183 postulated mechanisms of insulin resistance
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This document discusses several potential mechanisms of insulin resistance including increased levels and activity of PTP-1B, impaired phosphorylation of the insulin receptor and IRS-1, reduced PI-3 kinase activity, and attenuated insulin signaling. This leads to reduced phosphorylation of ApoB or its chaperone, enhanced stability and accelerated assembly of ApoB, and overproduction of VLDL. The document also discusses the contribution of intestinal lipoproteins to metabolic dyslipidemia in insulin resistance, and a hypothesis that fasting and postprandial hyperlipidemia in insulin resistant states may be attributable in part to intestinal oversecretion of apoB-48 containing lipoproteins.
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Plaque thermography uses a catheter with a single thermistor to measure heat levels in arteries and identify areas of plaque buildup. The technique works best in vessels with stenoses over 50% and has limitations in large vessels where the thermistor can flutter or "flail". The catheter comes in sizes from 3 to 4.5 French.
042 introducing a novel model
This document summarizes studies examining methods to track macrophage recruitment into atherosclerotic plaques. Initial EM studies in pigs found bi-directional movement of foam cells through the endothelium. Subsequent studies labeled monocytes with fluorescent dyes or microspheres and tracked their recruitment to plaques in pigs and mice. A newer method used PCR to detect transfusion of male monocytes into female mice. The presented study examined the effects of cytokines on SPIO uptake in plaques of ApoE-deficient mice, finding greater iron particle deposition in cytokine-treated mice, indicating increased monocyte recruitment. This suggests SPIO could non-invasively monitor monocyte recruitment during MRI.
035 respiratory infection of apo e ko mice
1) Acute respiratory infection caused by influenza virus led to excessive plaque inflammation in the aortas of ApoE knockout mice, implicating acute infection in triggering acute coronary events.
2) Influenza infection increased plaque inflammation and macrophage infiltration in the mice with or without plaque rupture/erosion.
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114 evaluation of atherosclerotic plaque
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Plaque thermography uses a catheter with a single thermistor to measure heat levels in arteries and identify areas of plaque buildup. The technique works best in vessels with stenoses over 50% and has limitations in large vessels where the thermistor can flutter or "flail". The catheter comes in sizes from 3 to 4.5 French.
042 introducing a novel model
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035 respiratory infection of apo e ko mice
1) Acute respiratory infection caused by influenza virus led to excessive plaque inflammation in the aortas of ApoE knockout mice, implicating acute infection in triggering acute coronary events.
2) Influenza infection increased plaque inflammation and macrophage infiltration in the mice with or without plaque rupture/erosion.
3) Further examination of infected mice tissue found polymorphic inflammatory cell infiltrates associated with platelets and fibrin near the plaques, indicating proinflammatory and procoagulant effects of acute influenza infection.
114 evaluation of atherosclerotic plaque
1. The study measured temperature, pH, and lactate levels in atherosclerotic plaques from human and animal subjects.
2. They found significant heterogeneity and variation in pH within and between plaques. Lipid-rich, inflamed areas tended to have higher temperatures and lower pH levels compared to calcified areas.
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145 intravascular elastography
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156 intravascular elastography
This document summarizes research on intravascular elastography, a technique using ultrasound to assess the mechanical properties of arterial plaques. It discusses how vulnerable plaques can be identified based on their high strain regions and mechanical properties. Studies showed elastography can detect vulnerable plaques in vitro and in animal models with high sensitivity and specificity compared to histology. Clinical studies in humans demonstrated elastography can identify high risk plaque features pre and post stenting. The technique shows potential to identify vulnerable plaques and guide treatment.
198 pulse sequences
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213 oral apo ai mimetic peptide for reduction of atherosclerosis
I. The document discusses studies on the effects of oral administration of apolipoprotein A-I mimetic peptides synthesized from D-amino acids in reducing atherosclerosis in mice. It was found to dramatically decrease lesions by 75-79% independent of changes in total or HDL cholesterol.
II. The peptide is proposed to be useful for preventing and treating atherosclerosis and other inflammatory diseases caused by oxidized lipids. Its ability to reduce lesions orally suggests potential as a therapeutic agent.
III. Further studies are referenced that examine the mechanisms of action of apo A-I and analogs in protecting against atherosclerosis through reverse cholesterol transport and removal of oxidized lipids.
507 stenosis severity and risk benefit
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1) Two studies found that coronary segments with 50-80% stenosis at baseline had higher risks of total occlusion at follow-up than segments with less severe stenosis.
2) Another study found that prior to myocardial infarction, 29% of culprit lesions showed 0-50% stenosis, while 4.1-7.9% showed 50-90% stenosis.
3) A review concluded that the majority of infarcts evolve from angiographically mild to moderate stenoses, not severe stenoses.
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210 atherosclerosis, is it an autoimmune disease
1) The document discusses evidence that atherosclerosis may be an autoimmune disease triggered by heat shock proteins (HSPs) like HSP60 and HSP70.
2) Studies in mice show these HSPs are expressed early at lesion-prone sites and by endothelial cells, then decrease in older mice with advanced lesions.
3) Macrophages and T-cells in lesions also express these HSPs, suggesting an immune response role in atherosclerosis development and progression.
218 pharmacologic stabilization of vulnerable plaque
This document discusses potential pharmacologic approaches to stabilizing vulnerable plaque. It lists various categories of drugs that may help stabilize plaque, including anti-inflammatory agents, antioxidants, lipid-lowering agents, antiplatelets, anticoagulants, anti-microbials, and drugs that target specific biological processes in plaque development like angiogenesis and MMP inhibition. The document provides examples of specific drugs within each category that have been or could be studied for plaque stabilization, such as aspirin, statins, antibiotics, vitamins C and E, and MMP inhibitors. It also discusses non-pharmacologic triggers of plaque rupture that could potentially be addressed.
250 patients with very abnormal test results
1) Clinical data confirms that coronary calcium detected by electron beam computed tomography (EBT) is found in 96% of patients presenting with or developing acute coronary syndromes, and that these patients have significantly greater coronary artery calcium scores at baseline compared to asymptomatic matched individuals.
2) Histologic studies show that coronary artery calcium occurs in all types of plaques, including stable (43%), rupture-prone (54%), and erosion-prone (77%) plaques.
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092 il18 and il18 bp in atherosclerosis
The document discusses the role of interleukin-18 (IL-18) and its binding protein (IL-18BP) in atherosclerosis. It finds that higher levels of IL-18 are associated with more unstable atherosclerotic plaques and acute coronary events. Experiments inhibiting IL-18 signaling through overexpression of IL-18BP in mice prevented atherosclerosis and produced more stable plaques with reduced macrophages, increased smooth muscle cells and collagen. The conclusion is that IL-18/IL-18BP regulation critically impacts atherosclerosis and inhibiting IL-18 may help reduce plaque progression and promote stability.
172 nir spectroscopy
This document discusses the use of near-infrared (NIR) spectroscopy to analyze atherosclerotic plaques. It provides definitions of NIR spectroscopy and describes how it allows chemical analysis of plaques. Studies are cited that have used NIR spectroscopy to detect plaque components like lipid pools, thin fibrous caps, and inflammatory cells. The document discusses both advantages and disadvantages of using NIR spectroscopy for in vivo chemical analysis of plaques. It concludes that NIR spectroscopy shows potential for identifying vulnerable plaques but questions remain about its ability to distinguish plaque types in living patients.
046 respiratory infection of apoe ko mice and plaque inflammation
1) The study investigated whether acute influenza infection could increase plaque inflammation and macrophage infiltration in atherosclerotic plaques of ApoE knockout mice, potentially triggering acute coronary events.
2) 42 ApoE mice were infected with influenza virus, and measurements were taken over 15 days before sacrifice. Infected mice showed significant weight loss.
3) Upon examination of plaques, over 1/3 of infected mice showed inflammatory infiltrates in plaques associated with platelets and fibrin, containing macrophages, smooth muscle cells, and T-lymphocytes. Further staining identified upregulation of inflammatory cytokines and receptors.
181 cholesterol independent therapeutic effects of hdl
The document discusses the therapeutic effects of high-density lipoproteins (HDL) on cardiovascular disease that are independent of cholesterol. It summarizes a study that found HDL administered before ischemia improved cardiac function recovery in rats and reduced markers of injury. The protective effects of HDL are thought to be due to anti-inflammatory, antioxidant, and anti-apoptotic properties, in addition to reversing cholesterol transport. Questions are raised about the underlying mechanisms of HDL's direct protective effects on heart tissue and whether these effects may be more important for reducing cardiovascular events than HDL's anti-atherosclerotic role.
233 cd40
CD40 and its ligand CD40L play an important role in atherosclerosis by promoting inflammation. Statins can limit the expression of CD40 and CD40L, thereby reducing inflammation. Oxidized LDL increases the expression of CD40 and CD40L on endothelial cells, smooth muscle cells, and macrophages, further promoting atherosclerosis. CD40L also contributes to thrombosis and restenosis. While CD40 does not seem to affect early plaque formation, its deficiency is associated with more stable plaques at advanced stages of atherosclerosis.
3rd vulnerable plaque rumberger 3 16-02 4
The document discusses that less obstructive plaques pose a greater risk of coronary occlusion than severely obstructed plaques due to their greater numbers. It also states that the aggregate risk of rupture from many non-significant lesions exceeds that of fewer significant lesions, so a myocardial infarction is more likely to originate from a non-significant lesion. Additionally, it explains that while electron beam tomography (EBT) cannot identify vulnerable plaques directly, it can identify vulnerable patients based on their coronary artery calcium (CAC) scores and percentile ranks, as risk increases with higher scores. EBT is also useful for estimating prognosis and tracking changes in plaque in response to treatment over time.
104 new advances in thermography
Thermography is a new technique for detecting atherosclerotic plaque vulnerability. A new catheter-based system called the Epiphany Thermography System can precisely measure plaque temperature and has shown higher temperatures in proximal versus distal plaque segments. Studies have found that greater temperature differences between segments predicts future cardiovascular events, with 86% sensitivity and 79% specificity. Preliminary research also indicates thermography may help identify vulnerable patients by measuring inflammation levels in coronary sinus blood draining the heart.
236 complement inhibitor
This document discusses the role of the complement system in the pathogenesis of atherosclerosis. It summarizes several studies that have found activation of the complement system and deposition of complement components in atherosclerotic plaques. C3 deficiency in mice is shown to result in larger lipid-positive areas and higher macrophage accumulation in plaques. The conclusion is that plaque maturation beyond early foam cell formation depends on an intact complement system, and complement activation should be considered in evaluating other inflammatory parameters associated with atherosclerosis. Complement inhibitors may have potential for preventing or stabilizing vulnerable plaques.
054 vulnerable plaques and vulnerable patients
This document outlines guidelines for defining vulnerable plaques and vulnerable patients from the Association for Eradication of Heart Attack. It discusses how atherosclerotic diseases are not limited to developed countries and are a major cause of death worldwide. Vulnerable plaques, myocardium, and hypercoagulable blood can lead to sudden cardiac death and heart attacks. The document proposes histological and clinical criteria for defining vulnerable plaques and screening methods. It also discusses diagnosing plaque inflammation, thin caps, endothelial dysfunction, and other factors at both the plaque and systemic level.
226 statins are overrated
Statins are not effective enough and their benefits are delayed. Vulnerable plaques are usually found in multiple locations. While statins may lower lipids and have anti-inflammatory effects within 6 weeks, they do not significantly reduce mortality within the first year of treatment. Over 40% of deaths in statin trials still occurred in the statin groups. Local therapies in addition to statins may be needed to stabilize vulnerable plaques and buy more time for other treatments to have an effect.
228 crp, is it a risk factor not a risk marker
This document summarizes several studies on C-reactive protein (CRP) and its role in atherosclerosis. It finds that CRP is an active player in atherosclerosis rather than just a risk marker. CRP was found to directly promote endothelial cell adhesion molecule expression, macrophage LDL uptake, and monocyte chemoattractant protein-1 secretion. Blocking CRP's effects through endothelin receptor antagonism or interleukin-6 inhibition reduced these proatherogenic effects. Therefore, CRP may directly facilitate the inflammatory process in atherosclerosis and represent a potential therapeutic target for reducing cardiovascular risk.
Adeli 21 24
1) The document discusses insulin signaling and VLDL overproduction in insulin resistance. It examines how fructose feeding impairs hepatic tyrosine phosphorylation of the insulin receptor, IRS-1, and IRS-2 in hamsters.
2) It also finds evidence for reduced PI3-kinase activity, reduced Akt phosphorylation, and enhanced PTP-1B mass and activity in fructose-fed hamsters.
3) The document shows that inhibition of cellular phosphatase activity with vanadate enhances insulin signaling, increases insulin receptor phosphorylation, reduces cellular and secreted ApoB levels, and stabilizes ApoB, reducing its secretion.
Slides 21 24
1) The document discusses insulin signaling and VLDL overproduction in insulin resistance. It examines how fructose feeding impairs hepatic tyrosine phosphorylation of the insulin receptor, IRS-1, and IRS-2 in hamsters.
2) It also finds evidence for reduced PI3-kinase activity, reduced Akt phosphorylation, and enhanced PTP-1B mass and activity in fructose-fed hamsters.
3) The document shows that inhibition of cellular phosphatase activity with vanadate enhances insulin signaling, increases insulin receptor phosphorylation, reduces cellular and secreted ApoB levels, and stabilizes ApoB, reducing its secretion.
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145 intravascular elastography
This document summarizes research on intravascular ultrasound elastography, a technique to identify vulnerable plaques. It discusses how elastography works by measuring the strain (deformation) of tissues under pressure changes. Studies found elastography could detect plaque composition like lipid pools and distinguish vulnerable plaques with high strain regions and thin fibrous caps. In vivo studies in humans and animals demonstrated elastography identified mechanically weak high risk plaques and correlated plaque strain with composition. The technique shows potential as a method to predict vulnerable plaques at high risk of rupture.
156 intravascular elastography
This document summarizes research on intravascular elastography, a technique using ultrasound to assess the mechanical properties of arterial plaques. It discusses how vulnerable plaques can be identified based on their high strain regions and mechanical properties. Studies showed elastography can detect vulnerable plaques in vitro and in animal models with high sensitivity and specificity compared to histology. Clinical studies in humans demonstrated elastography can identify high risk plaque features pre and post stenting. The technique shows potential to identify vulnerable plaques and guide treatment.
198 pulse sequences
There are three basic varieties of gradient echo pulse sequences: conventional, spoiled, and T2 enhanced. Gradient echo sequences have less T1 weighting than spin echo and more T2* effect with longer echo times. Desired contrasts include T1 with spoiled gradient echo, proton density with short echo times, and T2 with longer echo times. Artifacts include magnetic susceptibility effects and phase cancellation of water and fat. Gradient echo is useful for cartilage imaging, tumor delineation, motion studies, and MRA. Three dimensional spoiled gradient echo allows multiplanar imaging of joints.
213 oral apo ai mimetic peptide for reduction of atherosclerosis
I. The document discusses studies on the effects of oral administration of apolipoprotein A-I mimetic peptides synthesized from D-amino acids in reducing atherosclerosis in mice. It was found to dramatically decrease lesions by 75-79% independent of changes in total or HDL cholesterol.
II. The peptide is proposed to be useful for preventing and treating atherosclerosis and other inflammatory diseases caused by oxidized lipids. Its ability to reduce lesions orally suggests potential as a therapeutic agent.
III. Further studies are referenced that examine the mechanisms of action of apo A-I and analogs in protecting against atherosclerosis through reverse cholesterol transport and removal of oxidized lipids.
507 stenosis severity and risk benefit
This document discusses several studies on the relationship between stenosis severity and risks of coronary occlusion and acute coronary syndrome:
1) Two studies found that coronary segments with 50-80% stenosis at baseline had higher risks of total occlusion at follow-up than segments with less severe stenosis.
2) Another study found that prior to myocardial infarction, 29% of culprit lesions showed 0-50% stenosis, while 4.1-7.9% showed 50-90% stenosis.
3) A review concluded that the majority of infarcts evolve from angiographically mild to moderate stenoses, not severe stenoses.
4) A study on plaque rupture found that two-thirds of acute coronary disease
210 atherosclerosis, is it an autoimmune disease
1) The document discusses evidence that atherosclerosis may be an autoimmune disease triggered by heat shock proteins (HSPs) like HSP60 and HSP70.
2) Studies in mice show these HSPs are expressed early at lesion-prone sites and by endothelial cells, then decrease in older mice with advanced lesions.
3) Macrophages and T-cells in lesions also express these HSPs, suggesting an immune response role in atherosclerosis development and progression.
218 pharmacologic stabilization of vulnerable plaque
This document discusses potential pharmacologic approaches to stabilizing vulnerable plaque. It lists various categories of drugs that may help stabilize plaque, including anti-inflammatory agents, antioxidants, lipid-lowering agents, antiplatelets, anticoagulants, anti-microbials, and drugs that target specific biological processes in plaque development like angiogenesis and MMP inhibition. The document provides examples of specific drugs within each category that have been or could be studied for plaque stabilization, such as aspirin, statins, antibiotics, vitamins C and E, and MMP inhibitors. It also discusses non-pharmacologic triggers of plaque rupture that could potentially be addressed.
250 patients with very abnormal test results
1) Clinical data confirms that coronary calcium detected by electron beam computed tomography (EBT) is found in 96% of patients presenting with or developing acute coronary syndromes, and that these patients have significantly greater coronary artery calcium scores at baseline compared to asymptomatic matched individuals.
2) Histologic studies show that coronary artery calcium occurs in all types of plaques, including stable (43%), rupture-prone (54%), and erosion-prone (77%) plaques.
3) Therefore, coronary artery calcium detected by imaging is a marker of atherosclerotic plaque burden but not necessarily a marker of stable or unstable plaque, as there is considerable overlap in calcium presence between different plaque types.
092 il18 and il18 bp in atherosclerosis
The document discusses the role of interleukin-18 (IL-18) and its binding protein (IL-18BP) in atherosclerosis. It finds that higher levels of IL-18 are associated with more unstable atherosclerotic plaques and acute coronary events. Experiments inhibiting IL-18 signaling through overexpression of IL-18BP in mice prevented atherosclerosis and produced more stable plaques with reduced macrophages, increased smooth muscle cells and collagen. The conclusion is that IL-18/IL-18BP regulation critically impacts atherosclerosis and inhibiting IL-18 may help reduce plaque progression and promote stability.
172 nir spectroscopy
This document discusses the use of near-infrared (NIR) spectroscopy to analyze atherosclerotic plaques. It provides definitions of NIR spectroscopy and describes how it allows chemical analysis of plaques. Studies are cited that have used NIR spectroscopy to detect plaque components like lipid pools, thin fibrous caps, and inflammatory cells. The document discusses both advantages and disadvantages of using NIR spectroscopy for in vivo chemical analysis of plaques. It concludes that NIR spectroscopy shows potential for identifying vulnerable plaques but questions remain about its ability to distinguish plaque types in living patients.
046 respiratory infection of apoe ko mice and plaque inflammation
1) The study investigated whether acute influenza infection could increase plaque inflammation and macrophage infiltration in atherosclerotic plaques of ApoE knockout mice, potentially triggering acute coronary events.
2) 42 ApoE mice were infected with influenza virus, and measurements were taken over 15 days before sacrifice. Infected mice showed significant weight loss.
3) Upon examination of plaques, over 1/3 of infected mice showed inflammatory infiltrates in plaques associated with platelets and fibrin, containing macrophages, smooth muscle cells, and T-lymphocytes. Further staining identified upregulation of inflammatory cytokines and receptors.
181 cholesterol independent therapeutic effects of hdl
The document discusses the therapeutic effects of high-density lipoproteins (HDL) on cardiovascular disease that are independent of cholesterol. It summarizes a study that found HDL administered before ischemia improved cardiac function recovery in rats and reduced markers of injury. The protective effects of HDL are thought to be due to anti-inflammatory, antioxidant, and anti-apoptotic properties, in addition to reversing cholesterol transport. Questions are raised about the underlying mechanisms of HDL's direct protective effects on heart tissue and whether these effects may be more important for reducing cardiovascular events than HDL's anti-atherosclerotic role.
233 cd40
CD40 and its ligand CD40L play an important role in atherosclerosis by promoting inflammation. Statins can limit the expression of CD40 and CD40L, thereby reducing inflammation. Oxidized LDL increases the expression of CD40 and CD40L on endothelial cells, smooth muscle cells, and macrophages, further promoting atherosclerosis. CD40L also contributes to thrombosis and restenosis. While CD40 does not seem to affect early plaque formation, its deficiency is associated with more stable plaques at advanced stages of atherosclerosis.
3rd vulnerable plaque rumberger 3 16-02 4
The document discusses that less obstructive plaques pose a greater risk of coronary occlusion than severely obstructed plaques due to their greater numbers. It also states that the aggregate risk of rupture from many non-significant lesions exceeds that of fewer significant lesions, so a myocardial infarction is more likely to originate from a non-significant lesion. Additionally, it explains that while electron beam tomography (EBT) cannot identify vulnerable plaques directly, it can identify vulnerable patients based on their coronary artery calcium (CAC) scores and percentile ranks, as risk increases with higher scores. EBT is also useful for estimating prognosis and tracking changes in plaque in response to treatment over time.
104 new advances in thermography
Thermography is a new technique for detecting atherosclerotic plaque vulnerability. A new catheter-based system called the Epiphany Thermography System can precisely measure plaque temperature and has shown higher temperatures in proximal versus distal plaque segments. Studies have found that greater temperature differences between segments predicts future cardiovascular events, with 86% sensitivity and 79% specificity. Preliminary research also indicates thermography may help identify vulnerable patients by measuring inflammation levels in coronary sinus blood draining the heart.
236 complement inhibitor
This document discusses the role of the complement system in the pathogenesis of atherosclerosis. It summarizes several studies that have found activation of the complement system and deposition of complement components in atherosclerotic plaques. C3 deficiency in mice is shown to result in larger lipid-positive areas and higher macrophage accumulation in plaques. The conclusion is that plaque maturation beyond early foam cell formation depends on an intact complement system, and complement activation should be considered in evaluating other inflammatory parameters associated with atherosclerosis. Complement inhibitors may have potential for preventing or stabilizing vulnerable plaques.
054 vulnerable plaques and vulnerable patients
This document outlines guidelines for defining vulnerable plaques and vulnerable patients from the Association for Eradication of Heart Attack. It discusses how atherosclerotic diseases are not limited to developed countries and are a major cause of death worldwide. Vulnerable plaques, myocardium, and hypercoagulable blood can lead to sudden cardiac death and heart attacks. The document proposes histological and clinical criteria for defining vulnerable plaques and screening methods. It also discusses diagnosing plaque inflammation, thin caps, endothelial dysfunction, and other factors at both the plaque and systemic level.
226 statins are overrated
Statins are not effective enough and their benefits are delayed. Vulnerable plaques are usually found in multiple locations. While statins may lower lipids and have anti-inflammatory effects within 6 weeks, they do not significantly reduce mortality within the first year of treatment. Over 40% of deaths in statin trials still occurred in the statin groups. Local therapies in addition to statins may be needed to stabilize vulnerable plaques and buy more time for other treatments to have an effect.
228 crp, is it a risk factor not a risk marker
This document summarizes several studies on C-reactive protein (CRP) and its role in atherosclerosis. It finds that CRP is an active player in atherosclerosis rather than just a risk marker. CRP was found to directly promote endothelial cell adhesion molecule expression, macrophage LDL uptake, and monocyte chemoattractant protein-1 secretion. Blocking CRP's effects through endothelin receptor antagonism or interleukin-6 inhibition reduced these proatherogenic effects. Therefore, CRP may directly facilitate the inflammatory process in atherosclerosis and represent a potential therapeutic target for reducing cardiovascular risk.
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181 cholesterol independent therapeutic effects of hdl
181 cholesterol independent therapeutic effects of hdl
Similar to 183 postulated mechanisms of insulin resistance
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1) The document discusses insulin signaling and VLDL overproduction in insulin resistance. It examines how fructose feeding impairs hepatic tyrosine phosphorylation of the insulin receptor, IRS-1, and IRS-2 in hamsters.
2) It also finds evidence for reduced PI3-kinase activity, reduced Akt phosphorylation, and enhanced PTP-1B mass and activity in fructose-fed hamsters.
3) The document shows that inhibition of cellular phosphatase activity with vanadate enhances insulin signaling, increases insulin receptor phosphorylation, reduces cellular and secreted ApoB levels, and stabilizes ApoB, reducing its secretion.
Slides 21 24
1) The document discusses insulin signaling and VLDL overproduction in insulin resistance. It examines how fructose feeding impairs hepatic tyrosine phosphorylation of the insulin receptor, IRS-1, and IRS-2 in hamsters.
2) It also finds evidence for reduced PI3-kinase activity, reduced Akt phosphorylation, and enhanced PTP-1B mass and activity in fructose-fed hamsters.
3) The document shows that inhibition of cellular phosphatase activity with vanadate enhances insulin signaling, increases insulin receptor phosphorylation, reduces cellular and secreted ApoB levels, and stabilizes ApoB, reducing its secretion.
170 insulin signaling & vldl overproduction
1) The document discusses insulin signaling and VLDL overproduction in insulin resistance. It examines how fructose feeding impairs tyrosine phosphorylation of the insulin receptor, IRS-1, and IRS-2 in hepatocytes, reducing PI3-kinase activity and Akt phosphorylation while enhancing PTP-1B mass and activity.
2) It also finds that inhibition of cellular phosphatase activity with vanadate enhances insulin signaling and reduces ApoB secretion from hepatocytes by increasing insulin receptor phosphorylation, stabilizing cellular ApoB levels, and decreasing ApoB secretion.
3) The findings provide evidence that impaired insulin signaling and reduced PI3-kinase activity contribute to overproduction of VLDL in
170 insulin signaling & vldl overproduction
1) The document discusses insulin signaling and VLDL overproduction in insulin resistance. It examines how fructose feeding impairs hepatic tyrosine phosphorylation of the insulin receptor, IRS-1, and IRS-2 in hamsters.
2) It also finds evidence for reduced PI3-kinase activity, reduced Akt phosphorylation, and enhanced PTP-1B mass and activity in fructose-fed hamsters.
3) The document shows that inhibition of cellular phosphatase activity with vanadate enhances insulin signaling, increases insulin receptor phosphorylation, reduces cellular and secreted ApoB levels, and stabilizes ApoB, reducing its secretion.
Slides2124
1) The document discusses insulin signaling and VLDL overproduction in insulin resistance. It notes that insulin signaling activates the PI3-kinase pathway leading to Akt phosphorylation and VLDL assembly.
2) Data is presented showing impaired hepatic tyrosine phosphorylation of the insulin receptor, IRS-1, and IRS-2 in fructose-fed hamsters compared to controls. This provides evidence of reduced insulin signaling.
3) Additional data demonstrates reduced PI3-kinase activity, reduced Akt phosphorylation, and enhanced PTP-1B mass and activity in fructose-fed hamsters, suggesting disrupted insulin signaling.
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Glycolysis .pptx
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3) Insulin is now primarily produced through recombinant DNA technology allowing for the mass production of human insulin to treat diabetes.
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Insulin resistance causes and consequences
Insulin resistance is caused by decreased biological response to normal insulin levels and is often seen with conditions like diabetes, metabolic syndrome, obesity, and pregnancy. It can cause an inability to focus, increased hunger, weight gain, and high blood pressure. Insulin resistance is associated with increased insulin production by the pancreas and can lead to diabetes, cardiovascular disease, and other health issues. It involves defects in insulin signaling pathways involving proteins like PKB, IRS, and PI3 kinase. Treatment involves lifestyle changes and medications to lower blood sugar and insulin levels.
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The document discusses pancreatic hormones and insulin. It describes the four main cell types in the islets of Langerhans and the hormones they secrete, including insulin secreted by beta cells. Insulin was discovered in 1921 and contains two polypeptide chains connected by disulfide bonds. Insulin regulates glucose levels by facilitating glucose transport and storage and inhibiting gluconeogenesis. Various insulin preparations are discussed, from conventional insulin to highly purified pork insulin to human insulin produced through recombinant DNA technology to analogues like insulin lispro and glargine which have altered pharmacokinetic properties.
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This document discusses glycogen storage disorders (GSDs), which are caused by defects in glycogen metabolism. It describes the various enzymes involved and the biochemical tests used to diagnose different types of GSDs. Predominantly hepatic GSDs include defects in glucose-6-phosphatase (GSD I), debranching enzyme (GSD III), branching enzyme (GSD IV) and phosphorylase (GSD VI, IX). Muscle-affecting GSDs involve acid α-glucosidase deficiency (GSD II/Pompe disease), muscle phosphorylase (GSD V), and muscle phosphofructokinase (GSD VII). Diagnosis involves tests on red blood cells
Slides18
This document discusses metabolic dyslipidemia in insulin resistant states. It provides an overview of insulin resistance and its biological manifestations. It also summarizes recent observations from a animal model showing evidence of hepatic VLDL overproduction, hepatic insulin resistance, and intestinal lipoprotein overproduction in insulin resistant states. Putative candidate genes involved in insulin resistance and its effects on glucose and lipid metabolism are listed. Features of metabolic dyslipidemia such as hypertriglyceridemia, reduced HDL, and small dense LDL particles are described. Mechanisms of increased VLDL production in the liver during insulin resistance are also summarized.
201 metabolic dyslipidemia
This document discusses metabolic dyslipidemia in insulin resistant states. It provides an overview of insulin resistance and its biological manifestations. It also summarizes recent observations from a animal model showing evidence of hepatic VLDL overproduction, hepatic insulin resistance, and intestinal lipoprotein overproduction in insulin resistant states. Putative candidate genes involved in insulin resistance and its effects on glucose and lipid metabolism are listed. Features of metabolic dyslipidemia such as hypertriglyceridemia, reduced HDL, and small dense LDL particles are described. Mechanisms of increased VLDL production in the liver under insulin resistant conditions are also summarized.
201 metabolic dyslipidemia
This document discusses metabolic dyslipidemia in insulin resistant states. It provides an overview of insulin resistance and its biological manifestations. It also summarizes recent observations from a animal model showing evidence of hepatic VLDL overproduction, hepatic insulin resistance, and intestinal lipoprotein overproduction in insulin resistant states. Putative candidate genes involved in insulin resistance and its effects on glucose and lipid metabolism are listed. Features of metabolic dyslipidemia such as hypertriglyceridemia, reduced HDL, and small dense LDL particles are described. Mechanisms of increased VLDL production in the liver under insulin resistant conditions are also summarized.
Adeli 1 8
This document discusses metabolic dyslipidemia in insulin resistant states. It provides an overview of insulin resistance and its biological manifestations. It also summarizes recent observations from a animal model showing evidence of hepatic VLDL overproduction, hepatic insulin resistance, and intestinal lipoprotein overproduction in insulin resistant states. Putative candidate genes involved in insulin resistance and its effects on glucose and lipid metabolism are listed. Features of metabolic dyslipidemia such as hypertriglyceridemia, reduced HDL, and small dense LDL particles are described. Mechanisms of increased VLDL production in the liver under insulin resistant conditions are also summarized.
Slides 1 8
This document discusses metabolic dyslipidemia in insulin resistant states. It provides an overview of insulin resistance and its biological manifestations. It also summarizes recent observations from a animal model showing evidence of hepatic VLDL overproduction, hepatic insulin resistance, and intestinal lipoprotein overproduction in insulin resistant states. Putative candidate genes involved in insulin resistance and its effects on glucose and lipid metabolism are listed. Features of metabolic dyslipidemia such as hypertriglyceridemia, reduced HDL, and small dense LDL particles are described. Mechanisms of increased VLDL production in the liver under insulin resistant conditions are also summarized.
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Zahi A. Fayad is an Associate Professor who studies molecular imaging of atherosclerosis using MRI. His research focuses on developing targeted contrast agents to noninvasively detect unstable plaque. Some agents under investigation include annexin A5 labeled with a radioisotope to detect apoptosis, FDG-PET to assess plaque activity, and fibrin-targeted and MMP-targeting Gd-based contrasts. Additional work involves lipid-based particulate agents using reconstituted HDL or iron oxide nanoparticles. The goal is to improve MRI detection sensitivity and specificity for high-risk plaque characterization.
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183 postulated mechanisms of insulin resistance
- 1. Postulated Mechanisms of Insulin ResistancePostulated Mechanisms of Insulin Resistance PTP-1BPTP-1B Mass & ActivityMass & Activity Impaired Phosphorylation ofImpaired Phosphorylation of Insulin Receptor, IRS-1Insulin Receptor, IRS-1 PI-3 Kinase ActivityPI-3 Kinase Activity Attenuated Insulin SignalingAttenuated Insulin Signaling Reduced Phosphorylation of ApoB orReduced Phosphorylation of ApoB or an apoB-chaperonean apoB-chaperone Enhanced Stability and Accelerated Assembly of ApoBEnhanced Stability and Accelerated Assembly of ApoB Overproduction of VLDLOverproduction of VLDL ER-60MTP
- 2. Intestine Contribution of the Intestinal LipoproteinsContribution of the Intestinal Lipoproteins to Metabolic Dyslipidemia in Insulin Resistanceto Metabolic Dyslipidemia in Insulin Resistance Liver ApoB48 ApoB100 Intestinal Lipoprotein Metabolism
- 3. DietaryDietary CholesterolCholesterol DietaryDietary FatFat LuminalLuminal TriglycerideTriglyceride LipasesLipases Bile AcidsBile Acids Fatty AcidsFatty Acids Mocellar CholesterolMocellar Cholesterol Fatty AcidsFatty Acids CholrdyrtolCholrdyrtol ApoB48 + TG + CEApoB48 + TG + CE TGTG CMCM ABCA1ABCA1 ABCG5ABCG5 ABCG8ABCG8 Fatty Acid TransportersFatty Acid Transporters Intestinal Epithelial CellIntestinal Epithelial Cell (Intake)(Intake) (Uptake)(Uptake) (Chylomicron(Chylomicron Assembly)Assembly) (Cholesterol(Cholesterol Excretion)Excretion) Intestinal Lipid Absorption (Trigleride(Trigleride Synthesis)Synthesis)
- 4. Hypothesis III: Fasting and postprandial hyperlipidemia in insulin resistant states may be attributable in part to intestinal oversecretion of apoB-48 containing lipoproteins Experimental Approach: • Dietary induction of an insulin resistant state in the hamster by high fructose feeding • Isolation of adult viable villi from Syrian hamster small intestine. • -In Vivo Studies to assess production rate of intestinal (apoB48- containing) lipoproteins • -Ex Vivo Studies to assess intestinal apoB48 lipoprotein synthesis and secretion, mechanisms of chylomicron assembly, role of de novo lipogenesis in intestinal lipoprotein secretion in the fasting and postprandial states
Editor's Notes
- Key point: The process of cholesterol absorption is complex and currently only partly understood. Cholesterol absorption is a complex, multistep process. Methods of affecting these processes include reducing dietary cholesterol by decreasing intake. Bile acid sequestrants such as cholestyramine and colestipol bind to bile acids, blocking their normal resorption. This increases bile acid excretion resulting in a net cholesterol loss.4,10 The packaging of cholesterol in micelles can be reduced through the use of plant stanol esters, such as sitostanol. These esters are structurally similar to cholesterol and competitively compete with cholesterol for incorporation into micelles.2,5,11,12 Since cholesterol must be packaged in micelles in order to cross the basement membrane of enterocytes, this effectively decreases cholesterol uptake and increases cholesterol secretion. ABCG5 and ABCG8 are proteins involved in sterol excretion.13 ABCA1 is up-regulated by cellular cholesterol and functions to transport cholesterol out of the cell.7-9