Phospholipid Metabolism in Apoptosis


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To determine the level of blood glucose and lipids, adenosine monophosphate-activated protein kinase AMPK expression of liver and hipppocamual neuronal apoptosis. The changes in the function of XIAP, which is an anti-apoptotic protein in the hippocampus, may affect the metabolism of glucose and lipids. Diabetes and Alzheimer's disease AD are a group of complex, interrelated diseases. Diabetes and AD share many pathophysiological factors, such as an abnormal insulin signaling pathway, an increase in advanced glycation end products AGEs , oxidative stress, and inflammation reactions, that may be involved in disease development; however, the exact mechanisms are still unknown.

Due to its close relationship to diabetes, AD is also known as type 3 diabetes. Anatomically, the hippocampus is part of the cortex structure of the limbic forebrain, and its relation to cognitive function has become a popular research topic [ 1 , 2 ]. The hippocampus, which is the visceral integration hub, can also regulate visceral activities through autonomic pathways. The hippocampus receives the visceral afferent nerve fibers and has extensive fiber connections with the part of the central nervous system that regulates visceral activities, such as the hypothalamus, brain stem and spinal cord.

The hippocampus regulates visceral functions through sympathetic and parasympathetic nerves. In clinical practice, AD patients often have abnormal levels of blood glucose and lipids [ 3 ], and hippocampal neuron apoptosis is the pathological characteristic and outcome of the hippocampus in AD patients [ 1 , 2 , 4 , 5 ]. Despite the similarities between diabetes and AD, whether hippocampal neuron apoptosis affects the levels of peripheral blood glucose and lipids and the underlying mechanisms are still unknown. This study aims to develop an in-depth understanding of the effect and mechanism of hippocampal cognitive impairment on the metabolism of blood glucose and lipids.

The relationship between the changes in blood glucose and lipid levels and hippocampal neuron apoptosis, the expression of AMPK, and gastrointestinal motility was analyzed. Dowdy USA. The water maze test was performed to screen 30 rats for cognitive impairment. The inclusion criterion was cognitive impairment as confirmed by a significant difference in the location orientation and spatial exploration of the water maze relative to the control group. An additional 10 rats were used as the blank group absence of any interference. The water maze was a round pool that was cm in diameter, 50 cm tall, and 30 cm deep.

After the water maze was filled with water, milk powder was added approximately 1. The pool was divided into quadrants 1, 2, 3 and 4 clockwise. A quadrant was chosen, and a round transparent platform that was 10 cm in diameter and 28 cm high was placed in its center with the top of platform located 2 cm below the water surface. A camera was installed above the maze for real-time recording of the rat's movements. The external references of the maze remained constant, the curtain was closed, and the laboratory light source was kept hidden with a consistent brightness.

On the day prior to the location orientation test, the rats were individually placed into the pool no platform to swim freely for minutes to become familiar with the maze environment. If the rat was unable to locate the platform after seconds, it was guided towards the platform and stayed there for 10 seconds, and the escape latency was recorded as seconds.

For the spatial exploration test, the platform was removed, a pool entry point was randomly selected, and the rats were placed into the pool facing the maze wall. The following information was recorded: the distance that the rat swam in each quadrant, the ratio to the total swimming distance, and the number of times the rat crossed the platform during the seconds. The transformation was performed following the instructions for BL21plysS competent cells, and ampicillin Amp was used to screen positive colonies.

The protein samples were subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis SDS-PAGE and electrically transferred to a nitrocellulose membrane for western blot analysis. Mouse anti-6His monoclonal antibody was used as the primary antibody, HRP-labeled goat anti-mouse IgG was used as the secondary antibody, ECL reagents were used for chemiluminescence, and the membrane was exposed to X-rays and observed.

The rats were raised for 4 additional weeks. Next, under anesthesia with chloral hydrate, blood samples were taken from the heart, and the plasma was separated and loaded into an automatic biochemical analyzer to determine the levels of fasting plasma glucose FPG , triglyceride TG , cholesterol TC , high-density lipoprotein HDL cholesterol and low-density lipoprotein LDL cholesterol.

B-mode ultrasonography was performed to dynamically observe the gastrointestinal motility of the rats. The method of [ 6 ] was used to determine the gastric emptying rate and intestinal propulsive rate. The gastric cardia and pylorus were ligated. The gastric emptying rate and intestinal propulsive rate were calculated. The heart was perfused and fixed.

Table of contents

The neck was broken, and the brain was removed. An equal volume of labeling solution no terminal transferase was used in place of the TUNEL working solution as the negative control. Neurons were considered positive if brown or yellow particles were present in the nucleus. High-resolution microscopic fields were randomly selected to count the number of apoptotic neurons. The liver tissue samples were ground into powder in liquid nitrogen, and total RNA was then extracted.

Each sample was run in triplicate, and the average value was used for the final analysis. An automatic digital gel imaging system was used to determine and analyze the optical density of the western blot bands. The SPSS Model group. A TUNEL assay was performed to detect hippocampal neuron apoptosis in the rats and showed that apoptotic neuron nuclei were stained with varying shades of brown or yellow. A significant difference in neuron apoptosis was observed between the groups, especially in the hippocampal CA1 region.

The results showed that the apoptosis index was Only isolated apoptotic neurons with light staining were observed in the CA1 region of the blank group, and the apoptosis index was The gastric emptying rate and intestinal propulsive rate were significantly lower in the model group than in the blank group. Hippocampal neuron apoptosis is the main pathological change of many cognitive disorders, such as AD [ 7 , 8 ].

Cysteinyl aspartate specific proteinase caspase plays a critical role in apoptosis and mediates apoptosis through many pathways [ 9 , 10 , 11 ]. Based on the central role of caspase in neuron apoptosis and injury, researchers are focusing on the inhibition of apoptosis and the protection of neurons by inhibiting caspase activity.

XIAP is the most potent caspase inhibitor and can prevent apoptosis by binding to and inhibiting caspase-3, 7, 9 and reducing the release of cytochrome C [ 13 ]. Esser , J. Shimabukuro , M. Ohneda , Y. Lee , and R. Role of nitric oxide in obesity-induced beta cell disease. Kharroubi , I. Cardozo , Z.

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Ravazzola , and A. Chronic palmitate but not oleate exposure induces endoplasmic reticulum stress, which may contribute to INS-1 pancreatic beta-cell apoptosis. Laybutt , D. Preston , M. Akerfeldt , J.

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Lipid Asymmetry

Cheng , and H. Interleukin alleviated palmitate-induced endoplasmic reticulum stress in INS-1 cells through activation of autophagy. Prause , M. Christensen , N. Billestrup , and T. Kokas , J. Mandl , G. Metformin attenuates palmitate-induced endoplasmic reticulum stress, serine phosphorylation of IRS-1 and apoptosis in rat insulinoma cells. Puyal , J.

Chatton , J. Duprez , F. Allagnat , M. Frias , R. James , G. Waeber , J. Jonas , and C. HDLs protect pancreatic beta-cells against ER stress by restoring protein folding and trafficking. Petremand , G. Dubuis , C. Rummel , and C. Hong , D.

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Lipid metabolism, apoptosis and cancer therapy.

Gao , X. Wang , C. Luo , Y. Bai , and G. High-density lipoprotein prevents endoplasmic reticulum stress-induced downregulation of liver LOX-1 expression. Engin , F. Yermalovich , T. Nguyen , S. Hummasti , W. Eizirik , D. Mathis , and G. Restoration of the unfolded protein response in pancreatic beta cells protects mice against type 1 diabetes. Restoring endoplasmic reticulum function by chemical chaperones: an emerging therapeutic approach for metabolic diseases.

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Lipid Metabolism, Apoptosis and Cancer Therapy

Zhang , J. Chen , W. Cheng , W. Shen , and Z. Laybutt , M. Zhao , J. Chan , and G. Bip overexpression, but not CHOP inhibition, attenuates fatty-acid-induced endoplasmic reticulum stress and apoptosis in HepG2 liver cells. Life Sci. Pan , Q. Ren , W. Liu , Y. Zheng , Y. Xu , and G. Resveratrol prevents hepatic steatosis and endoplasmic reticulum stress and regulates the expression of genes involved in lipid metabolism, insulin resistance, and inflammation in rats.

Yang , X. Wang , and J. Glucagon-like peptide-1 preserves non-alcoholic fatty liver disease through inhibition of the endoplasmic reticulum stress-associated pathway. Pierre , N. Deldicque , C. Barbe , D. Naslain , P. Cani , and M. Toll-like receptor 4 knockout mice are protected against endoplasmic reticulum stress induced by a high-fat diet.

Miyamoto , Y. Mauer , S. Kumar , J. Mott , and H. Listenberger , L. Palmitate-induced apoptosis can occur through a ceramide-independent pathway. Egnatchik , R. Leamy , D. Jacobson , M. Shiota , and J. ER calcium release promotes mitochondrial dysfunction and hepatic cell lipotoxicity in response to palmitate overload. Rong , X. Albert , C. Hong , M. Duerr , B. Chamberlain , E.

Frontiers | The Role of Lipid Metabolism in T Lymphocyte Differentiation and Survival | Immunology

Tarling , A. Ito , J. Gao , B. Wang , P. Edwards , et al. LXRs regulate ER stress and inflammation through dynamic modulation of membrane phospholipid composition. Leamy , A. Egnatchik , M. Shiota , P. Ivanova , D. Myers , H. Brown , and J. Enhanced synthesis of saturated phospholipids is associated with ER stress and lipotoxicity in palmitate treated hepatic cells.

Flowers , M. Keller , Y. Choi , H. Lan , C. Kendziorski , J. Ntambi , and A. Liver gene expression analysis reveals endoplasmic reticulum stress and metabolic dysfunction in SCD1-deficient mice fed a very low-fat diet. Yang , P. Hofmann , L. Dicker , W. Hide , X. Lin , S. Watkins , A. Ivanov , and G. Aberrant lipid metabolism disrupts calcium homeostasis causing liver endoplasmic reticulum stress in obesity. Damiano , F. Alemanno , G. Gnoni , and L. Rochira , R. Tocci , S. Alemanno , A. Fang , D. Wan , W. Cao , Z. Zhang , W. Cheng , J.

Chen , and B. Endoplasmic reticulum stress leads to lipid accumulation through upregulation of SREBP-1c in normal hepatic and hepatoma cells. Choe , K. Shin , H. Jang , J. Seong , S. Back , and J. Endoplasmic reticulum stress induces hepatic steatosis via increased expression of the hepatic very low-density lipoprotein receptor. Tsai , E. Qiu , E. Bereczki , M. Santha , and K. Apolipoprotein B acts as a molecular link between lipid-induced endoplasmic reticulum stress and hepatic insulin resistance. Baker , P. Christian , M. Naples , X. Tong , K.

Hepatic mitochondrial and ER stress induced by defective PPARalpha signaling in the pathogenesis of hepatic steatosis. Chan , S. Sun , X. Zeng , Z. Choong , H. Watt , and J. Activation of PPARalpha ameliorates hepatic insulin resistance and steatosis in high fructose-fed mice despite increased endoplasmic reticulum stress. Xiong , X. Wang , Z. Yang , H. Zhang , and X. Hepatic steatosis exacerbated by endoplasmic reticulum stress-mediated downregulation of FXR in aging mice. Watanabe , M. Houten , L. Wang , A. Moschetta , D.

Mangelsdorf , R. Heyman , D. Moore , and J. Mayoral , N. Agra , M. Valdecantos , V. Pardo , M. Miquilena-Colina , J. Lo Iacono , M. Corazzari , G. Fimia , et al. Impaired autophagic flux is associated with increased endoplasmic reticulum stress during the development of NAFLD. Cell Death Dis. Peter , A. Weigert , H. Staiger , F. Machicao , F. Schick , J. Machann , N. Stefan , C. Thamer , H. Haring , and E.

Individual stearoyl-CoA desaturase 1 expression modulates endoplasmic reticulum stress and inflammation in human myotubes and is associated with skeletal muscle lipid storage and insulin sensitivity in vivo. Deldicque , L. Cani , A. Philp , J. Raymackers , P. Meakin , M. Ashford , N. Delzenne , M. Francaux , and K. The unfolded protein response is activated in skeletal muscle by high-fat feeding: potential role in the downregulation of protein synthesis. Kars , M. Yang , M. Gregor , B. Mohammed , T. Pietka , B. Finck , B. Patterson , J. Horton , B.

Mittendorfer , G. Hotamisligil , et al. Tauroursodeoxycholic acid may improve liver and muscle but not adipose tissue insulin sensitivity in obese men and women. Zhang , G. Peng , F. Yang , et al. Proteome of skeletal muscle lipid droplet reveals association with mitochondria and apolipoprotein a-I. Proteome Res. Coll , A. Barroso , X. Palomer , and M. Oleate prevents saturated-fatty-acid-induced ER stress, inflammation and insulin resistance in skeletal muscle cells through an AMPK-dependent mechanism. Barroso , A. Palomer , L. Michalik , W. Wahli , and M. Van Proeyen , M.

Francaux , and P. The unfolded protein response in human skeletal muscle is not involved in the onset of glucose tolerance impairment induced by a fat-rich diet. Hage Hassan , R. Hainault , J. Vilquin , C. Samama , F. Lasnier , P. Ferre , F. Foufelle , and E. Endoplasmic reticulum stress does not mediate palmitate-induced insulin resistance in mouse and human muscle cells.

Rieusset , J.


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Chauvin , A. Durand , A. Bravard , F. Laugerette , M. Michalski , and H. Reduction of endoplasmic reticulum stress using chemical chaperones or Grp78 overexpression does not protect muscle cells from palmitate-induced insulin resistance. Nielsen , L. Perko , H. Arendrup , and C. Microsomal triglyceride transfer protein gene expression and triglyceride accumulation in hypoxic human hearts. Marfella , R. Di Filippo , M. Portoghese , M.

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Phospholipid Metabolism in Apoptosis Phospholipid Metabolism in Apoptosis
Phospholipid Metabolism in Apoptosis Phospholipid Metabolism in Apoptosis
Phospholipid Metabolism in Apoptosis Phospholipid Metabolism in Apoptosis
Phospholipid Metabolism in Apoptosis Phospholipid Metabolism in Apoptosis
Phospholipid Metabolism in Apoptosis Phospholipid Metabolism in Apoptosis
Phospholipid Metabolism in Apoptosis Phospholipid Metabolism in Apoptosis
Phospholipid Metabolism in Apoptosis Phospholipid Metabolism in Apoptosis
Phospholipid Metabolism in Apoptosis Phospholipid Metabolism in Apoptosis
Phospholipid Metabolism in Apoptosis Phospholipid Metabolism in Apoptosis

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