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Gerald I. Shulman
Yale University
575Publications
142H-index
80.6kCitations
Publications 575
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#1Rachel J. Perry (Yale University)H-Index: 15
#2Aviva Rabin-Court (Yale University)H-Index: 2
Last.Gerald I. Shulman (Yale University)H-Index: 142
view all 7 authors...
Sodium-glucose transport protein 2 (SGLT2) inhibitors are a class of anti-diabetic agents; however, concerns have been raised about their potential to induce euglycemic ketoacidosis and to increase both glucose production and glucagon secretion. The mechanisms behind these alterations are unknown. Here we show that the SGLT2 inhibitor (SGLT2i) dapagliflozin promotes ketoacidosis in both healthy and type 2 diabetic rats in the setting of insulinopenia through increased plasma catecholamine and co...
#1Naim Alkhouri (University of Texas at Austin)H-Index: 1
#2Eric Lawitz (University of Texas at Austin)H-Index: 3
Last.Gerald I. Shulman (Yale University)H-Index: 142
view all 5 authors...
ABSTRACTIntroduction: De novo lipogenesis (DNL) plays a major role in fatty acid metabolism and contributes significantly to triglyceride accumulation within the hepatocytes in patients with nonalc...
#1Christine J. Pol (TU: Temple University)H-Index: 2
#2Nina M. Pollak (University of Graz)H-Index: 8
Last.Iannis Aifantis (HHMI: Howard Hughes Medical Institute)H-Index: 52
view all 10 authors...
Abstract Cardiac metabolism affects systemic energetic balance. Previously, we showed that Kruppel-like factor (KLF)-5 regulates cardiomyocyte PPARα and fatty acid oxidation-related gene expression in diabetes. We surprisingly found that cardiomyocyte-specific KLF5 knockout mice ( αMHC-KLF5 −/− ) have accelerated diet-induced obesity, associated with increased white adipose tissue (WAT). Alterations in cardiac expression of the mediator complex subunit 13 ( Med13 ) modulates obesity. αMHC-KLF5 −...
#1Rachel J. Perry (Yale University)H-Index: 15
#2Jon M. Resch (BIDMC: Beth Israel Deaconess Medical Center)H-Index: 9
Last.Gerald I. Shulman (Yale University)H-Index: 142
view all 10 authors...
Leptin informs the brain about sufficiency of fuel stores. When insufficient, leptin levels fall, triggering compensatory increases in appetite. Falling leptin is first sensed by hypothalamic neurons, which then initiate adaptive responses. With regard to hunger, it is thought that leptin-sensing neurons work entirely via circuits within the central nervous system (CNS). Very unexpectedly, however, we now show this is not the case. Instead, stimulation of hunger requires an intervening endocrine...
#1Abudukadier Abulizi (Yale University)H-Index: 3
#2João-Paulo G. Camporez (Yale University)H-Index: 22
Last.Daniel F. Vatner (Yale University)H-Index: 9
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The connection between adipose glucocorticoid action and whole-body metabolism is incompletely understood. Thus, we generated adipose tissue–specific glucocorticoid receptor–knockout (Ad-GcR−/−) mice to explore potential mechanisms. Ad-GcR−/− mice had a lower concentration of fasting plasma nonesterified fatty acids and less hepatic steatosis. This was associated with increased protein kinase B phosphorylation and increased hepatic glycogen synthesis after an oral glucose challenge. High-fat die...
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