RBP4 is the only specific transport protein for retinol/ vitamin A in serum. Since 2005, this protein has been the focus of diabetes research as it was shown to be more highly expressed in adipose tissue and detectable in higher concentrations in blood of insulin-resistant/ obese patients. Circulating RBP4 has therefore been attributed a causative role in the development of insulin resistance and type 2 diabetes. The group of Prof. Schupp and colleagues from the University of Potsdam could now show that in a new mouse model with increased circulating RBP4 levels in serum by liver-specific overexpression, RBP4 does not induce a metabolic deterioration. This finding is leading the path in order to shift the focus of future scientific studies on the function of RBP4 to other aspects, such as its intracellular effects, and to determine whether modulation of RBP4 could function as a therapeutic strategy for metabolic diseases.
Liver-secreted RBP4 does not impair glucose homeostasis in mice.
Fedders R, Muenzner M, Weber P, Sommerfeld M, Knauer M, Kedziora S, Kast N, Heidenreich S, Raila J, Weger S, Henze A, Schupp M.
J Biol Chem. 2018 Aug 20. pii: jbc.RA118.004294. doi: 10.1074/jbc.RA118.004294. [Epub ahead of print] PMID: 30126844 DOI: 10.1074/jbc.RA118.004294
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