A5066507748- Diabetes, Cardiovascular Risks, and Lipoproteins
- Lipid metabolism and disorders
- Cancer, Lipids, and Metabolism
- Peroxisome Proliferator-Activated Receptors
- Lipoproteins and Cardiovascular Health
- Adipose Tissue and Metabolism
- Lipid metabolism and biosynthesis
- Cardiovascular Function and Risk Factors
- Metabolism, Diabetes, and Cancer
- Atherosclerosis and Cardiovascular Diseases
- Adipokines, Inflammation, and Metabolic Diseases
- Kruppel-like factors research
- Cholesterol and Lipid Metabolism
- Diabetes Treatment and Management
- Liver Disease Diagnosis and Treatment
- Diet and metabolism studies
- Antioxidant Activity and Oxidative Stress
- Diet, Metabolism, and Disease
- Retinoids in leukemia and cellular processes
- Cancer, Hypoxia, and Metabolism
- Diabetes and associated disorders
- Pancreatic function and diabetes
- Caveolin-1 and cellular processes
- Diabetes Management and Research
- Glycosylation and Glycoproteins Research
New York University
2016-2025
NYU Langone Health
2016-2025
Icahn School of Medicine at Mount Sinai
1982-2024
Diabetes & Endocrine Associates
2018-2024
Royal Perth Hospital
2024
Sorbonne Université
2024
Inserm
2024
Arrowhead Pharmaceuticals (United States)
2024
Hinge Health
2023
University of New Haven
2021
Although it has been known for over 50 years that lipoprotein lipase (LPL) hydrolyzes triglyceride in chylomicrons, during the past half decade there a reinterest physiologic and pathophysiologic actions of this enzyme.In part, coincided with clinical studies implicating increased postprandial lipemia as risk factor atherosclerosis development.In addition, recent creation genetically altered mice hypertriglyceridemia fo- cused interest geneticists physiologists on pathophysiology...
Insulin resistance in skeletal muscle and liver may play a primary role the development of type 2 diabetes mellitus, mechanism by which insulin occurs be related to alterations fat metabolism. Transgenic mice with muscle- liver-specific overexpression lipoprotein lipase were studied during 2-h hyperinsulinemic-euglycemic clamp determine effect tissue-specific increase on action signaling. Muscle-lipoprotein had 3-fold triglyceride content resistant because decreases insulin-stimulated...
Previous data suggest that apolipoprotein (apo) CIII may inhibit both triglyceride hydrolysis by lipoprotein lipase (LPL) and apo E-mediated uptake of triglyceride-rich lipoproteins the liver. We studied B metabolism in very low density (VLDL), intermediate (IDL), (LDL) two sisters with CIII-apo AI deficiency. The subjects had reduced levels VLDL triglyceride, normal LDL cholesterol, near absence high (HDL) cholesterol. Compartmental analysis kinetics after injection 125I-VLDL 131I-LDL...
Cells obtain FAs either from LPL-catalyzed hydrolysis of lipoprotein triglyceride or unesterified FFAs associated with albumin. LPL also influences uptake esterified lipids such as cholesteryl and retinyl esters that are not hydrolyzed in the plasma. This process might involve enzymatic activity. is regulated by feeding/fasting, insulin, exercise. Although a number molecules may affect cellular FFAs, best characterized CD36. Genetic deletion this multiligand receptor reduces FFA into...
Lipoprotein lipase is the principal enzyme that hydrolyzes circulating triglycerides and liberates free fatty acids can be used as energy by cardiac muscle. Although lipoprotein expressed found on surface of cardiomyocytes, its transfer to luminal endothelial cells thought required for actions. To study whether nontransferable has physiological actions, we placed an α-myosin heavy-chain promoter upstream a human minigene construct with glycosylphosphatidylinositol anchoring sequence carboxyl...
Three forms of PPARs are expressed in the heart. In animal models, PPARgamma agonist treatment improves lipotoxic cardiomyopathy; however, humans is associated with peripheral edema and increased heart failure. To directly assess effects on function, we created transgenic mice expressing PPARgamma1 via cardiac alpha-myosin heavy chain (alpha-MHC) promoter. PPARgamma1-transgenic had expression fatty acid oxidation genes lipoprotein triglyceride (TG) uptake. Unlike PPARalpha-transgenic mice,...
Hepatic steatosis is often associated with insulin resistance and obesity can lead to steatohepatitis cirrhosis. In this study, we have demonstrated that hormone-sensitive lipase (HSL) adipose triglyceride (ATGL), two enzymes critical for lipolysis in tissues, also contribute the liver mobilize hepatic triglycerides vivo vitro. Adenoviral overexpression of HSL and/or ATGL reduced by 40-60% both ob/ob mice high fat diet-induced obesity. However, these did not affect fasting plasma free fatty...
We previously observed that treatment of mice with a dominant negative form cJun (dn-cJun) increased the expression genes involved in lipid metabolism and modulated nine microRNAs (miR). To investigate potential effect these miRs on metabolism, we performed studies cultured HepG2 cells. Transfection cells sense or antisense miR-370 miR-122 upregulated downregulated, respectively, transcription factor sterol-regulatory element binding protein 1c (SREBP-1c) enzymes diacylglycerol...
Background— Heart failure is associated with impaired myocardial metabolism a shift from fatty acids to glucose use for ATP generation. We hypothesized that cardiac accumulation of toxic lipid intermediates inhibits insulin signaling in advanced heart and mechanical unloading the failing myocardium corrects metabolism. Methods Results— analyzed serum 61 patients (body mass index, 26.5±5.1 kg/m 2 ; age, 51±12 years) obtained during left ventricular assist device implantation at explantation...
Hypertriglyceridemia is an independent risk factor for cardiovascular disease, and plasma triglycerides (TGs) correlate strongly with apolipoprotein C-III (ApoC-III) levels. Antisense oligonucleotides (ASOs) ApoC-III reduce TGs in primates mice, but the underlying mechanism of action remains controversial. We determined that a murine-specific ApoC-III-targeting ASO reduces fasting TG levels through dependent on low-density lipoprotein receptors (LDLRs) LDLR-related protein 1 (LRP1)....
Movement of circulating fatty acids (FAs) to parenchymal cells requires their transfer across the endothelial cell (EC) barrier. The multiligand receptor cluster differentiation 36 (CD36) facilitates tissue FA uptake and is expressed in ECs such as myocytes adipocytes. Whether FAs dependent on EC or CD36, both, unknown. Using a cell-specific deletion approach, we show that EC, but not cell, CD36 increased fasting plasma postprandial triglycerides. EC-Cd36–KO mice had reduced radiolabeled...