Abstract

Introduction. During the Hajj, millions of pilgrims are exposed to extreme heat while many carry diagnosed or undiagnosed type 2 diabetes. Standard WHO oral rehydration salts (ORS) contain 75 mmol/L of free glucose and depend primarily on SGLT1-mediated intestinal water absorption. We hypothesize that this glucose-dependent pathway may be counterproductive in hyperglycemic patients: the additional glucose load could exacerbate renal glucosuria and osmotic diuresis, potentially converting a rehydration intervention into a dehydration accelerant. The expanding use of SGLT2 inhibitors, now recommended as first-line therapy in NICE 2026 guidelines, introduces additional dehydration risk under heat stress. Many pilgrims also lose access to their medications during transit between Hajj sites.

Hypothesis. We propose that an ORS in which most free glucose is replaced by L-glutamine and L-alanine (exploiting the B0AT1 and SNAT2 sodium-amino acid symporters), supplemented with high-amylose maize starch for delayed colonic short-chain fatty acid-driven fluid salvage and low-dose magnesium to support intracellular potassium handling, may achieve clinical rehydration in hyperglycemic heat-stressed adults without worsening glycemia. We designate this formulation AA-HAMS-ORS(Amr and Khulood ORS).

Evaluation. Each component draws on established transporter biology. B0AT1 and SNAT2 are insulin-insensitive and can mediate sodium and water absorption independently of luminal glucose. Amylase-resistant starch undergoes colonic fermentation to acetate and butyrate, which drive electroneutral sodium and water absorption through NHE2/NHE3. Magnesium supports basolateral Na+/K+-ATPase function and helps restore the magnesium-dependent gating of renal ROMK channels. We translate these mechanisms into formal, testable statistical hypotheses.