa hay. Transrectal ultrasonography was performed to verify ovulation and corpus luteum (CL) volume before AI (day 0), on days 7 and 15. After ultrasonography on day 15, cows diagnosed without a CL on day 0, but with a CL greater than 0.38 cm3 in volume on days 7 and 15 (2 or 3 cows per pen; CSSO, n = 20; CON, n = 24), were assigned to conceptus collection via transcervical flushing and endometrial biopsy in the uterine horn ipsilateral to the CL. Blood samples were collected for FA analysis on days 0, 7, and 15. Blood was collected from cows not assigned to conceptus collection for whole-blood RNA extraction on day 20 and for pregnancy diagnosis on day 30 by measuring concentrations of pregnancy-associated glycoproteins. Cows receiving CSSO had greater (P ≤ 0.04) mean plasma concentrations of linoleic acid and ω-6 FA compared with CON on days 7 and 15. Moreover, CSSO supplementation increased (P = 0.05) mRNA expression of interferon-tau by the conceptus and blood mRNA expression of interferon-stimulated gene 15 and 20,50-oligoadenylate synthetase on day 20 in gestating cows. Hence, post-AI CSSO supplementation to B. taurus beef cows improved pregnancy rates to timed AI, which can be associated with increased mRNA expression of interferon-tau by the conceptus when CSSO is supplemented during early gestation.

A major obstacle to nanodrugs-mediated cancer therapy is their rapid uptake by the reticuloendothelial system that decreases the systemic exposure of the nanodrugs to tumors and also increases toxicities. Intralipid has been shown to reduce nano-oxaliplatin-mediated toxicity while improving bioavailability. Here, we have found that Intralipid reduces the cytotoxicity of paclitaxel for human monocytic cells, but not for breast, lung, or pancreatic cancer cells. Intralipid also promotes the polarization of macrophages to the anti-cancer M1-like phenotype. Using a xenograft breast cancer mouse model, we have found that Intralipid pre-treatment significantly increases the amount of paclitaxel reaching the tumor and promotes tumor apoptosis. The combination of Intralipid with half the standard clinical dose of Abraxane reduces the tumor growth rate as effectively as the standard clinical dose. Our findings suggest that pre-treatment of Intralipid has the potential to be a powerful agent to enhance the tumor cytotoxic effects of Abraxane and to reduce its off-target toxicities.

Endothelial dysfunction (ED) is closely associated with most cardiovascular diseases. Experimental models are needed to analyze the potential impact of ED on cardioprotection in constant pressure Langendorff systems (CPLS). One cardioprotective strategy against ischemia/reperfusion injury (I/RI) is conditioning with the lipid emulsion Intralipid (IL). Whether ED modulates the cardioprotective effect of IL remains unknown. The aim of the study was to transfer a protocol using a constant flow Langendorff system for the induction of ED into a CPLS, without the loss of smooth muscle cell functionality, and to analyze the cardioprotective effect of IL against I/RI under ED. In isolated hearts of male Wistar rats, ED was induced by 10 min perfusion of a Krebs–Henseleit buffer containing 60 mM KCl (K+), and the vasodilatory response to the vasodilators histamine (endothelial-dependent) and sodium–nitroprusside (SNP, endothelial-independent) was measured. A CPLS was employed to determine cardioprotection of pre- or postconditioning with 1% IL against I/RI. The constant flow perfusion of K+ reduced endothelial response to histamine but not to SNP, indicating reduced vasodilatory functionality of endothelial cells but not smooth muscle cells. Preconditioning with IL reduced infarct size and improved cardiac function while postconditioning with IL had no effect. The induction of ED neither influenced infarct size nor affected the cardioprotective effect by preconditioning with IL. This protocol allows for studies of cardioprotective strategies under ED in CLPS. The protection by preconditioning with IL seems to be mediated independently of a functional endothelium.

Weaning stress results in gastrointestinal dysfunction and depressed performance in pigs. This study aimed to investigate the effect of soy oil, glucose, and glutamine on the growth and health of weaned piglets. Compared with those in the glutamine group, piglets in the glucose and soy oil groups had greater average daily gain, average daily feed intake, and gain: feed ratio from day 0 to 14, and gain: feed ratio for the overall period. There were no differences with regard to serum amino acids among the three groups on day 14, except glycine and threonine. The serum concentration of histidine, serine, threonine, proline, and cysteine was the highest in the glutamine group, while the content of glycine and lysine in the soy oil group on day 28 was the highest among all groups. Piglets fed with glutamine had greater serum glucose and creatinine on day 14, high-density lipoprotein on day 28, and serum IgG and IgM on day 28. Piglets in the glutamine group demonstrated lower serum total superoxide dismutase on day 14 and 28; however, they demonstrated higher total superoxide dismutase and total antioxidant capacity in the duodenum and ileum on day 14. Weaned pigs supplemented with glucose or soy oil demonstrate better growth performance possibly due to their enhanced feed intake, whereas those supplemented with glutamine may have improved immunity and intestinal oxidative capacity.

This study aimed to examine the effect of lipid emulsion on the vasodilation induced by a toxic dose of amlodipine in isolated rat aorta and elucidate its mechanism, with a particular focus on nitric oxide. The effects of endothelial denudation, NW-nitro-L-arginvine methyl ester (L-NAME), methylene blue, lipid emulsion, and linolenic acid on the amlodipine-induced vasodilation and amlodipine-induced cyclic guanosine monophosphate (cGMP) production were examined. Furthermore, the effects of lipid emulsion, amlodipine, and PP2, either alone or combined, on endothelial nitric oxide synthase (eNOS), caveolin-1, and Src-kinase phosphorylation were examined. Amlodipine-induced vasodilation was higher in endothelium-intact aorta than in endothelium-denuded aorta. L-NAME, methylene blue, lipid emulsion, and linolenic acid inhibited amlodipine-induced vasodilation and amlodipine-induced cGMP production in the endothelium-intact aorta. Lipid emulsion reversed the increased stimulatory eNOS (Ser1177) phosphorylation and decreased inhibitory eNOS (Thr495) phosphorylation induced via amlodipine. PP2 inhibited stimulatory eNOS, caveolin-1, and Src-kinase phosphorylation induced via amlodipine. Lipid emulsion inhibited amlodipine-induced endothelial intracellular calcium increase. These results suggest that lipid emulsion attenuated the vasodilation induced via amlodipine through inhibiting nitric oxide release in isolated rat aorta, which seems to be mediated via reversal of stimulatory eNOS (Ser1177) phosphorylation and inhibitory eNOS (Thr495) dephosphorylation, which are also induced via amlodipine.