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Showing 1–6 of 6 results
Advanced filters: Author: Sudha B. Biddinger Clear advanced filters
  • The hepatic enzyme FMO3 has been linked to atherosclerosis. Here the authors show that FMO3 is upregulated in various models of diabetes and link FMO3 with key transcriptional regulators of hepatic glucose and cholesterol synthesis, thus proposing a mechanistic connection between diabetes and atherosclerosis.

    • Ji Miao
    • Alisha V. Ling
    • Sudha B. Biddinger
    ResearchOpen Access
    Nature Communications
    Volume: 6, P: 1-10
  • People with the metabolic syndrome often develop gallstones. Why these two disorders are linked has not been not clear, but now Kahn and his colleagues have shown that lack of insulin signaling in the liver leads to dysregulation of genes that control the transport and synthesis of bile acids, thus altering the proper profile of bile salts and resulting in the formation of gallstones.

    • Sudha B Biddinger
    • Joel T Haas
    • C Ronald Kahn
    Research
    Nature Medicine
    Volume: 14, P: 778-782
  • A soluble form of insulin receptor in human plasma has been previously reported. Here the authors demonstrate that insulin receptor is cleaved by BACE1 that can regulate biological active insulin receptor levels in a glucose concentration-dependent manner, both in physiological and diabetic conditions.

    • Paul J. Meakin
    • Anna Mezzapesa
    • Franck Peiretti
    ResearchOpen Access
    Nature Communications
    Volume: 9, P: 1-14
  • Insulin dials down endogenous hepatic glucose production after a meal by deactivating the transcription factor FoxO1. In a mouse model of insulin resistance, Umut Ozcan and his colleagues now show that hepatic overexpression of Xbp-1s, a factor involved in the cell stress response, leads to the protein degradation of FoxO1, thus reducing serum glucose levels. These results suggest a way to bypass one aspect of insulin resistance.

    • Yingjiang Zhou
    • Justin Lee
    • Umut Ozcan
    Research
    Nature Medicine
    Volume: 17, P: 356-365
  • During fasting SIRT3 is induced in liver and brown adipose tissue. One of SIRT3's substrates is shown to be long–chain acyl co-enzyme A dehydrogenase (LCAD). Without SIRT3 LCAD becomes hyperacetylated, which diminishes its activity, and reduces fatty acid oxidation. Mice without SIRT3 have all the hallmarks of fatty acid oxidation disorders during fasting, including reduced ATP levels and intolerance to cold. Thus, acetylation is a novel regulatory mechanism for fatty acid oxidation.

    • Matthew D. Hirschey
    • Tadahiro Shimazu
    • Eric Verdin
    Research
    Nature
    Volume: 464, P: 121-125
  • Consuming diets rich in plant versus animal products changes the microbes found in the human gut within days, with important implications for our health and evolution.

    • Lawrence A. David
    • Corinne F. Maurice
    • Peter J. Turnbaugh
    Research
    Nature
    Volume: 505, P: 559-563