Research output

De novo lipogenesis in human fat and liver is linked to ChREBP-beta and metabolic health

Research output: Contribution to journalArticleAcademicpeer-review

Associated researcher

  • Eissing, L.
  • Scherer, T.
  • Todter, K.
  • Knippschild, U.
  • Greve, J.W.M.

  • Buurman, W. A.
  • Pinnschmidt, H. O.
  • Rensen, S.S.M.

  • Wolf, A. M.
  • Bartelt, A.
  • Heeren, J.
  • Buettner, C.
  • Scheja, L.

Associated organisations

Abstract

Clinical interest in de novo lipogenesis has been sparked by recent studies in rodents demonstrating that de novo lipogenesis specifically in white adipose tissue produces the insulin-sensitizing fatty acid palmitoleate. By contrast, hepatic lipogenesis is thought to contribute to metabolic disease. How de novo lipogenesis in white adipose tissue versus liver is altered in human obesity and insulin resistance is poorly understood. Here we show that lipogenic enzymes and the glucose transporter-4 are markedly decreased in white adipose tissue of insulin-resistant obese individuals compared with non-obese controls. By contrast, lipogenic enzymes are substantially upregulated in the liver of obese subjects. Bariatric weight loss restored de novo lipogenesis and glucose transporter-4 gene expression in white adipose tissue. Notably, lipogenic gene expression in both white adipose tissue and liver was strongly linked to the expression of carbohydrate-responsive element-binding protein-beta and to metabolic risk markers. Thus, de novo lipogenesis predicts metabolic health in humans in a tissue-specific manner and is likely regulated by glucose-dependent carbohydrate-responsive element-binding protein activation.

    Research areas

  • ENDOPLASMIC-RETICULUM STRESS, ADIPOSE-TISSUE, INSULIN-RESISTANCE, HEPATIC STEATOSIS, WEIGHT-LOSS, TRANSCRIPTION FACTOR, COA DESATURASE, ACID SYNTHESIS, GLUCOSE, OBESE
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Details

Original languageEnglish
Article number1528
Number of pages11
JournalNature Communications
Volume4
DOIs
Publication statusPublished - Feb 2013