scholarly journals PEX11 promotes peroxisome division independently of peroxisome metabolism

2002 ◽  
Vol 156 (4) ◽  
pp. 643-651 ◽  
Author(s):  
Xiaoling Li ◽  
Stephen J. Gould

The PEX11 peroxisomal membrane proteins are the only factors known to promote peroxisome division in multiple species. It has been proposed that PEX11 proteins have a direct role in peroxisomal fatty acid oxidation, and that they only affect peroxisome abundance indirectly. Here we show that PEX11 proteins are unique in their ability to promote peroxisome division, and that PEX11 overexpression promotes peroxisome division in the absence of peroxisomal metabolic activity. We also observed that mouse cells lacking PEX11β display reduced peroxisome abundance, even in the absence of peroxisomal metabolic substrates, and that PEX11β−/− mice are partially deficient in two distinct peroxisomal metabolic pathways, ether lipid synthesis and very long chain fatty acid oxidation. Based on these and other observations, we propose that PEX11 proteins act directly in peroxisome division, and that their loss has indirect effects on peroxisome metabolism.

2020 ◽  
Vol 477 (12) ◽  
pp. 2347-2361
Author(s):  
Emily A. Day ◽  
Rebecca J. Ford ◽  
Jessie H. Lu ◽  
Rachel Lu ◽  
Lucie Lundenberg ◽  
...  

Sodium-glucose cotransporter 2 inhibitors such as canagliflozin lower blood glucose and reduce cardiovascular events in people with type 2 diabetes through mechanisms that are not fully understood. Canagliflozin has been shown to increase the activity of the AMP-activated protein kinase (AMPK), a metabolic energy sensor important for increasing fatty acid oxidation and energy expenditure and suppressing lipogenesis and inflammation, but whether AMPK activation is important for mediating some of the beneficial metabolic effects of canagliflozin has not been determined. We, therefore, evaluated the effects of canagliflozin in female ApoE−/− and ApoE−/−AMPK β1−/− mice fed a western diet. Canagliflozin increased fatty acid oxidation and energy expenditure and lowered adiposity, blood glucose and the respiratory exchange ratio independently of AMPK β1. Canagliflozin also suppressed liver lipid synthesis and the expression of ATP-citrate lyase, acetyl-CoA carboxylase and sterol response element-binding protein 1c independently of AMPK β1. Canagliflozin lowered circulating IL-1β and studies in bone marrow-derived macrophages indicated that in contrast with the metabolic adaptations, this effect required AMPK β1. Canagliflozin had no effect on the size of atherosclerotic plaques in either ApoE−/− and ApoE−/−AMPK β1−/− mice. Future studies investigating whether reductions in liver lipid synthesis and macrophage IL-1β are important for the cardioprotective effects of canagliflozin warrant further investigation.


2019 ◽  
Author(s):  
Helena Urquijo ◽  
Emma N Panting ◽  
Roderick N Carter ◽  
Emma J Agnew ◽  
Caitlin S Wyrwoll ◽  
...  

1999 ◽  
Vol 22 (4) ◽  
pp. 487-502 ◽  
Author(s):  
J. M. Saudubray ◽  
D. Martin ◽  
P. De Lonlay ◽  
G. Touati ◽  
F. Poggi-Travert ◽  
...  

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