C
Carl Grunfeld
Researcher at University of California, San Francisco
Publications - 372
Citations - 35694
Carl Grunfeld is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Tumor necrosis factor alpha & Adipose tissue. The author has an hindex of 99, co-authored 368 publications receiving 34037 citations. Previous affiliations of Carl Grunfeld include San Francisco General Hospital & Veterans Health Administration.
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Journal ArticleDOI
Effects of infection and inflammation on lipid and lipoprotein metabolism: mechanisms and consequences to the host.
Weerapan Khovidhunkit,Min Sun Kim,Riaz A. Memon,Judy K. Shigenaga,Arthur H. Moser,Kenneth R. Feingold,Carl Grunfeld +6 more
TL;DR: APR-induced alterations initially protect the host from the harmful effects of bacteria, viruses, and parasites, however, if prolonged, these changes in the structure and function of lipoproteins will contribute to atherogenesis.
Journal ArticleDOI
Lipids, lipoproteins, triglyceride clearance, and cytokines in human immunodeficiency virus infection and the acquired immunodeficiency syndrome.
Carl Grunfeld,Miyin Pang,William T. Doerrler,Judy K. Shigenaga,Peter S. Jensen,Kenneth R. Feingold +5 more
TL;DR: In this article, the authors studied plasma lipids, lipoproteins, triglyceride (TG) metabolism, and serum cytokines in three groups: patients with the acquired immunodeficiency syndrome (AIDS) without active secondary infection, patients with evidence of HIV infection but without clinical AIDS (HIV+), and controls.
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Endotoxin and cytokines induce expression of leptin, the ob gene product, in hamsters.
TL;DR: Induction of leptin during the host response to infection may contribute to the anorexia of infection, as assessed by immuknoprecipitation and Western blotting.
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Leptin regulation of the immune response and the immunodeficiency of malnutrition
TL;DR: Low leptin levels occurring during starvation mediate the neuroendocrine and immune dysfunction of starvation, and may represent a protective component of the host response to inflammation.
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Hyperlipidemia and insulin resistance are induced by protease inhibitors independent of changes in body composition in patients with HIV infection.
Kathleen Mulligan,Carl Grunfeld,Viva W. Tai,Heather Algren,Miyin Pang,David Chernoff,Joan C. Lo,Morris Schambelan +7 more
TL;DR: In this paper, the authors analyzed paired data in HIV-infected patients before and after beginning antiretroviral therapy that included a PI (PI, N = 20) or lamivudine (3TC) but no PI (3 TC), and a control group on stable regimens that included neither of these agents (CONT: N = 12).