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Sulforaphane improves disrupted ER-mitochondria interactions and suppresses exaggerated hepatic glucose production

Artikel i vetenskaplig tidskrift
Författare E. Tubbs
A. S. Axelsson
G. Vial
C. B. Wollheim
J. Rieusset
Anders H. Rosengren
Publicerad i Molecular and Cellular Endocrinology
Volym 461
Nummer/häfte C
Sidor 205-214
ISSN 0303-7207
Publiceringsår 2018
Publicerad vid Institutionen för neurovetenskap och fysiologi
Sidor 205-214
Språk en
Länkar dx.doi.org/10.1016/j.mce.2017.09.01...
Ämnesord Mitochondria-associated ER membranes, Type 2 diabetes, Sulphoraphane, endoplasmic-reticulum stress, induced insulin-resistance, type-2, diabetes-mellitus, high-fat diet, oxidative stress, dysfunction, nrf2, disease, cells, lipogenesis, Cell Biology, Endocrinology & Metabolism, fronzo ra, 1989, metabolism-clinical and experimental, v38, p387
Ämneskategorier Endokrinologi och diabetes

Sammanfattning

Aims: Exaggerated hepatic glucose production is one of the hallmarks of type 2 diabetes. Sulforaphane (SFN) has been suggested as a new potential anti-diabetic compound. However, the effects of SFN in hepatocytes are yet unclear. Accumulating evidence points to the close structural contacts between the ER and mitochondria, known as mitochondria-associated ER membranes (MAMs), as important hubs for hepatic metabolism. We wanted to investigate whether SFN could affect hepatic glucose production and MAMs. Materials and methods: We used proximity ligation assays, analysis of ER stress markers and glucose production assays in hepatoma cell lines, primary mouse hepatocytes and diabetic animal models. Results: SFN counteracted the increase of glucose production in palmitate-treated mouse hepatocytes. SFN also counteracted palmitate-induced MAM disruptions. Moreover, SFN decreased the ER stress markers CHOP and Grp78. In ob/ob mice, SFN improved glucose tolerance and reduced exaggerated glucose production. In livers of these mice, SFN increased MAM protein content, restored impaired VDAC1-IP3R1 interactions and reduced ER stress markers. In mice on HFHSD, SFN improved glucose tolerance, MAM protein content and ER-mitochondria interactions to a similar extent to that of metformin. Conclusions: The present findings show that MAMs are severely reduced in animal models of glucose intolerance, which reinforces the role of MAMs as a hub for insulin signaling in the liver. We also show that SFN restores MAMs and improves glucose tolerance by a similar magnitude to that of metformin. These data highlight SFN as a new potential anti-diabetic compound. (C) 2017 Elsevier B.V. All rights reserved.

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