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Adipose Tissue and RBP Generation
Serum Retinol-Binding Protein: a Link between Obesity, Insulin Resistance, and Type 2 Diabetes
https://academic.oup.com/
There are several interesting points made in this report. One of the more important ones is that the RBPs are actually being generated in the adipocytes.
Insulin resistance has a causal role in type 2 diabetes. Serum levels of retinol-binding protein 4 (RBP4), a protein secreted by adipocytes, are increased in insulin-resistant states.
This information is quite contrary to many other reports where it is stated that the RBPs are generated by the primarily the hepatic cells of the liver. Since the adipocytes are generating the RBPs, it suggests the liver's storage of retinol is not to store it and then safely deliver it to stem cells at some later time. Rather, it’s probably just to sequester it away and dispose of it.
"In fact, it is now accepted that the elevations of RBP4 detected in T2D are largely from adipose tissue and not liver "
In 2006, Kahn and colleagues demonstrated that obesity and insulin resistance in mice and humans led to elevations in serum levels of RBP4[24,25]. RBP4 is synthesized in the liver and is the primary carrier of serum vitamin A (retinol)[1]. Other researchers also reported an association between elevated serum RBP4 levels and T2D[26]; however, subsequent studies failed to detect this relationship[27,28]. Human, experimental animal and cell culture studies eventually demonstrated that the prodiabetic effect of RBP4 is not related to vitamin A or RBP4’s role as a vitamin A carrier[29–31]. In fact, it is now accepted that the elevations of RBP4 detected in T2D are largely from adipose tissue and not liver, further supporting a nonvitamin A role for any prodiabetic properties of RBP4[25,32]. Despite increasing data on the molecular mechanisms responsible for the prodiabetic effects of RBP4[29], little is known regarding the biological functions of RBP4 outside of its role as the major serum vitamin A carrier. Nevertheless, anti-T2D therapies that block RBP4 are being developed[25]. However, as RBP4 is the major carrier of serum vitamin A, a thorough understanding of how these therapeutic approaches might affect vitamin A metabolism is essential, as anti-RBP4 therapies can compromise vitamin A status in rodents and humans[33–35].
https://www.ncbi.nlm.nih.gov/
It seriously puts into question the supposition that the liver is storing retinol for some later use. If the primary transport protein for retinol originates in the adipose tissues, then why is it being "stored" it in the liver? It just does not add up.
Interesting! I hope this gets more attention.