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Scott M. Turner

Researcher at University of California, Berkeley

Publications -  68
Citations -  4077

Scott M. Turner is an academic researcher from University of California, Berkeley. The author has contributed to research in topics: Fibrosis & Lipogenesis. The author has an hindex of 33, co-authored 67 publications receiving 3452 citations.

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Measurement in vivo of proliferation rates of slow turnover cells by 2H2O labeling of the deoxyribose moiety of DNA.

TL;DR: 2H2O labeling of dR in DNA allows safe, convenient, reproducible, and inexpensive measurement of cell proliferation in humans and experimental animals and is well suited for slow turnover cells.
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Short-term alterations in carbohydrate energy intake in humans. Striking effects on hepatic glucose production, de novo lipogenesis, lipolysis, and whole-body fuel selection.

TL;DR: It is concluded that altered CHO intake alters HGP specifically and in a dose-dependent manner, that HGP may mediate the effects of CHO on whole-body fuel selection both by providing substrate and by altering serum insulin concentrations, that altered lipolysis and tissue oxidation efficiency contribute to changes in fat oxidation, and that surplus CHO is not substantially converted by the liver to fat as it spares fat oxidation.
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Mice fed a lipogenic methionine-choline-deficient diet develop hypermetabolism coincident with hepatic suppression of SCD-1.

TL;DR: It is found that MCD feeding causes profound hepatic suppression of the gene encoding stearoyl-coenzyme A desaturase-1 (SCD-1) in the liver, which likely contributes to hypermetabolism and weight loss.
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Hepatic gluconeogenic fluxes and glycogen turnover during fasting in humans. A stable isotope study.

TL;DR: Hepatic gluconeogenic flux into glycogen and glycogen turnover persist during fasting in humans, reconciling inconsistencies in the literature and interposing another locus of control in the normal pathway of GP.
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Mfge8 diminishes the severity of tissue fibrosis in mice by binding and targeting collagen for uptake by macrophages

TL;DR: A critical role is demonstrated for Mfge8 in decreasing the severity of murine tissue fibrosis by facilitating the removal of accumulated collagen through binding and targeting collagen for cellular uptake through its discoidin domains.