Recovery from exercise refers to the period between the end of a bout of exercise and the subsequent return to a resting or recovered state. It is a dynamic period in which many physiological changes occur. A large amount of research has evaluated the effect of training on intramuscular lipid metabolism. However, data are limited regarding intramuscular lipid metabolism during the recovery period. In this study, lipid metabolism-related proteins were examined after a single bout of exercise in a time-dependent way to explore the mechanism of how exercise induces intramuscular lipid metabolism adaptation. Firstly, all rats in the exercise group underwent a five-week training protocol (HIIT, five times/week), and then performed a more intense HIIT session after 72 h of the last-time five-week training. After that, rats were sampled in a time-dependent way, including 0 h, 6 h, 12 h, 24 h, 48 h, 72 h, and 96 h following the acute training session. Our results discovered that five weeks of HIIT increased the content of intramuscular triglyceride (IMTG) and enhanced the lipolytic and lipogenesis-related proteins in skeletal muscle. Furthermore, IMTG content decreased immediately post HIIT and gradually increased to baseline levels 48 h postexercise, continuing to over-recover up to 96 h postexercise. Following acute exercise, lipolytic-related proteins showed an initial increase (6-12 h) before decreasing during recovery. Conversely, lipogenesis-related proteins decreased following exercise (6-12 h), then increased in the recovery period. Based on the changes, we speculate that skeletal muscle is predominated by lipid oxidative at the first 12 h postexercise. After this period, lipid synthesis-related proteins increased, which may be the result of body recovery. Together, these results may provide insight into how the lipid metabolism-related signaling changes after chronic and acute HIIT and how protein levels lipid metabolism correlates to IMTG recovery., Min Chen, Lei Zhou, Siyu Chen, Ruonan Shangguan, Yaqian Qu, Jingquan Sun., and Obsahuje bibliografii
Ruminants are often fed a high-concentrate (HC) diet to meet lactating demands, yet long-term concentrate feeding induces subacute ruminal acidosis (SARA) and leads to a decrease in milk fat. Buffering agent could enhance the acid base buffer capacity and has been used to prevent ruminant rumen SARA and improve the content of milk fat. Therefore, we tested whether a buffering agent increases lipid anabolism in the livers of goats and influences of milk fat synthesis. Twelve Saanen-lactating goats were randomly assigned to two groups: one group received a HC diet (Concentrate: Forage=60:40, Control) and the other group received the same diet with a buffering agent added (10 g sodium butyrate, C4H7NaO2; 10 g sodium bicarbonate, NaHCO3; BG) over a 20-week experimental period. Overall, milk fat increase (4.25±0.08 vs. 3.24±0.10; P<0.05), and lipopolysaccharide levels in the jugular (1.82±0.14 vs. 3.76±0.33) and rumen fluid (23,340±134 vs. 42,550±136) decreased in the buffering agent group (P<0.05). Liver consumption and release of nonesterified fatty acid (NEFA) into the bloodstream increased (P<0.05). Phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT) and ribosomal protein S6 kinase (p70S6K) up-regulated significantly in the livers of the buffering agent group (P<0.05). It also up-regulated expression of the transcription factor sterol regulatory element binding protein-1c (SREBP-1c) and its downstream targets involved in fatty acid synthetic, including fatty acid synthetase (FAS), stearoyl-CoA desaturase (SCD-1) and acetyl-CoA carboxylase 1 (ACC1) (P<0.05). The BG diet increased insulin levels in blood (19.43±0.18 vs. 13.81±0.10, P<0.05), and insulin receptor was likewise elevated in the liver (P<0.05). Cumulatively, the BG diet increased plasma concentrations of NEFA by INS-PI3K/AKTSREBP- 1c signaling pathway promoting their synthesis in the liver., L. Li, M. L. He, K. Wang, Y. S. Zhang., and Obsahuje bibliografii
Insulin resistance associated with dyslipidemia enhances cardiovascular risk. Several atherogenic indexes have been suggested to give more precise information about the risk. The aim of our study was to estimate, which atherogenic index correlates better with parameters of insulin resistance. Furthermore, we compared the parameters of lipid metabolism and insulin resistance between smokers and non-smokers. In our cross-sectional study we enrolled 729 patients with dyslipidemia which were divided into two groups - non-smokers (586) and smokers (143). We measured lipid profile, parameters of insulin resistance (fasting glycemia, insulin, HOMA-IR, C-peptide, proinsulin) and calculated atherogenic indexes - atherogenic index of plasma (log (TAG/HDL-C), AIP), ApoB/ApoA1 index and nonHDL-C. AIP was found out to show stronger correlations with parameters of insulin resistance (p<0.001, correlation coefficients ranging between 0.457 and 0.243) than other indexes (ApoB/ApoA1 or nonHDL cholesterol). AIP correlated with parameters of insulin resistance both in smokers and nonsmokers, but after adjustment (for age, body mass index, waist circumference) persisting only in non-smokers. Smokers had a wider waist circumference and a proatherogenic lipid profile. Smoking increases the risk of developing metabolic syndrome. AIP can be used in daily praxis for predicting insulin resistance in patients with dyslipidemia, predominantly in non-smokers., L'. Cibičková, D. Karásek, K. Langová, H. Vaverková, J. Orság, J. Lukeš, D. Novotný., and Obsahuje bibliografii
Dehydroepiandrosterone (DHEA) possesses fat-reducing effect, while little information is available on whether DHEA regulates cell proliferation and mitochondrial function, which would, in turn, affect lipid droplet accumulation in the broiler. In the present study, the lipid droplet accumulation, cell proliferation, cell cycle and mitochondrial membrane potential were analysis in primary chicken hepatocytes after DHEA treated. The results showed that total area and counts of lipid droplets were significantly decreased in hepatocytes treated with DHEA. The cell viability was significantly increased, while cell proliferation was significantly inhibited in a dose-dependent manner in primary chicken hepatocytes after DHEA treated. DHEA treatment significantly increased the cell population in S phase and decreased the population in G2/M in primary chicken hepatocytes. Meanwhile, the cyclin A and cyclin-dependent kinases 2 (CDK2) mRNA abundance were significantly decreased in hepatocytes after DHEA treated. No significant differences were observed in the number of mitochondria, while the mitochondrial membrane permeability and succinate dehydrogenase (SDH) activity were significantly increased in hepatocytes after DHEA treated. In conclusion, our results demonstrated that DHEA reduced lipid droplet accumulation by inhibiting hepatocytes proliferation and enhancing mitochondrial function in primary chicken hepatocytes., Long-Long Li, Dian Wang, Chong-Yang Ge, Lei Yu, Jin-Long Zhao, Hai-Tian Ma., and Obsahuje bibliografii
A high VO2max in middle-age is related to high metabolic flexibility and lowered risk of metabolic diseases. However, the influence of a high VO2max induced by years of regular training in middle-age on protein expression related to muscle metabolism is not well studied. This study measures key proteins involved in mitochondrial oxidation, glucose and lipid metabolism in skeletal muscle of trained and untrained middle-aged men. 16 middle-aged men, matched for lean body mass, were recruited into an endurance trained (TR, n=8) or an untrained (CON, n=8) group based on their VO2max. A muscle biopsy was obtained from m. vastus lateralis and protein levels were analyzed by Western blotting. The TR had higher protein levels of mitochondrial complex III-V, endothelial lipase (EL) and perilipin 5 compared to the CON. Glycogen synthase (P=0.05), perilipin 3 (P=0.09) and ATGL (P=0.09) tended to be higher in TR than CON, but there was no difference in AKT I/II, HKII, GLUT4 and LPL protein expression. Lastly, there was a positive correlation between plasma HDL and EL (R2=0.53, P<0.01). In conclusion, a high VO2max in middle-aged men was as expected is reflected in higher muscle oxidative capacity, but also in higher endothelial lipase and perilipin 5 expression and a borderline higher glycogen synthase protein expression, which may contribute to a higher metabolic flexibility., A. Vigelsø, C. Prats, T. Ploug, F. Dela, J. W. Helge., and Obsahuje bibliografii
With the increasing prevalence of obesity and especially abdominal obesity, a simple clinical tool is needed that identifies the cardiometabolic risk for cardiovascular disease and type 2 diabetes. The aim of our study was to evaluate a broad spectrum of metabolic variables and IMT in subjects with and without hypertriglyceridemic waist (HTGW) and compare it with the harmonized definition of metabolic syndrome (MS) with both a higher (MS- I) and lower waist circumference (MS -II) for Europids. We enrolled 607 asymptomatic dyslipidemic subjects (295 men and 312 women) into our cross -sectional study. The subjects with HTGW had an atherogenic lipid profile (significantly higher triglycerides, AIP, non -HDL -C, lower HDL -C and ApoA -1, and the women also higher TC and ApoB), increased markers of insulin resistance (insulin, HOMA, C -peptide, proinsulin), inflammation (hsCRP), thrombosis (fibrinogen, PAI -1), SBP and DBP, and lower adiponectin (p<0.05 -0.001 for all). These risk factors were entirely similar in HTGW, MS- I and MS -II. Age -adjusted IMT was significantly higher only in the women with HTGW but this significance disappeared after further adjustment for TC, SBP, and smoking. Our results support the routine use of HTGW as a simple and inexpensive screening tool to detect subjects at increased cardiometabolic risk in clinical practice., H. Vaverková, D. Karásek, D. Novotný, M. Halenka, J. Orság, L. Slavík., and Obsahuje bibliografii
In the present study the hypothesis that there is a feedback between juvenile hormone and adipokinetic hormones (AKHs) was investigated by topical application of the juvenoid methoprene on 9-day-old adult males of the firebug Pyrrhocoris apterus. This juvenoid (2 µg) induced a significant reduction of haemolymph lipids 24 h after treatment; however, it did not significantly reduce the ability of Pyrap-AKH (10 pmol/bug) to mobilize fat body lipids 6-72 h after the methoprene application. The same methoprene treatment elicited a significant increase of AKH content in the CNS (central nervous system: brain + corpora cardiaca + corpora allata) of experimental males 24 and 48 h after the juvenoid application. A significant decrease in the AKH level in the haemolymph was recorded at the same times and under the same experimental conditions. Similar results were observed when production of the AKHs from the CNS of topically treated males was measured under in vitro conditions. It is suggested that methoprene may reduce AKH release from the CNS resulting in an increase in the AKH content of the CNS due to accumulation rather than stimulation of AKH synthesis. Possible consequences of this phenomenon on the physiology of P. apterus are discussed.
Circadian clock plays an essential role in orchestrating daily physiology, and its disruption can evoke metabolic diseases such as obesity. L-Carnitine can reduce blood lipid levels, and ameliorate fatty liver through regulating lipid metabolism. However, whether L-Carnitine administration may affect the disturbance of lipid metabolism and circadian rhythm of mice induced by prolonged circadian disruption is still unknown. Herein, we investigated the effects of L-Carnitine on conditions of circadian clock and lipid metabolism through a chronic jet-lag mice model which was developed by reversing 12 h light/12 h dark cycle every 4 days for a continuous 12 weeks. Results showed that L-Carnitine administration significantly decreased levels of serum glutamic-oxaloacetic transaminase (GOT) and triglycerides (TG), which were remarkably elevated by chronic jet-lag. More importantly, quantitative real-time polymerase chain reaction (qRT-PCR) analysis indicated that L-Carnitine supplementation would effectively counteract the negative
alterations in gene expression which related to lipid metabolism (Srebp1, Acaca, Fasn, and Scd1), metabolic regulator (mTOR)
and circadian rhythm (Bmal1 , Per1, Cry1 and Dec1 ) in the liver of
mice subjected to the chronic jet-lag. As a conclusion, L-Carnitine was partly effective in preventing the disruption of circadian clock and lipid metabolic disorders induced by the chronic jet-lag.
Activation of calmodulin dependent protein kinase (CaMK)II by exercise is beneficial in controlling membrane lipids associated with type 2 diabetes and obesity. Regulation of lipid metabolism is crucial in the improvement of type 2 diabetes and obesity associated symptoms. The role of CaMKII in membrane associated lipid metabolism was the focus of this study. Five to six weeks old male Wistar rats were used in this study. GC×GC-TOFMS technique was used to determine the levels of polyunsaturated fatty acids (linoleic acid, arachidonic acid and 11,14-eicosadienoic acid). Carnitine palmitoyltransferase (Cpt-1) and acetyl-CoA carboxylase (Acc-1) genes expression were assessed using quantitative real time PCR (qPCR). From the results, CaMKII activation by exercise increased the levels of arachidonic acid and 11,14-eicosadienoic acid while a decrease in the level of linolenic acid was observed in the skeletal muscle. The results indicated that exercise-induced CaMKII activation increased CPT-1 expression and decreased ACC-1 expression in rat skeletal muscle. All the observed increases with activation of CaMKII by exercise were aborted when KN93, an inhibitor of CaMKII was injected in exercising rats. This study demonstrated that CaMKII activation by exercise regulated lipid metabolism. This study suggests that CaMKII can be a vital target of
therapeutic approach in the management of diseases such as type 2 diabetes and obesity that have increased to epidemic proportions recently.
Stať popisuje design, realizaci a výsledky prospektivně uspořádaného dvoufázového šetření, jehož cílem bylo ověřit na souboru ekonomicky aktivních českých mužů a žen potenciální souvislosti mezi syndromem vyhoření, vybranými psychosociálními charakteristikami a hlavními známými riziky kardiovaskulárních chorob. Součástí projektu byla intervence směřující ke snížení výskytu rizikových faktorů KVO a syndromu vyhoření. Dalším cílem projektu byla snaha zhodnotit vliv edukace probandů na snížení rizik KVO (i syndromu vyhoření), jak již bylo dříve, pokud jde o rizika KVO, prokázáno. Soubor probandů (78 osob, 64 žen, 14 mužů; průměrný věk 48,4; SD 11,6; min.věk 22, max. věk 67) byl získán oslovením českých i zahraničních firem, podniků a institucí. Pokud jde o změny biochemických proměnných v důsledku intervence, snížení celkového cholesterolu a LDL cholesterolu lze pokládat za velmi příznivý nález. Změny psychologických proměnných lze rovněž pokládat za příznivé: došlo ke snížení řady rizikových charakteristik a ke zvýšení úrovně vnímané sociální opory, která je protektivním faktorem. Z výsledků vyplývá, že koncentrace lipidů a jejich metabolismus jsou relativně velmi citlivé na osobnostní a psychosociální charakteristiky, jež lze pokládat za obecně rizikové pro zdraví. Jednotlivé proměnné se jako prediktory uplatňovaly v menší míře než faktory, jež zastupovaly několik proměnných.