Fig. 2.

The effects of cellular and nutritional therapies on the prevention of diabetic retinopathy. a In a model of type 1 diabetes with ACE2 deficiency (ACE2^−/y-Akita), intraperitoneal injection of FACS-sorted wild-type (WT) bone marrow myeloid angiogenic cells (MACs) was shown to restructure the gut microbiota and repair the gut–vascular barrier (GVB). The intact GVB resulted in a decrease in the levels of systemic peptidoglycan (PGN), inhibiting a noncanonical TLR2-mediated signaling cascade in the retina, reducing retinal barrier dysfunction. b In a model of type 2 diabetes (db/db), intermittent fasting on an alternate-day regimen was shown to restructure the gut microbiota and activate production of beneficial secondary bile acids, specifically tauroursodeoxycholate (TUDCA), in the liver. TUDCA prevented progression of DR via activation of its receptor, TGR5, in the neural retina