Nahrungs- und Futtermittel in der Fischaufzucht

Die Erfindung betrifft ein Nahrungs- oder Futtermittel mit einer Beimengung von Phytohaemagglutinin und/oder von wenigstens einer Isoform einer Phytohaemagglutinin-Untereinheit, insbesondere die Verwendung von Phytohaemagglutinin als Fischfutterzusatz in kommerziellen Brutfuttern zur Unterstützung der Reifung des Verdauungstraktes und damit zur Steigerung der larvalen Verdauungseffizienz. Des Weiteren betrifft sie die Verwendung von Phytohaemagglutinin zur Einsparung von Lebendfutter in der Fischzucht

Plasma Orexin-A Levels Do Not Undergo Circadian Rhythm in Young Healthy Male Subjects

Orexin-A (OXA) has been originally isolated from a precursor peptide prepro-orexin from the lateral hypothalamus. The orexin system has been attributed to important functions in sleep, arousal and regulation of energy homeostasis. In addition to its high levels in cerebrospinal fluid, OXA is present in blood. However, reported peptide concentrations in plasma vary significantly depending on the method used. Therefore, a specific and sensitive OXA radioimmunoassay (RIA) with solid phase extraction method was developed to determine whether plasma OXA concentrations is affected by acute feeding and/or wake and sleep in young healthy males. Blood samples were collected for 24 h from nine healthy males (aged 20–24 years; BMI 20.7–26.5) every 2 h starting at 11 a.m. Food was served at 12 p.m, 5:30 p.m, 8 p.m and 8 a.m and the sleep time was between 10 p.m and 7 a.m. Plasma samples were analyzed in addition for cortisol and melatonin levels. Blood pressure was monitored through the experimental period. OXA antibody was raised in rabbits. OXA antiserum had only minor cross-reactivity with prepro-orexin precursor (<0.001%), amino-terminal peptide (<0.001%), carboxy-terminal peptide (0.001%), and orexin-B (0.3%) with high sensitivity (0.15 pg/tube). Plasma OXA levels varied between 0.5 and 16 pg/ml in seven subjects and were undetectable (below 0.5 pg/ml) in two subjects. The OXA concentrations did not correlate to feeding nor wake/sleep, whereas cortisol, melatonin and mean arterial blood pressure presented a clear circadian rhythm in each subject. In conclusion, OXA is present in blood in low amounts and its levels do not follow autonomic nor neuroendocrine circadian rhythms. Thereby, studies examining regulatory mechanisms and influences of OXA from blood samples should interpret results very cautiously

Metabolic flexibility is unimpaired during exercise in the cold following acute glucose ingestion in young healthy adults

AbstractPurpose: Metabolic flexibility is compromised in individuals suffering from metabolic diseases, lipo- and glucotoxicity, and mitochondrial dysfunctions. Exercise studies performed in cold environments have demonstrated an increase in lipid utilization, which could lead to a compromised substrate competition, glycotoxic-lipotoxic state, or metabolic inflexibility. Whether metabolic flexibility is altered during incremental maximal exercise to volitional fatigue in a cold environment remains unclear.Methods: Ten young healthy participants performed four maximal incremental treadmill tests to volitional fatigue, in a fasted state, in a cold (0 °C) or a thermoneutral (22.0 °C) environment, with and without a pre-exercise ingestion of a 75-g glucose solution. Metabolic flexibility was assessed via indirect calorimetry using the change in respiratory exchange ratio (ΔRER), maximal fat oxidation (ΔMFO), and where MFO occurred along the exercise intensity spectrum (ΔFatmax), while circulating lactate and glucose levels were measured pre and post exercise.Results: Multiple linear mixed-effects regressions revealed an increase in glucose oxidation from glucose ingestion and an increase in lipid oxidation from the cold during exercise (p vs. 0.05 ± 0.03; p = 0.734), ΔMFO (0.21 ± 0.18 vs. 0.16 ± 0.13 g min−1; p = 0.133) and ΔFatmax (13.3 ± 19.0 vs. 0.6 ± 21.3 %V̇O2peak; p = 0.266) in cold and thermoneutral, respectively.Conclusions: Following glucose loading, metabolic flexibility was unaffected during exercise to volitional fatigue in a cold environment, inducing an increase in lipid oxidation. These results suggest that competing pathways responsible for the regulation of fuel selection during exercise and cold exposure may potentially be mechanistically independent. Whether long-term metabolic influences of high-fat diets and acute lipid overload in cold and warm environments would impact metabolic flexibility remain unclear.Abstract Purpose: Metabolic flexibility is compromised in individuals suffering from metabolic diseases, lipo- and glucotoxicity, and mitochondrial dysfunctions. Exercise studies performed in cold environments have demonstrated an increase in lipid utilization, which could lead to a compromised substrate competition, glycotoxic-lipotoxic state, or metabolic inflexibility. Whether metabolic flexibility is altered during incremental maximal exercise to volitional fatigue in a cold environment remains unclear. Methods: Ten young healthy participants performed four maximal incremental treadmill tests to volitional fatigue, in a fasted state, in a cold (0 °C) or a thermoneutral (22.0 °C) environment, with and without a pre-exercise ingestion of a 75-g glucose solution. Metabolic flexibility was assessed via indirect calorimetry using the change in respiratory exchange ratio (ΔRER), maximal fat oxidation (ΔMFO), and where MFO occurred along the exercise intensity spectrum (ΔFatmax), while circulating lactate and glucose levels were measured pre and post exercise. Results: Multiple linear mixed-effects regressions revealed an increase in glucose oxidation from glucose ingestion and an increase in lipid oxidation from the cold during exercise (p < 0.001). No differences were observed in metabolic flexibility as assessed via ΔRER (0.05 ± 0.03 vs. 0.05 ± 0.03; p = 0.734), ΔMFO (0.21 ± 0.18 vs. 0.16 ± 0.13 g min−1; p = 0.133) and ΔFatmax (13.3 ± 19.0 vs. 0.6 ± 21.3 %V̇O2peak; p = 0.266) in cold and thermoneutral, respectively. Conclusions: Following glucose loading, metabolic flexibility was unaffected during exercise to volitional fatigue in a cold environment, inducing an increase in lipid oxidation. These results suggest that competing pathways responsible for the regulation of fuel selection during exercise and cold exposure may potentially be mechanistically independent. Whether long-term metabolic influences of high-fat diets and acute lipid overload in cold and warm environments would impact metabolic flexibility remain unclear

Exogenous Ketone Salt Supplementation and Whole-Body Cooling Do Not Improve Short-Term Physical Performance

Publisher Copyright: © Copyright © 2021 Clark, Munten, Herzig and Gagnon.Exogenous ketone supplementation and whole-body cooling (WBC) have shown to independently influence exercise metabolism. Whether readily available ketone salts, with and without WBC, would provide similar metabolic benefits during steady-state aerobic and time-trial performances was investigated. Nine active males (VO2peak: 56.3 ± 2.2 mL·kg−1·min−1) completed three single-blind exercise sessions preceded by: (1) ingestion of placebo (CON), (2) ketone supplementation (0.3 g·kg−1 β-OHB) (KET), and (3) ketone supplementation with WBC (KETCO). Participants cycled in steady-state (SS, 60% Wmax) condition for 30-min, immediately followed by a 15-min time trial (TT). Skin and core temperature, cardio-metabolic, and respiratory measures were collected continuously, whereas venous blood samples were collected before and after supplementation, after SS and TT. Venous β-OHB was elevated, while blood glucose was lower, with supplementation vs. CON (p < 0.05). TT power output was not different between conditions (p = 0.112, CON: 190 ± 43.5 W, KET: 185 ± 40.4 W, KETCO: 211 ± 50.7 W). RER was higher during KETCO (0.97 ± 0.09) compared to both CON (0.88 ± 0.04, p = 0.012) and KET (0.88 ± 0.05, p = 0.014). Ketone salt supplementation and WBC prior to short-term exercise sufficiently increase blood β-OHB concentrations, but do not benefit metabolic shifts in fuel utilization or improve time trial performance.Peer reviewe

Effect of Physical Activity on Plasma PCSK9 in Subjects With High Risk for Type 2 Diabetes

BackgroundProprotein convertase subtilisin/kexin type 9 (PCSK9) is a liver serine protease regulating LDL cholesterol metabolism. PCSK9 binds to LDL receptors and guides them to lysosomes for degradation, thus increasing the amount of circulating LDL cholesterol. The aim of the study was to investigate associations between physical activity and plasma PCSK9 in subjects with high risk for type 2 diabetes (T2D).MethodsSixty-eight subjects from both genders with a high risk for T2D were included to a randomized controlled trial with a 3-month physical activity intervention. Physical activity intensities and frequencies were monitored throughout the intervention using a hip worn portable accelerometer. The plasma was collected before and after intervention for analysis of PCSK9 and cardiovascular biomarkers.ResultsPlasma PCSK9 did not relate to physical activity although number of steps were 46% higher in the intervention group than in the control group (p &lt; 0.029). Total cholesterol was positively correlated with plasma PCSK9 (R = 0.320, p = 0.008), while maximal oxygen uptake was negatively associated (R = -0.252, p = 0.044). After the physical activity intervention PCSK9 levels were even stronger inversely associated with maximal oxygen uptake (R = -0.410, p = 0.0008) and positively correlated with HDL cholesterol (R = 0.264, p = 0.030). Interestingly, plasma PCSK9 levels were higher in the beginning than at the end of the study.ConclusionThe low physical activity that our subjects with high risk for T2D could perform did not influence plasma PCSK9 levels. Intervention with higher physical activities might be more effective in influencing PCSK9 levels