niacin has been researched along with Disease Exacerbation in 30 studies
Niacin: A water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is required by the body for the formation of coenzymes NAD and NADP. It has PELLAGRA-curative, vasodilating, and antilipemic properties.
vitamin B3 : Any member of a group of vitamers that belong to the chemical structural class called pyridines that exhibit biological activity against vitamin B3 deficiency. Vitamin B3 deficiency causes a condition known as pellagra whose symptoms include depression, dermatitis and diarrhea. The vitamers include nicotinic acid and nicotinamide (and their ionized and salt forms).
nicotinic acid : A pyridinemonocarboxylic acid that is pyridine in which the hydrogen at position 3 is replaced by a carboxy group.
| Excerpt | Relevance | Reference |
|---|---|---|
| "The change in logarithmic reactive hyperemia index between 1 month and 12 months was similar in patients receiving ER-niacin vs placebo (0." | 6.80 | Effect of Extended-Release Niacin on Carotid Intima Media Thickness, Reactive Hyperemia, and Endothelial Progenitor Cell Mobilization: Insights From the Atherosclerosis Lesion Progression Intervention Using Niacin Extended Release in Saphenous Vein Grafts ( Abdurrahim, G; Banerjee, S; Brilakis, ES; Chao, H; Christopoulos, G; Coleman, A; de Lemos, JA; Guerra, A; Han, H; Kotsia, A; McGuire, DK; Packer, M; Rangan, BV; Roesle, M; Sosa, A; Xu, H, 2015) |
| "Niacin-treated subjects compared to untreated subjects had significantly less change in mean coronary stenosis (0." | 6.78 | Effects of niacin on glucose levels, coronary stenosis progression, and clinical events in subjects with normal baseline glucose levels (<100 mg/dl): a combined analysis of the Familial Atherosclerosis Treatment Study (FATS), HDL-Atherosclerosis Treatment ( Brown, BG; Isquith, D; Muñoz, L; Phan, BA; Shadzi, P; Triller, M; Zhao, XQ, 2013) |
| "Niacin treatment to rats with preexisting hepatic steatosis induced by the HF diet significantly regressed steatosis." | 5.40 | Therapeutic role of niacin in the prevention and regression of hepatic steatosis in rat model of nonalcoholic fatty liver disease. ( Ganji, SH; Kamanna, VS; Kashyap, ML; Kukes, GD; Lambrecht, N, 2014) |
| "We examined the effects of simvastatin-niacin and antioxidant vitamins on changes in high-density lipoprotein (HDL) subpopulations and alterations in coronary artery stenosis, as assessed by angiography." | 5.10 | Change in alpha1 HDL concentration predicts progression in coronary artery stenosis. ( Asztalos, BF; Batista, M; Brown, GB; Cox, CE; Dallal, GE; Horvath, KV; Morse, JS; Schaefer, EJ, 2003) |
| "The use of FDA-approved niacin (nicotinic acid or vitamin B3) formulations at therapeutic doses, alone or in combination with statins or other lipid therapies, is safe, improves multiple lipid parameters, and reduces atherosclerosis progression." | 4.88 | Niacin: the evidence, clinical use, and future directions. ( Gore, RS; Kim, AS; Taylor, AJ; Villines, TC, 2012) |
| "Nicotinic acid (niacin) is a drug used to reduce the progression of atherosclerosis." | 3.77 | Nicotinic acid inhibits progression of atherosclerosis in mice through its receptor GPR109A expressed by immune cells. ( Gille, A; Kero, J; Lukasova, M; Malaval, C; Offermanns, S, 2011) |
| "The change in logarithmic reactive hyperemia index between 1 month and 12 months was similar in patients receiving ER-niacin vs placebo (0." | 2.80 | Effect of Extended-Release Niacin on Carotid Intima Media Thickness, Reactive Hyperemia, and Endothelial Progenitor Cell Mobilization: Insights From the Atherosclerosis Lesion Progression Intervention Using Niacin Extended Release in Saphenous Vein Grafts ( Abdurrahim, G; Banerjee, S; Brilakis, ES; Chao, H; Christopoulos, G; Coleman, A; de Lemos, JA; Guerra, A; Han, H; Kotsia, A; McGuire, DK; Packer, M; Rangan, BV; Roesle, M; Sosa, A; Xu, H, 2015) |
| "Niacin-treated subjects compared to untreated subjects had significantly less change in mean coronary stenosis (0." | 2.78 | Effects of niacin on glucose levels, coronary stenosis progression, and clinical events in subjects with normal baseline glucose levels (<100 mg/dl): a combined analysis of the Familial Atherosclerosis Treatment Study (FATS), HDL-Atherosclerosis Treatment ( Brown, BG; Isquith, D; Muñoz, L; Phan, BA; Shadzi, P; Triller, M; Zhao, XQ, 2013) |
| "Niacin was the first hypolipidemic drug to significantly reduce both major cardiovascular events and mortality in patients with cardiovascular disease." | 2.53 | Pleiotropic effects of niacin: Current possibilities for its clinical use. ( Hrib, J; Hromádka, R; Perlík, F; Širc, J; Staňková, B; Tvrzická, E; Vecka, M; Žák, A; Zeman, M, 2016) |
| "Niacin has a favorable unique impact on factors affecting the rate of glomerular filtration rate decline, including high-density lipoprotein (HDL) particle number and function, triglyceride levels, oxidant stress, inflammation and endothelial function, and lowering of serum phosphorus levels by reducing dietary phosphorus absorption in the gastrointestinal tract." | 2.52 | Niacin and progression of CKD. ( Kalantar-Zadeh, K; Kashyap, ML; Kovesdy, CP; Moradi, H; Streja, DA; Streja, E, 2015) |
| "Niacin has been shown to regress atherosclerosis when used as monotherapy, in combination with a statin, and in combination with nonstatin therapies (including cholesterol-binding resins) and fibrates." | 2.44 | Evidence to support aggressive management of high-density lipoprotein cholesterol: implications of recent imaging trials. ( Taylor, AJ, 2008) |
| "Treatment of dyslipidemia to prevent CHD depends on the pattern and severity of dyslipidemia, the presence of overt CHD, and the patient's response to diet." | 2.40 | Perspectives in the treatment of dyslipidemias in the prevention of coronary heart disease. ( Borgia, MC; Medici, F, 1998) |
| "Recent studies suggest that treating dyslipidemia in persons with coronary atherosclerosis may decrease morbidity and mortality." | 2.39 | Number-needed-to-treat analysis of the prevention of myocardial infarction and death by antidyslipidemic therapy. ( Rembold, CM, 1996) |
| "Niacin serves as a high-affinity ligand for the receptor HCAR2 (GPR109A)." | 1.72 | The niacin receptor HCAR2 modulates microglial response and limits disease progression in a mouse model of Alzheimer's disease. ( Casali, BT; Coronel, I; Lamb, BT; Landreth, GE; Lasagna-Reeves, CA; Lin, PB; Martinez, P; Moutinho, M; Oblak, AL; Puntambekar, SS; Tsai, AP, 2022) |
| "Niacin treatment to rats with preexisting hepatic steatosis induced by the HF diet significantly regressed steatosis." | 1.40 | Therapeutic role of niacin in the prevention and regression of hepatic steatosis in rat model of nonalcoholic fatty liver disease. ( Ganji, SH; Kamanna, VS; Kashyap, ML; Kukes, GD; Lambrecht, N, 2014) |
| "Lipodystrophy is defined as the defective metabolism of fat, and it is characterized by distinct physical changes, such as an increased waist size or an accumulation of fatty tissue at the base of the neck." | 1.30 | Update on lipodystrophy. ( Gaucher, M, 1999) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 3 (10.00) | 18.2507 |
| 2000's | 14 (46.67) | 29.6817 |
| 2010's | 12 (40.00) | 24.3611 |
| 2020's | 1 (3.33) | 2.80 |
| Authors | Studies |
|---|---|
| Moutinho, M | 1 |
| Puntambekar, SS | 1 |
| Tsai, AP | 1 |
| Coronel, I | 1 |
| Lin, PB | 1 |
| Casali, BT | 1 |
| Martinez, P | 1 |
| Oblak, AL | 1 |
| Lasagna-Reeves, CA | 1 |
| Lamb, BT | 1 |
| Landreth, GE | 1 |
| Santidrian, AF | 1 |
| Matsuno-Yagi, A | 1 |
| Ritland, M | 1 |
| Seo, BB | 1 |
| LeBoeuf, SE | 1 |
| Gay, LJ | 1 |
| Yagi, T | 1 |
| Felding-Habermann, B | 1 |
| Ganji, SH | 1 |
| Kukes, GD | 1 |
| Lambrecht, N | 1 |
| Kashyap, ML | 2 |
| Kamanna, VS | 2 |
| Streja, E | 1 |
| Kovesdy, CP | 1 |
| Streja, DA | 1 |
| Moradi, H | 1 |
| Kalantar-Zadeh, K | 1 |
| Kotsia, AP | 1 |
| Rangan, BV | 2 |
| Christopoulos, G | 2 |
| Coleman, A | 2 |
| Roesle, M | 2 |
| Cipher, D | 1 |
| de Lemos, JA | 2 |
| McGuire, DK | 2 |
| Packer, M | 2 |
| Banerjee, S | 2 |
| Brilakis, ES | 2 |
| Guerra, A | 1 |
| Xu, H | 1 |
| Kotsia, A | 1 |
| Sosa, A | 1 |
| Chao, H | 1 |
| Han, H | 1 |
| Abdurrahim, G | 1 |
| Zeman, M | 1 |
| Vecka, M | 1 |
| Perlík, F | 1 |
| Staňková, B | 1 |
| Hromádka, R | 1 |
| Tvrzická, E | 1 |
| Širc, J | 1 |
| Hrib, J | 1 |
| Žák, A | 1 |
| Robinson, JG | 1 |
| Linke, A | 1 |
| Sonnabend, M | 1 |
| Fasshauer, M | 1 |
| Höllriegel, R | 1 |
| Schuler, G | 1 |
| Niebauer, J | 1 |
| Stumvoll, M | 1 |
| Blüher, M | 1 |
| Avis, HJ | 1 |
| Vissers, MN | 1 |
| Wijburg, FA | 1 |
| Kastelein, JJ | 1 |
| Hutten, BA | 1 |
| Cho, KH | 1 |
| Kim, HJ | 1 |
| Vaziri, ND | 1 |
| Lee, JM | 1 |
| Choudhury, RP | 1 |
| Lukasova, M | 1 |
| Malaval, C | 1 |
| Gille, A | 1 |
| Kero, J | 1 |
| Offermanns, S | 1 |
| Villines, TC | 1 |
| Kim, AS | 1 |
| Gore, RS | 1 |
| Taylor, AJ | 2 |
| Phan, BA | 1 |
| Muñoz, L | 1 |
| Shadzi, P | 1 |
| Isquith, D | 1 |
| Triller, M | 1 |
| Brown, BG | 2 |
| Zhao, XQ | 1 |
| Hecht, HS | 1 |
| Harman, SM | 1 |
| Asztalos, BF | 1 |
| Batista, M | 1 |
| Horvath, KV | 1 |
| Cox, CE | 1 |
| Dallal, GE | 1 |
| Morse, JS | 1 |
| Brown, GB | 1 |
| Schaefer, EJ | 1 |
| Kuvin, JT | 1 |
| Karas, RH | 1 |
| Whitney, EJ | 1 |
| Krasuski, RA | 1 |
| Personius, BE | 1 |
| Michalek, JE | 1 |
| Maranian, AM | 1 |
| Kolasa, MW | 1 |
| Monick, E | 1 |
| Gotto, AM | 1 |
| Wierzbicki, AS | 1 |
| Athanasiadis, I | 1 |
| Konstantinidis, A | 1 |
| Kyprianou, I | 1 |
| Robinson, R | 1 |
| Moschou, V | 1 |
| Kouzi-Koliakos, K | 1 |
| Rembold, CM | 1 |
| Borgia, MC | 1 |
| Medici, F | 1 |
| Mack, WJ | 2 |
| Xiang, M | 1 |
| Selzer, RH | 2 |
| Hodis, HN | 2 |
| LaBree, L | 1 |
| Liu, C | 1 |
| Chesney, CM | 1 |
| Elam, MB | 1 |
| Herd, JA | 1 |
| Davis, KB | 1 |
| Garg, R | 1 |
| Hunninghake, D | 1 |
| Kennedy, JW | 1 |
| Applegate, WB | 1 |
| Gaucher, M | 1 |
| Kapas, I | 1 |
| Majtenyi, K | 1 |
| Törö, K | 1 |
| Keller, E | 1 |
| Voigtländer, T | 1 |
| Kovacs, GG | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Effect of Alirocumab on Saphenous Vein Graft Atherosclerosis: The Alirocumab for Stopping Atherosclerosis Progression in Saphenous Vein Grafts (ASAP-SVG) Pilot Trial[NCT03542110] | Phase 4 | 46 participants (Actual) | Interventional | 2018-08-04 | Terminated (stopped due to Withdrawal of medication and funding support by Sponsor) | ||
| Effect of Extended-Release Niacin on Saphenous Vein Graft Atherosclerosis: The Atherosclerosis Lesion Progression Intervention Using Niacin Extended Release in Saphenous Vein Grafts (ALPINE-SVG) Pilot Trial[NCT01221402] | Phase 2 | 38 participants (Actual) | Interventional | 2010-10-31 | Completed | ||
| Carotid Plaque Composition by Magnetic Resonance Imaging During Lipid Lowering Therapy[NCT00715273] | Phase 4 | 217 participants (Actual) | Interventional | 2001-05-01 | Completed | ||
| Heartmatters Challenge - First Responders[NCT03322046] | 185 participants (Actual) | Observational | 2013-10-08 | Completed | |||
| High Density Lipoprotein Subspecies and Coronary Disease[NCT00005676] | 2,700 participants (Actual) | Observational | 2000-04-30 | Completed | |||
| Randomized, Double-blind, Placebo-controlled Trial of Niaspan® in Patients With Overt Diabetic Nephropathy and Moderate Renal Impairment[NCT00108485] | Phase 3 | 9 participants (Actual) | Interventional | 2005-04-30 | Terminated (stopped due to Unable to recruit sufficient study subjects) | ||
| Correlates of Angiographic Changes and Coronary Events: The Cholesterol-Lowering Atherosclerosis Study (CLAS)[NCT00005433] | 188 participants (Actual) | Observational | 1996-04-30 | Completed | |||
| [NCT00000539] | Phase 3 | 0 participants | Interventional | 1992-09-30 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
"The primary endpoint of this study is carotid plaque lipid composition identified by MRI. The determination of plaque lipid content for each carotid artery will be performed using the automated interactive system. These measurements will be performed from the MRI scans at four time points blinded to time sequence of MRI examinations, patient treatment, lipid levels and clinical course.~Volume Measurements: Contours were placed around the lumen, outer-wall boundaries, and plaque features of carotid artery. (Arterial wall area) = (outer-wall area) - (lumen area). Volume calculated as: area x 2 mm (slice thickness). Tissue volume/wall volume x (100%) is presented as percentage. Annualized change presented mm^3/year (for volume) and as percentage change/year." (NCT00715273)
Timeframe: Measured at Years 1, 2, and 3
| Intervention | mm^3/year (Mean) |
|---|---|
| 1 - Single Therapy Group | -4.6 |
| 2 - Double Therapy Group | -15.1 |
| 3 - Triple Therapy Group | -9.4 |
"The primary endpoint of this study is carotid plaque lipid composition identified by MRI. The determination of plaque lipid content for each carotid artery will be performed using the automated interactive system. These measurements will be performed from the MRI scans at four time points blinded to time sequence of MRI examinations, patient treatment, lipid levels and clinical course.~Volume Measurements: Contours were placed around the lumen, outer-wall boundaries, and plaque features of carotid artery. (Arterial wall area) = (outer-wall area) - (lumen area). Volume calculated as: area x 2 mm (slice thickness). Tissue volume/wall volume x (100%) is presented as percentage. Annualized change presented mm^3/year (for volume) and as percentage change/year." (NCT00715273)
Timeframe: Measured at Years 1, 2, and 3
| Intervention | percentage change/year (Mean) | |
|---|---|---|
| LRNC change | Wall Volume change | |
| 1 - Single Therapy Group | -1.6 | -0.6 |
| 2 - Double Therapy Group | -3.6 | -1.4 |
| 3 - Triple Therapy Group | -2.8 | -1.2 |
Any cardiovascular events such as death from any cause, nonfatal myocardial infarction, stroke, and revascularization procedures (PCI or CABG) due to unstable ischemia will be recorded and verified. (NCT00715273)
Timeframe: Measured at Years 3, 4, and 5
| Intervention | Participants (Count of Participants) | ||
|---|---|---|---|
| Composite Measured at Year 3 | Composite Measured at Year 4 (cumulative) | Composite Measured at Year 5 (cumulative) | |
| 1 - Single Therapy Group | 6 | 7 | 9 |
| 2 - Double Therapy Group | 6 | 11 | 11 |
| 3 - Triple Therapy Group | 7 | 9 | 9 |
(NCT00108485)
Timeframe: Baseline, 1 year
| Intervention | mg/dL (Number) |
|---|---|
| Extended Release Niacin | 42 |
| Placebo | 63 |
11 reviews available for niacin and Disease Exacerbation
| Article | Year |
|---|---|
Niacin and progression of CKD.
Topics: Comorbidity; Coronary Artery Disease; Disease Progression; Endothelium, Vascular; Humans; Hypolipide | 2015 |
Pleiotropic effects of niacin: Current possibilities for its clinical use.
Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Atherosclerosis; Disease Progression | 2016 |
LDL reduction: how low should we go and is it safe?
Topics: Allylamine; Anticholesteremic Agents; Azetidines; Cholesterol, LDL; Colesevelam Hydrochloride; Coron | 2008 |
The use of lipid-lowering drug therapy in children and adolescents.
Topics: Adolescent; Atherosclerosis; Azetidines; Bile Acids and Salts; Cardiovascular Diseases; Child; Chole | 2009 |
Atherosclerosis regression and high-density lipoproteins.
Topics: Animals; Atherosclerosis; Cholesterol Ester Transfer Proteins; Disease Progression; Humans; Hypolipi | 2010 |
Niacin: the evidence, clinical use, and future directions.
Topics: Atherosclerosis; Disease Progression; Dyslipidemias; Humans; Hypolipidemic Agents; Lipids; Niacin | 2012 |
The effects of LDL reduction and HDL augmentation on physiologic and inflammatory markers.
Topics: Arteriosclerosis; Biomarkers; C-Reactive Protein; Cholesterol, HDL; Cholesterol, LDL; Disease Progre | 2003 |
Have we forgotten the pivotal role of high-density lipoprotein cholesterol in atherosclerosis prevention?
Topics: Arteriosclerosis; Cholesterol, HDL; Clofibric Acid; Coronary Artery Disease; Disease Progression; Hu | 2005 |
Evidence to support aggressive management of high-density lipoprotein cholesterol: implications of recent imaging trials.
Topics: Anticholesteremic Agents; Cholesterol, HDL; Clofibric Acid; Coronary Artery Disease; Disease Progres | 2008 |
Number-needed-to-treat analysis of the prevention of myocardial infarction and death by antidyslipidemic therapy.
Topics: Coronary Angiography; Coronary Artery Disease; Disease Progression; Female; Humans; Hydroxymethylglu | 1996 |
Perspectives in the treatment of dyslipidemias in the prevention of coronary heart disease.
Topics: Cholesterol; Cholesterol, HDL; Cholesterol, LDL; Combined Modality Therapy; Coronary Artery Disease; | 1998 |
9 trials available for niacin and Disease Exacerbation
| Article | Year |
|---|---|
Effect of Extended-Release Niacin on Saphenous Vein Graft Atherosclerosis: Insights from the Atherosclerosis Lesion Progression Intervention Using Niacin Extended Release in Saphenous Vein Grafts (ALPINE-SVG) Pilot Trial.
Topics: Aged; Atherosclerosis; Coronary Angiography; Coronary Artery Bypass; Coronary Stenosis; Delayed-Acti | 2015 |
Effect of Extended-Release Niacin on Saphenous Vein Graft Atherosclerosis: Insights from the Atherosclerosis Lesion Progression Intervention Using Niacin Extended Release in Saphenous Vein Grafts (ALPINE-SVG) Pilot Trial.
Topics: Aged; Atherosclerosis; Coronary Angiography; Coronary Artery Bypass; Coronary Stenosis; Delayed-Acti | 2015 |
Effect of Extended-Release Niacin on Saphenous Vein Graft Atherosclerosis: Insights from the Atherosclerosis Lesion Progression Intervention Using Niacin Extended Release in Saphenous Vein Grafts (ALPINE-SVG) Pilot Trial.
Topics: Aged; Atherosclerosis; Coronary Angiography; Coronary Artery Bypass; Coronary Stenosis; Delayed-Acti | 2015 |
Effect of Extended-Release Niacin on Saphenous Vein Graft Atherosclerosis: Insights from the Atherosclerosis Lesion Progression Intervention Using Niacin Extended Release in Saphenous Vein Grafts (ALPINE-SVG) Pilot Trial.
Topics: Aged; Atherosclerosis; Coronary Angiography; Coronary Artery Bypass; Coronary Stenosis; Delayed-Acti | 2015 |
Effect of Extended-Release Niacin on Carotid Intima Media Thickness, Reactive Hyperemia, and Endothelial Progenitor Cell Mobilization: Insights From the Atherosclerosis Lesion Progression Intervention Using Niacin Extended Release in Saphenous Vein Grafts
Topics: Aged; Atherosclerosis; Carotid Arteries; Carotid Intima-Media Thickness; Coronary Artery Disease; De | 2015 |
Effects of extended-release niacin on lipid profile and adipocyte biology in patients with impaired glucose tolerance.
Topics: Adipocytes; Adipose Tissue; Adult; Cholesterol, HDL; Cholesterol, LDL; Delayed-Action Preparations; | 2009 |
Effects of niacin on glucose levels, coronary stenosis progression, and clinical events in subjects with normal baseline glucose levels (<100 mg/dl): a combined analysis of the Familial Atherosclerosis Treatment Study (FATS), HDL-Atherosclerosis Treatment
Topics: Blood Glucose; Carotid Stenosis; Cholesterol, HDL; Cholesterol, LDL; Coronary Angiography; Coronary | 2013 |
Change in alpha1 HDL concentration predicts progression in coronary artery stenosis.
Topics: Aged; Antioxidants; Apolipoprotein A-I; Apolipoprotein A-II; Coronary Stenosis; Disease Progression; | 2003 |
Change in alpha1 HDL concentration predicts progression in coronary artery stenosis.
Topics: Aged; Antioxidants; Apolipoprotein A-I; Apolipoprotein A-II; Coronary Stenosis; Disease Progression; | 2003 |
Change in alpha1 HDL concentration predicts progression in coronary artery stenosis.
Topics: Aged; Antioxidants; Apolipoprotein A-I; Apolipoprotein A-II; Coronary Stenosis; Disease Progression; | 2003 |
Change in alpha1 HDL concentration predicts progression in coronary artery stenosis.
Topics: Aged; Antioxidants; Apolipoprotein A-I; Apolipoprotein A-II; Coronary Stenosis; Disease Progression; | 2003 |
A randomized trial of a strategy for increasing high-density lipoprotein cholesterol levels: effects on progression of coronary heart disease and clinical events.
Topics: Aged; Cholesterol, HDL; Cholestyramine Resin; Coronary Angiography; Coronary Disease; Disease Progre | 2005 |
Serial quantitative coronary angiography and coronary events.
Topics: Adult; Cholesterol, LDL; Colestipol; Collateral Circulation; Coronary Angiography; Coronary Artery D | 2000 |
Correlations between measures of atherosclerosis change using carotid ultrasonography and coronary angiography.
Topics: Adult; Carotid Artery, Common; Carotid Stenosis; Colestipol; Coronary Angiography; Coronary Artery D | 2000 |
Effect of niacin, warfarin, and antioxidant therapy on coagulation parameters in patients with peripheral arterial disease in the Arterial Disease Multiple Intervention Trial (ADMIT).
Topics: Aged; Anticoagulants; Antioxidants; Arterial Occlusive Diseases; Ascorbic Acid; beta Carotene; Blood | 2000 |
10 other studies available for niacin and Disease Exacerbation
| Article | Year |
|---|---|
The niacin receptor HCAR2 modulates microglial response and limits disease progression in a mouse model of Alzheimer's disease.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Disease Models, Animal; Disease Progression; Mice | 2022 |
Mitochondrial complex I activity and NAD+/NADH balance regulate breast cancer progression.
Topics: Acrylamides; Animals; Autophagy; Autophagy-Related Protein 5; Brain Neoplasms; Cell Line, Tumor; Cel | 2013 |
Therapeutic role of niacin in the prevention and regression of hepatic steatosis in rat model of nonalcoholic fatty liver disease.
Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Disease Models, Animal; Disease Progression; Fatty | 2014 |
Niacin improves renal lipid metabolism and slows progression in chronic kidney disease.
Topics: Animals; ATP Binding Cassette Transporter 1; ATP-Binding Cassette Transporters; Basic Helix-Loop-Hel | 2010 |
Nicotinic acid inhibits progression of atherosclerosis in mice through its receptor GPR109A expressed by immune cells.
Topics: Adipocytes; Animals; Aorta; Atherosclerosis; ATP Binding Cassette Transporter, Subfamily G, Member 1 | 2011 |
Comparison of the effects of atorvastatin versus simvastatin on subclinical atherosclerosis in primary preventionas determined by electronbeam tomography.
Topics: Analysis of Variance; Anticholesteremic Agents; Arteriosclerosis; Atorvastatin; Chi-Square Distribut | 2003 |
Summaries for patients. Targeting cholesterol treatment toward increasing high-density lipoprotein levels.
Topics: Aged; Cholesterol, HDL; Cholestyramine Resin; Coronary Angiography; Coronary Disease; Disease Progre | 2005 |
Rapidly progressing bilateral cataracts in a patient with beta thalassemia and pellagra.
Topics: Adult; beta-Thalassemia; Cataract; Disease Progression; Female; Glutathione; Humans; Iron Overload; | 2007 |
Update on lipodystrophy.
Topics: Diet; Disease Progression; Exercise; Female; HIV Infections; HIV Protease Inhibitors; Human Growth H | 1999 |
Pellagra encephalopathy as a differential diagnosis for Creutzfeldt-Jakob disease.
Topics: 14-3-3 Proteins; Adult; Aged; Aged, 80 and over; Brain; Creutzfeldt-Jakob Syndrome; Dementia; Diagno | 2012 |