THE LONG-TERM GOAL OF THE PROPOSED STUDIES IS TO DETERMINE WHETHER DIETARY RESISTANT STARCH (RS) PREVENTS DISRUPTION OF RENAL VITAMIN D METABOLISM AND RELATED COMPLICATIONS IN TYPE 1 (T1) AND TYPE 2 DIABETES (T2D) BY ALTERING THE GUT MICROBIOME. VITAMIN D METABOLISM IS COMPROMISED IN RODENT MODELS OF T1 AND T2D DUE TO URINARY LOSS OF BOTH THE MAJOR CIRCULATING METABOLITE OF VITAMIN D, 25-HYDROXYVITAMIN D3 AND THE ACTIVE HORMONE, 1,25-DIHYDROXYVITAMIN D3. FEEDING T1 AND T2D RATS HIGH-AMYLOSE MAIZE CONTAINING ~35% RS PREVENTED URINARY LOSS OF VITAMIN D BY PROTECTING RENAL INTEGRITY. THOUGH MARKEDLY DIABETIC, RS-FED T2D RATS EXHIBITED ROBUST RENAL HANDLING OF VITAMIN D, INDICATING PROTEIN REABSORPTION CAPABILITIES WERE PROTECTED. THE PROPOSED WORK WILL DETERMINE HOW RS MAINTAINS VITAMIN D BALANCE AND SIGNALING IN T1 AND T2D. THE CENTRAL HYPOTHESIS IS THAT THE INTRARENAL RAS MODULATES EXCRETION AND SIGNALING OF VITAMIN D IN T1 AND T2D. A COROLLARY TO THIS HYPOTHESIS IS THAT VITAMIN D REUPTAKE AND SIGNALING WILL BE PROTECTED IN DIABETIC RATS FED DIETARY RS THROUGH SUPPRESSION OF THE INTRARENAL RAS AND THE PROMOTION OF KIDNEY HEALTH BY ALTERING THE GUT MICROBIOME. MOREOVER, PREVENTION OF VITAMIN D EXCRETION BY INHIBITING RAS THROUGH DIETARY MODIFICATIONS WILL ATTENUATE DIABETIC COMPLICATIONS. TWO SPECIFIC AIMS WILL TEST THE HYPOTHESIS: (1) TO DETERMINE WHETHER THE INTRARENAL RAS MODULATES THE ACTIONS OF VITAMIN D DURING T1 AND T2D; AND (2) TO DETERMINE WHETHER PREVENTION OF VITAMIN D EXCRETION BY RS IS MEDIATED BY THE MICROBIOME.