Multiorgan observations following consumption of ketogenic diet in prolonged experimental diabetes mellitus

Oxidative stress and inflammation have been identified as key mediators in either the progression, or amelioration of diabetes mellitus. Dietary interventions, especially ketogenic diet, has been reported to exert ameliorative effects in diabetes mellitus. However, its likely benefit in prolonged diabetes mellitus is unclear. This study was designed to evaluated the likely beneficial effects of ketogenic diet on systemic and selected organ oxidative stress and inflammation in experimentally induced diabetic Wistar rats. Wistar rats (N=40) were equally divided into Control and Diabetic (streptozotocin 55mg/kg in 2% citrate buffer) animals. Control (I-II) and diabetic animals (III-IV) where divided into 2 groups (n=10) and exposed to either standard chow (SC) or ketogenic diet (KD), for 14 days, respectively. Animals were exposed to the different diets, 7 days after induction of diabetes mellitus. Thereafter, blood samples were obtained and evaluated for blood glucose, lipid profile, liver and renal function tests, and serum oxidative stress and inflammations indices. Cardiac, renal, knee joint and hepatic samples were also obtained and evaluated for histology, and oxidative stress and inflammation indices. Blood glucose, systemic, cardiac, renal and knee joint oxidative stress and inflammation were elevated while hepatic and renal functions were impaired in the SC exposed diabetic group compared to controls. Exposure of diabetic animals to KD resulted in reduced blood glucose and alleviated systemic inflammation in varying degrees. Impaired renal and hepatic functions were however not reversed. Similarly, tissue specific oxidative stress and inflammation though somewhat ameliorated, were however still persistent. This study suggests that consumption of ketogenic diet alone in preexisting or prolonged diabetes mellitus may ameliorate fasting blood glucose and reduces systemic inflammation but does not reverse completely, tissue-specific aberrations caused by diabetic mellitus. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.