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Andrea L. Hevener

Researcher at University of California, Los Angeles

Publications -  89
Citations -  13177

Andrea L. Hevener is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Insulin resistance & Insulin. The author has an hindex of 47, co-authored 80 publications receiving 11396 citations. Previous affiliations of Andrea L. Hevener include University of California, Berkeley & Semel Institute for Neuroscience and Human Behavior.

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IKK-beta links inflammation to obesity-induced insulin resistance.

TL;DR: The importance of liver cell IKK-β in hepatic insulin resistance and the central role of myeloid cells in development of systemic insulin resistance are demonstrated and it is suggested that inhibition of Ikk-β, especially in myeloids cells, may be used to treat insulin resistance.
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Adipose-specific peroxisome proliferator-activated receptor gamma knockout causes insulin resistance in fat and liver but not in muscle.

TL;DR: Surprisingly, TZD treatment effectively reversed liver IR, whereas it failed to lower plasma free fatty acids, suggesting that syndrome X may be comprised of separable PPARγ-dependent components whose origins and therapeutic sites may reside in distinct tissues.
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The role of estrogens in control of energy balance and glucose homeostasis.

TL;DR: The literature in both rodents and humans on the role of estrogens and their receptors in the control of energy homeostasis and glucose metabolism in health and metabolic diseases is reviewed.
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The Effect of Thiazolidinediones on Plasma Adiponectin Levels in Normal, Obese, and Type 2 Diabetic Subjects

TL;DR: The findings show that TZD treatment increased adiponectin levels in all subjects, including normal subjects in which no other effects of TZDs are observed, and it may play a physiologic role in enhancing insulin sensitivity.
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New mitochondrial DNA synthesis enables NLRP3 inflammasome activation

TL;DR: It is shown that the synthesis of mitochondrial DNA (mtDNA), induced after the engagement of Toll-like receptors, is crucial for NLRP3 signalling, and the dependence on CMPK2 catalytic activity provides opportunities for more effective control ofNLRP3 inflammasome-associated diseases.