His main research concerns Internal medicine, Endocrinology, Insulin, Insulin receptor and Insulin resistance. His study in Insulin oscillation, Islet, Glucose homeostasis, IRS2 and Pancreatic islets is carried out as part of his Internal medicine studies. His studies in Endocrinology integrate themes in fields like Receptor, Protein kinase B and Cell biology.
His research in the fields of Beta cell overlaps with other disciplines such as Calcium metabolism. His study in Insulin receptor is interdisciplinary in nature, drawing from both Knockout mouse and Hyperinsulinemia. In his research, TRIB3, Incretin and Diabetes mellitus genetics is intimately related to Glucose uptake, which falls under the overarching field of Insulin resistance.
Rohit N. Kulkarni focuses on Internal medicine, Endocrinology, Insulin, Insulin resistance and Cell biology. All of his Endocrinology and Insulin receptor, Glucose homeostasis, Islet, Diabetes mellitus and Insulin oscillation investigations are sub-components of the entire Endocrinology study. His work carried out in the field of Insulin receptor brings together such families of science as PI3K/AKT/mTOR pathway, Downregulation and upregulation and Glucagon secretion.
The various areas that Rohit N. Kulkarni examines in his Insulin study include Adipose tissue, Protein kinase B, Knockout mouse and Carbohydrate metabolism. The study incorporates disciplines such as Epigenetics and Type 2 diabetes in addition to Insulin resistance. His Cell biology research incorporates themes from Cell, Receptor and Induced pluripotent stem cell.
His primary scientific interests are in Cell biology, Insulin resistance, Internal medicine, Endocrinology and Insulin. His Cell biology research is multidisciplinary, incorporating elements of Cell, Proteomics, Induced pluripotent stem cell, Translation and Islet. He interconnects Gene expression, FOXO1, Gene silencing, Epigenetics and Type 2 diabetes in the investigation of issues within Insulin resistance.
His Insulin receptor, Steatosis and Thiamine study in the realm of Internal medicine interacts with subjects such as Nonalcoholic fatty liver disease. His work in the fields of Diabetes mellitus genetics overlaps with other areas such as Solute carrier family. He has included themes like Diabetes mellitus, Messenger RNA, Transdifferentiation and Pharmacology in his Insulin study.
His scientific interests lie mostly in Insulin resistance, Islet, Internal medicine, Endocrinology and Cell. His Insulin resistance study results in a more complete grasp of Insulin. He has researched Islet in several fields, including Inflammation, Secretion, Cancer research and Cytokine.
His study in the field of Steatosis, Metabolic syndrome and Insulin receptor also crosses realms of Nonalcoholic fatty liver disease. His Endocrinology research incorporates elements of Downregulation and upregulation and Epigenetics. Rohit N. Kulkarni combines subjects such as MAPK/ERK pathway, Cell growth, Pancreas and Cell biology with his study of Cell.
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Loss of Insulin Signaling in Hepatocytes Leads to Severe Insulin Resistance and Progressive Hepatic Dysfunction
M.Dodson Michael;Rohit N. Kulkarni;Catherine Postic;Steven F. Previs.
Molecular Cell (2000)
Tissue-Specific Knockout of the Insulin Receptor in Pancreatic β Cells Creates an Insulin Secretory Defect Similar to that in Type 2 Diabetes
R N Kulkarni;J C Brüning;J N Winnay;C Postic.
New role of bone morphogenetic protein 7 in brown adipogenesis and energy expenditure
Yu Hua Tseng;Efi Kokkotou;Tim J. Schulz;Tian Lian Huang.
TRB3: A tribbles Homolog That Inhibits Akt/PKB Activation by Insulin in Liver
Keyong Du;Stephan Herzig;Rohit N. Kulkarni;Marc Montminy.
Melanin-concentrating hormone overexpression in transgenic mice leads to obesity and insulin resistance
David S. Ludwig;Nicholas A. Tritos;Jason W. Mastaitis;Rohit Kulkarni.
Journal of Clinical Investigation (2001)
cAMP promotes pancreatic β-cell survival via CREB-mediated induction of IRS2
Ulupi S. Jhala;Gianluca Canettieri;Robert A. Screaton;Rohit N. Kulkarni.
Genes & Development (2003)
PGC-1 promotes insulin resistance in liver through PPAR-α-dependent induction of TRB-3
Seung Hoi Koo;Hiroaki Satoh;Stephan Herzig;Chih Hao Lee.
Nature Medicine (2004)
Loss of ARNT/HIF1β Mediates Altered Gene Expression and Pancreatic-Islet Dysfunction in Human Type 2 Diabetes
Jenny E. Gunton;Rohit N. Kulkarni;Sun Hee Yim;Terumasa Okada.
beta-cell-specific deletion of the Igf1 receptor leads to hyperinsulinemia and glucose intolerance but does not alter beta-cell mass.
R N Kulkarni;M Holzenberger;D Q Shih;U Ozcan.
Nature Genetics (2002)
Abnormal glucose homeostasis in skeletal muscle–specific PGC-1α knockout mice reveals skeletal muscle–pancreatic β cell crosstalk
Christoph Handschin;Cheol Soo Choi;Sherry Chin;Sheene Kim.
Journal of Clinical Investigation (2007)
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