The germination of cucumber seeds begins with the degradation of reserved oil to fatty acids within the lipid body, which are then further metabolized to acyl-CoA. The acyl-CoA moves from the lipid body to the glyoxysome following β-oxidation for the production of acetyl-CoA. As an initial carbon source supplier, acetyl-CoA is an essential molecule in the glyoxylate cycle within the glyoxysome, which produces the metabolic intermediates of citrate and malate, among others. The glyoxylate cycle is a necessary metabolic pathway for oil seed plant germination because it produces the metabolic intermediates for the tricarboxylic acid (TCA) cycle and for gluconeogenesis, such as the oxaloacetate, which moves to the cytosol for the initiation of gluconeogenesis by phophoenolpyruvate carboxykinase (PEPCK). Following reserved oil mobilization, the production and transport of various metabolic intermediates are involved in the coordinated operation and activation of multiple metabolic pathways to supply directly usable carbohydrate in the form of glucose. Furthermore, corresponding gene expression regulation compatibly transforms the microbody to glyoxysome, which contains the organelle-specific malate synthase (MS) and isocitrate lyase (ICL) enzymes during oil seed germination. Together with glyoxylate cycle, carnitine, which mediates the supplementary route of the acetyl-CoA transport mechanism via the mitochondrial BOU (A BOUT DE SOUFFLE) system, possibly plays a secondary role in lipid metabolism for enhanced plant development.
Liver receptor homolog-1 (LRH-1) has emerged as a regulator of hepatic glucose, bile acid, and mitochondrial metabolism. However, the functional mechanism underlying the effect of LRH-1 on lipid mobilization has not been addressed. This study investigated the regulatory function of LRH-1 in lipid metabolism in maintaining a normal liver physiological state during fasting. The Lrh-1f/f and LRH-1 liver-specific knockout (Lrh-1LKO) mice were either fed or fasted for 24 h, and the liver and serum were isolated. The livers were used for qPCR, western blot, and histological analysis. Primary hepatocytes were isolated for immunocytochemistry assessments of lipids. During fasting, the Lrh-1LKO mice showed increased accumulation of triglycerides in the liver compared to that in Lrh-1f/f mice. Interestingly, in the Lrh-1LKO liver, decreases in perilipin 5 (PLIN5) expression and genes involved in β-oxidation were observed. In addition, the LRH-1 agonist dialauroylphosphatidylcholine also enhanced PLIN5 expression in human cultured HepG2 cells. To identify new target genes of LRH-1, these findings directed us to analyze the Plin5 promoter sequence, which revealed -1620/-1614 to be a putative binding site for LRH-1. This was confirmed by promoter activity and chromatin immunoprecipitation assays. Additionally, fasted Lrh-1f/f primary hepatocytes showed increased co-localization of PLIN5 in lipid droplets (LDs) compared to that in fasted Lrh-1LKO primary hepatocytes. Overall, these findings suggest that PLIN5 might be a novel target of LRH-1 to mobilize LDs, protect the liver from lipid overload, and manage the cellular needs during fasting.
This research was conducted to investigate the physiological consequences of undernourished yak. Twelve Maiwa yak ($110.3{\pm}5.85kg$) were randomly divided into two groups (baseline and starvation group). The yak of baseline group were slaughtered at day 0, while the other group of yak were kept in shed without feed but allowed free access to water, salt and free movement for 9 days. Blood samples of the starvation group were collected on day 0, 1, 2, 3, 5, 7, 9 and the starved yak were slaughtered after the final blood sample collection. The liver and muscle glycogen of the starvation group decreased (p<0.01), and the lipid content also decreased while the content of moisture and ash increased (p<0.05) both in Longissimus dorsi and liver compared with the baseline group. The plasma insulin and glucose of the starved yak decreased at first and then kept stable but at a relatively lower level during the following days (p<0.01). On the contrary, the non-esterified fatty acids was increased (p<0.01). Beyond our expectation, the ketone bodies of ${\beta}$-hydroxybutyric acid and acetoacetic acid decreased with prolonged starvation (p<0.01). Furthermore, the mRNA expression of lipogenetic enzyme fatty acid synthase and lipoprotein lipase in subcutaneous adipose tissue of starved yak were down-regulated (p<0.01), whereas the mRNA expression of lipolytic enzyme carnitine palmitoyltransferase-1 and hormone sensitive lipase were up-regulated (p<0.01) after 9 days of starvation. The phosphoenolpyruvate carboxykinase and pyruvate carboxylase, responsible for hepatic gluconeogenesis were up-regulated (p<0.01). It was concluded that yak derive energy by gluconeogenesis promotion and fat storage mobilization during starvation but without ketone body accumulation in the plasma.
It has been known that the pronounced hypotension resulting from hemorrhage gives rise to compensatory stimulation of the adrenosympathetic system, which leads to an increase of liberation of catecholamines from sympathetic nervous system and adrenal medulla. It is obvious, therefore, that numerous physiological and biochemical changes during the hemorrhagic hypotention might be mediated through the increased liberation of catecholamines. Although an extensive studies have been reported on changes of protein and carbohydrate metabolism in hemorrhagic shock a few studies on the changes of lipid metabolism have been reported. Levenson(1961) observed a marked increase of serum lipids content during hemorrhagic shock and also noticed a marked elevation of serum free fatty acids. He suggested that these effects were due to mobilization and accelerated metabolic breakdown of lipids which might be resulted by sympathetic stimulation as a cause. To elucidate the mechanism of this, author studied the change of serum free fatty acids and blood sugar with relation to catecholamines during experimentally induced hemorrhagic shock in dog. Healthy male mongrel dogs weighing approximately 15kg were used. Under the general anesthesia with pentobarbital, rapid hemorrhage was produced from the femoral artery maintaining blood pressure level of 40 mmHg measured by the manometer connected with the opposite femoral artery throughout the experiment. Serum free fatty acids(FFA) and blood sugar were measured by the methods of Dole(1956) and Folin-wu,(1920) respectively. Tissue catecholamine was measured by Shore and Olin method(1958) using Aminco-Bowman spectrophotofluorometer.
Mobilization of storage lipids is critical for the germination of oil seeds, as they supply carbon and energy until photosynthesis commences in cotyledons. In this study, we determined the levels of plant carnitine and associated changes in these levels from seed germination to cotyledon senescence. We also examined changes in the content of unsaturated fatty acids throughout seedling development. Carnitine levels peaked on day 3 at 14.5 nM in cotyledons and decreased sharply to 7.2 nM on day 4. On development day 3 carnitine levels were maintained at around 3 nM until day 7. The unsaturated fatty acid content dropped by half at the same time as carnitine peaked (day-3), and storage lipids were almost depleted by day 5. Thereafter, carnitine was hardly detected until the second stage of cotyledon senescence, at which stage the carnitine content was 6.8 nM, similar to that on day 4 at the time of fatty acid depletion in the cotyledons. Unsaturated fatty acids levels remained constant in green cotyledons but slightly increased in the senescing cotyledons. The latter can be explained by intracellular breakdown of membrane lipids. This is the first such discovery in developing cotyledons and may offer clues regarding other roles of the acetyl unit transport system in plants. The expression of BOU was closely associated with carnitine metabolism during seed germination and cotyledon development. The results provide support for the possibility of carbon re-routing during the glyoxylate cycle in the supply of energy for early germination and development.
The effect of starch infusion on production, metabolic parameters and relative mRNA abundance was investigated in low yield lactating cows from 86 days in milk. Six Holstein cows fitted with permanent ruminal cannulas were arranged into one of two complete $3{\times}3$ Latin squares and infused with a starch solution containing 800 grams starch for 16 days. The three treatments were: i) ruminal and abomasal infusion with water (Control); ii) ruminal infusion with cornstarch solution and abomasal infusion with water (Rumen); iii) ruminal infusion with water and abomasal infusion with cornstarch solution (Abomasum). There were no significant differences (p>0.05) among the three treatments with low yield lactating cows in feed and energy intake, milk yield and composition, plasma metabolism, or even on gene expression. However, cows receiving starch through rumen performed better than directly through the abomasum during the glucose tolerance test procedure with a higher area under the curve (AUC; p = 0.08) and shorter half-time ($t^{1/2}$; p = 0.11) of plasma insulin, therefore, it increased glucose disposal, which stated a lipid anabolism other than mobilization after energy supplementation. In conclusion, extra starch infusion at concentration of 800 g/d did not enhance energy supplies to the mammary gland and improve the lactating performance in low yield lactating cows.
Resveratrol is a non-flavonoid polyphenol which belongs to the stilbenes group and is naturally generated in several plants in response to damage or fungal invasion. It has been shown in published studies that resveratrol has an anti-adipogenic effect. A good consensus regarding the involvement of a down-regulation of $C/EBP{\alpha}$ and $PPAR{\gamma}$ in this effect has been reached. In addition, different metabolic pathways involved in triacylglycerol metabolism in white adipose tissue have been shown to be regulated by resveratrol. Concerning lipolysis, though this compound in itself seems to be unable to cause lipolysis, it increases lipid mobilization stimulated by ${\beta}-adrenergic$ agents. The increase in brown adipose tissue thermogenesis, and accordingly the associated energy dissipation, can attribute to accounting for the body-fat reducing effect of resveratrol. Besides its effects on adipose tissue, resveratrol can also acts on other organs and tissues. Therefore, it increases mitochondrial biogenesis and accordingly fatty acid oxidation in skeletal muscle and liver. This effect can also attribute to the body-fat reducing effect of this molecule. The present review purposes to collect the evidence concerning the potential mechanisms of action which underlie the anti-obesity effects of resveratrol, acquired either in cultured cells lines and animal models.
Kim, Moon-Young;Liang, Guo-Hua;Kim, Ji-Aee;Choi, Soo-Seung;Choi, Shin-Ku;Suh, Suk-Hyo
The Korean Journal of Physiology and Pharmacology
/
v.13
no.1
/
pp.27-32
/
2009
The effects of oxidized low-density lipoprotein(OxLDL) and its major lipid constituent lysophosphatidylcholine(LPC) on $Ca^{2+}$ entry were investigated in cultured human umbilical endothelial cells(HUVECs) using fura-2 fluorescence and patch-clamp methods. OxLDL or LPC increased intracellular $Ca^{2+}$ concentration($[Ca^{2+}]_i$), and the increase of $[Ca^{2+}]_i$ by OxLDL or by LPC was inhibited by $La^{3+}$ or heparin. LPC failed to increase $[Ca^{2+}]_i$ in the presence of an antioxidant tempol. In addition, store-operated $Ca^{2+}$ entry(SOC), which was evoked by intracellular $Ca^{2+}$ store depletion in $Ca^{2+}$-free solution using the sarcoplasmic reticulum $Ca^{2+}$ pump blocker, 2, 5-di-t-butyl-l,4-benzohydroquinone(BHQ), was further enhanced by OxLDL or by LPC. Increased SOC by OxLDL or by LPC was inhibited by U73122. In voltage-clamped cells, OxLDL or LPC increased $[Ca^{2+}]_i$ and simultaneously activated non-selective cation(NSC) currents. LPC-induced NSC currents were inhibited by 2-APB, $La^{3+}$ or U73122, and NSC currents were not activated by LPC in the presence of tempol. Furthermore, in voltage-clamped HUVECs, OxLDL enhanced SOC and evoked outward currents simultaneously. Clamping intracellular $Ca^{2+}$ to 1 ${\mu}M$ activated large-conductance $Ca^{2+}$-activated $K^+(BK_{ca})$ current spontaneously, and this activated $BK_{ca}$ current was further enhanced by OxLDL or by LPC. From these results, we concluded that OxLDL or its main component LPC activates $Ca^{2+}$-permeable $Ca^{2+}$-activated NSC current and $BK_{ca}$ current simultaneously, thereby increasing SOC.
Ginseng has been used as a general tonic agent to invigorate human body. In the present study, we isolated novel glycolipoproteins from ginseng that activate $Ca^{2+}$-activated $Cl^-$ channel (CaCC) in Xenopus oocytes and transiently increase intracellular free $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) in mouse Ehrlich ascites tumor cells. We named the active ingredients as gintonin. Gintonin exists in at least six different forms. The native molecular weight of gintonin is about 67 kDa but its apparent molecular weight is about 13 kDa, indicating that gintonin might be a pentamer. Gintonin is rich in hydrophobic amino acids. Its main carbohydrates are glucose and glucosamine. Its lipid components are linoleic, palmitic, oleic, and stearic acids. Gintonin actions were blocked by U73122, a phospholipase C inhibitor, 2-aminoethxydiphenyl borate, an inositol 1,4,5-trisphosphate receptor antagonist, or bis (o-aminophenoxy) ethane-N,N,N0,N0-tetracetic acid acetoxymethyl ester, a membrane permeable $Ca^{2+}$ chelator. In the present study, we for the first time isolated novel gintonin and showed the signaling pathways on gintonin-mediated CaCC activations and transient increase of $[Ca^{2+}]_i$. Since $[Ca^{2+}]_i$ as a second messenger plays a pivotal role in the regulation of diverse $Ca^{2+}$-dependent intracellular signal pathways, gintonin-mediated regulations of $[Ca^{2+}]_i$ might contribute to biological actions of ginseng.
Delfino, Nelson Carvalho;de Aragao Bulcao, Lucas Fialho;Alba, Henry Daniel Ruiz;da Silva Oliveira, Mauricio Xavier;de Queiroz, Filipe Pinheiro Soares;de Carvalho, Gleidson Giordano Pinto;Renno, Francisco Palma;de Freitas, Jose Esler Junior
Asian-Australasian Journal of Animal Sciences
/
v.31
no.11
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pp.1756-1765
/
2018
Objective: The purpose of this study was to evaluate the influence of body condition score (BCS) at calving on the metabolic status of female Murrah buffaloes in the transition period. Methods: Thirty-seven pregnant buffaloes (multiparous) were selected and monitored during the transition period based on their body condition score and on the estimated calving date. Two groups were formed: i) buffaloes with a BCS>3.5 (n = 17); this group was classified and named 'high BCS at calving' (HBCS); and ii) buffaloes with a $BCS{\leq}3.5$ (n = 20); this group was classified and named 'low BCS at calving' (LBCS). All animals were monitored during the last 30 days of pregnancy and the first 70 days post-calving and kept in the same environment and under the same feeding and management conditions. Mean values for BCS at calving were $2.98{\pm}0.9$ (mean${\pm}$standard error of the mean [SEM]) and $4.21{\pm}0.9$ (mean${\pm}$SEM) for the HBCS and LBCS groups, respectively. Results: The HBCS group showed higher milk fat content (p = 0.007) and milk fat yield (p = 0.027) and a higher concentration of milk urea nitrogen (p = 0.001) than LBCS buffaloes, which in turn had a lower urine pH value (p = 0.033) than HBCS buffaloes in the pre-calving period (7.86 for HBCS vs 7.76 for LBCS). The HBCS animals had a higher concentration of erythrocytes (p = 0.001) and hematocrit (p = 0.012) post-calving and a higher hemoglobin concentration (p = 0.004) pre-calving. Conclusion: Buffaloes during the transition period exhibited some variations in the oxidative stress related to their metabolic status. After calving, buffaloes with a high BCS at calving and greater lipid mobilization have a more marked alteration in oxidative status, but improved production performance.
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