scholarly journals Mori Fructus Polysaccharides Attenuate Alcohol-Induced Liver Damage by Regulating Fatty Acid Synthesis, Degradation and Glycerophospholipid Metabolism in Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Liang Bian ◽  
Hua-Guo Chen ◽  
Xiao-Jian Gong ◽  
Chao Zhao ◽  
Xin Zhou
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Liver Damage ◽  
Fatty Acid Synthesis ◽  
Serum Triglyceride ◽  
Acid Synthesis ◽  
Serum Triglyceride Level ◽  
Group Model ◽  
Model Group ◽  
Blank Group

Mori Fructus polysaccharides (MFP) are macromolecules extracted from Mori Fructus (MF), which has the biological activity of anti-liver damage. Our group found that MFP maybe down regulate the serum triglyceride level in mice with alcohol-induced liver damage, suggesting that MFP can regulate lipid metabolism, but its specific mechanism is still not clear. Fifty SPF-ICR male mice weighing 18–22 g were randomly divided into five groups, blank group, model group, bifendate group, MFPA1 group and MFPB1 group. The blood and liver tissues were taken from mice for nontargeted lipidomic analysis and histopathological examination after 7 day’s treatment. The histopathological changes indicated that the normal liver cells were intact and regular, with orderly arrangement and distinct cell boundaries; the liver of model mice showed inflammatory infiltration, ballooning degeneration in the cells and small lipid drops; the liver of mice in the bifendate, MFPA1 and MFPB1 groups showed similar symptoms to those of model mice, but the lesions were less severe and the ballooning degeneration were reduced. Multivariate analysis of all lipids in the serum of five groups of mice showed there were obvious differences in lipid metabolism between the model group and the blank group. At the same time, seven kinds of differential lipids were precisely identified after screening, including prostaglandins, long-chain fatty acids, glycerophospholipids, acyl carnitines. In summary, alcohol intake and MFP intervention have significant effects on fatty acid synthesis, degradation and glycerophospholipid metabolism.

LIF and CNTF, which share the gp130 transduction system, stimulate hepatic lipid metabolism in rats

1996 ◽  
Vol 271 (3) ◽  
pp. E521-E528 ◽  
Author(s):  
K. Nonogaki ◽  
X. M. Pan ◽  
A. H. Moser ◽  
J. Shigenaga ◽  
I. Staprans ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Acid Synthesis ◽  
Interleukin 4 ◽  
Dependent Manner ◽  
Hepatic Triglyceride ◽  
Serum Triglycerides ◽  
Triglyceride Secretion

We determined the effects of leukemia inhibitory factor (LIF) and ciliary neurotrophic factor (CNTF) on lipid metabolism in intact rats. Administration of LIF and CNTF increased serum triglycerides in a dose-dependent manner with peak values at 2 h. The effects of LIF and CNTF on serum cholesterol were very small, and serum glucose was unaffected. Both LIF and CNTF stimulated hepatic triglyceride secretion, hepatic de novo fatty acid synthesis, and lipolysis. Pretreatment with phenylisopropyl adenosine, which inhibits lipolysis, partially inhibited LIF- and CNTF-induced hypertriglyceridemia. Interleukin-4, which inhibits cytokine-induced hepatic fatty acid synthesis, also partially inhibited LIF- and CNTF-induced hypertriglyceridemia. These results indicate that both lipolysis and de novo fatty acid synthesis play a role in providing fatty acids for the increase in hepatic triglyceride secretion. Neither indomethacin nor adrenergic receptor antagonists affected the hypertriglyceridemia. The combination of LIF plus CNTF showed no additive effects consistent with the action of both cytokines through the gp130 transduction system. Thus LIF and CNTF have similar effects on lipid metabolism; they join a growing list of cytokines that stimulate hepatic triglyceride secretion and may mediate the changes in lipid metabolism that accompany the acute phase response.

scholarly journals Taurine-Mediated IDOL Contributes to Resolution of Streptococcus uberis Infection

2021 ◽  
Vol 89 (5) ◽  
Author(s):  
Zhixin Wan ◽  
Riguo Lan ◽  
Yilin Zhou ◽  
Yuanyuan Xu ◽  
Zhenglei Wang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Bacterial Load ◽  
Critical Role ◽  
Acid Synthesis ◽  
Content Type ◽  
Streptococcus Uberis

ABSTRACT Metabolic alterations occur in pathogenic infections, but the role of lipid metabolism in the progression of bacterial mastitis is unclear. Cross talk between lipid droplets (LDs) and invading bacteria occurs, and targeting of de novo lipogenesis inhibits pathogen reproduction. In this study, we investigate the role(s) of lipid metabolism in mammary cells during Streptococcus uberis infection. Our results indicate that S. uberis induces the synthesis of fatty acids and production of LDs. Importantly, taurine reduces fatty acid synthesis, the abundance of LDs and the in vitro bacterial load of S. uberis. These changes are mediated, at least partly, by the E3 ubiquitin ligase IDOL, which is associated with the degradation of low-density lipoprotein receptors (LDLRs). We have identified a critical role for IDOL-mediated fatty acid synthesis in bacterial infection, and we suggest that taurine may be an effective prophylactic or therapeutic strategy for preventing S. uberis mastitis.

scholarly journals Lipid Metabolism in Development and Progression of Hepatocellular Carcinoma

Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1419 ◽  
Author(s):  
Moris Sangineto ◽  
Rosanna Villani ◽  
Francesco Cavallone ◽  
Antonino Romano ◽  
Domenico Loizzi ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Fatty Acid Synthesis ◽  
Cell Signalling ◽  
Acid Synthesis ◽  
Environmental Adaptation ◽  
Metabolic Reprogramming ◽  
Therapeutic Approaches

Metabolic reprogramming is critically involved in the development and progression of cancer. In particular, lipid metabolism has been investigated as a source of energy, micro-environmental adaptation, and cell signalling in neoplastic cells. However, the specific role of lipid metabolism dysregulation in hepatocellular carcinoma (HCC) has not been widely described yet. Alterations in fatty acid synthesis, β-oxidation, and cellular lipidic composition contribute to initiation and progression of HCC. The aim of this review is to elucidate the mechanisms by which lipid metabolism is involved in hepatocarcinogenesis and tumour adaptation to different conditions, focusing on the transcriptional aberrations with new insights in lipidomics and lipid zonation. This will help detect new putative therapeutic approaches in the second most frequent cause of cancer-related death.

scholarly journals Tryptophan and the control of triglyceride and carbohydrate metabolism in the rat

1980 ◽  
Vol 43 (2) ◽  
pp. 349-356 ◽  
Author(s):  
R. Fears ◽  
Elspeth A. Murrellt
Keyword(s):  
Fatty Acid ◽  
Amino Acid ◽  
Fatty Acid Synthesis ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Specific Inhibitor ◽  
Serum Triglyceride ◽  
Acid Synthesis ◽  
Hepatic Fatty Acid ◽  
Metabolic States

1. Hepatic fatty acid synthesis, measured in vivo using 8H2O, was increased by a single dose of L-tryptophan (50 mg/kg body-weight) to both fed and fasted rats and by a supplement of tryptophan to the diet (2.5 g/kg diet for 7 d) when the rats were killed midway through the feeding period.2. Additional dietary tryptophan was hypotriglyceridaemic in normal rats but exacerbated the hyper- triglyceridaemia in rats when lipoprotein clearance was impaired 24 h after an injection of Triton WR 1339 (Chromatography Services Co., Birkenhead, Cheshire).3. The effects of tryptophan on hepatic fatty acid synthesis and the concentration of serum triglyceride were not directly related to the action of the amino acid on gluconeogenesis. A lack of correlation between inhibition of gluconeogenesis and enhancement of lipogenesis was confirmed using mercaptopicolinic acid, a specific inhibitor of phosphoenolpyruvate carboxykinase (EC 4.1.1.32).4. DL-Tryptophan itself did not provide a significant contribution of substrate to the total rate of lipogenesis. Other possible explanations for the activity of tryptophan noted in the present experiments are discussed.5. In conclusion, moderate intakes of tryptophan affect fatty acid and triglyceride metabolism under physiological conditions and it is proposed that the amino acid may be involved in the control of lipid metabolism in a variety of metabolic states.

scholarly journals Glucagon regulates ACC activity in adipocytes through the CAMKKβ/AMPK pathway

2012 ◽  
Vol 302 (12) ◽  
pp. E1560-E1568 ◽  
Author(s):  
I-Chen Peng ◽  
Zhen Chen ◽  
Wei Sun ◽  
Ying-Shiuan Li ◽  
Traci LaNai Marin ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Protein Kinase ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
Dependent Protein Kinase ◽  
Ampk Signaling ◽  
Dependent Protein

Glucagon is important for regulating lipid metabolism in part through its inhibition of fatty acid synthesis in adipocytes. Acetyl-CoA carboxylase 1 (ACC1) is the rate-limiting enzyme for fatty acid synthesis. Glucagon has been proposed to activate cAMP-dependent protein kinase A (PKA), which phosphorylates ACC1 to attenuate the lipogenic activity of ACC1. Because AMP-activated protein kinase (AMPK) also inhibits fatty acid synthesis by phosphorylation of ACC1, we examined the involvement of AMPK and its upstream kinase in the glucagon-elicited signaling in adipocytes in vitro and in vivo. LC-MS-MS analysis suggested that ACC1 was phosphorylated only at Ser79, an AMPK-specific site, in glucagon-treated adipocytes. Pharmacological inhibitors and siRNA knockdown of AMPK or PKA in adipocytes demonstrate that glucagon regulates ACC1 and ACC2 activity through AMPK but not PKA. By using Ca2+/calmodulin-dependent protein kinase kinase-β knockout (CaMKKβ−/−) mice and cultured adipocytes, we further show that glucagon activates the CaMKKβ/AMPK/ACC cascade. Additionally, fasting increases the phosphorylation of AMPK and ACC in CaMKKβ+/+ but not CaMKKβ−/− mice. These results indicate that CaMKKβ/AMPK signaling is an important molecular component in regulating lipid metabolism in adipocytes responding to glucagon and could be a therapeutic target for the dysregulation of energy storage.

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