What is he best known for?
The fields of study he is best known for:
His main research concerns Internal medicine, Endocrinology, Insulin, Genetics and Gene.
His research in Internal medicine intersects with topics in Diabetes mellitus and Type 2 diabetes.
He has researched Endocrinology in several fields, including Fibrosis and Receptor.
Specifically, his work in Insulin is concerned with the study of Insulin resistance.
Alan D. Attie studied Cholesterol and Stearoyl-CoA desaturase-1 that intersect with Very low-density lipoprotein and Stearoyl-CoA Desaturase.
His studies examine the connections between Low-density lipoprotein and genetics, as well as such issues in Mutant, with regards to LDL receptor.
His most cited work include:
- Loss of stearoyl–CoA desaturase-1 function protects mice against adiposity (910 citations)
- The Collaborative Cross, a community resource for the genetic analysis of complex traits (852 citations)
- Hypoxia-inducible factor 1α induces fibrosis and insulin resistance in white adipose tissue (563 citations)
What are the main themes of his work throughout his whole career to date?
Alan D. Attie mainly investigates Endocrinology, Internal medicine, Genetics, Biochemistry and Insulin.
His works in Diabetes mellitus, Insulin resistance, Cholesterol, Type 2 diabetes and Apolipoprotein B are all subjects of inquiry into Endocrinology.
His Diabetes mellitus study incorporates themes from Obesity and Leptin.
His study in the field of Reverse cholesterol transport and High-density lipoprotein is also linked to topics like Tangier disease.
His work carried out in the field of Apolipoprotein B brings together such families of science as LDL receptor and Lipoprotein.
His research combines Mutant and Internal medicine.
He most often published in these fields:
- Endocrinology (44.60%)
- Internal medicine (44.60%)
- Genetics (22.07%)
What were the highlights of his more recent work (between 2013-2021)?
- Genetics (22.07%)
- Cell biology (8.92%)
- Insulin (17.84%)
In recent papers he was focusing on the following fields of study:
Alan D. Attie focuses on Genetics, Cell biology, Insulin, Internal medicine and Endocrinology.
His study focuses on the intersection of Genetics and fields such as Gut flora with connections in the field of Genetic variation, Bile acid and Gastrointestinal tract.
His biological study spans a wide range of topics, including Lipid metabolism, Biogenesis, Endogeny and Proteomics.
While the research belongs to areas of Insulin, he spends his time largely on the problem of Exocytosis, intersecting his research to questions surrounding Insulin oscillation, Impaired glucose tolerance and Endosome.
His studies in Internal medicine integrate themes in fields like Diabetes mellitus, Mitochondrion and Mitochondrial DNA.
His Endocrinology research is multidisciplinary, incorporating elements of Gene targeting and Mitochondrial biogenesis.
Between 2013 and 2021, his most popular works were:
- Diet-Microbiota Interactions Mediate Global Epigenetic Programming in Multiple Host Tissues (202 citations)
- Energy Metabolic Reprogramming in the Hypertrophied and Early Stage Failing Heart A Multisystems Approach (129 citations)
- A Role for Peroxisome Proliferator-Activated Receptor γ Coactivator-1 in the Control of Mitochondrial Dynamics During Postnatal Cardiac Growth (121 citations)
In his most recent research, the most cited papers focused on:
Alan D. Attie mainly investigates Genetics, Receptor, Endocrinology, Internal medicine and Insulin.
His work on Quantitative trait locus, Genome and Chromatin remodeling as part of general Genetics research is often related to Epigenomics, thus linking different fields of science.
His study looks at the intersection of Receptor and topics like Cell biology with Transgene, Knockout mouse, Metabolic pathway and Acinar cell.
Endocrinology is often connected to Mitochondrion in his work.
His work deals with themes such as Cell culture, Glucagon-like peptide-1 and Protein kinase A, which intersect with Internal medicine.
His Insulin research incorporates themes from miR-132, Activator, Pancreas and Protein Kinase A Inhibitor.
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