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Ketogenic Diet Prevents Hypoglycemia Due to Endotoxin Sepsis
Prathima Nandivada, MD1; Melissa I. Chang, MD,MEng1; Sarah J. Carlson MD, MSc1; Amy H. Pan, BS1; Pei-Ra Ling, MD2; Bruce R Bistrian,MD,PhD2; Mark Puder, MD, PhD1
1Vascular Biology Program and Department of Surgery, Boston Children's Hospital, Boston, MA; 2Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA

Background: Hypoglycemia in patients with sepsis is associated with increased mortality. The purpose of this study was to determine if a ketogenic diet prevents hypoglycemia in mice with endotoxin sepsis.

Methods: Mice were fed a ketogenic diet (KD) with 90% fat kcal or a control diet (CD) with 2.5% fat kcal for 4 weeks. Mice subsequently received either 10 mg/kg of lipopolysaccharide (LPS) or saline (n=10 per group) intraperitoneally. Fasting glucose was measured for 4 hours, followed by serum and tissue analysis.

Results: KD and CD mice had an initial hyperglycemic response to LPS, while KD and CD mice maintained normal glucose after saline. Hypoglycemia (<80 mg/dL) developed after LPS in only the CD mice (47.8 mg/dL), whereas KD mice normalized their glucose (92 mg/dL, p=0.0001). Insulin resistance was 10-fold higher in KD than CD mice after LPS (p=0.01). Hepatic glycogen was undetectable in CD mice after LPS, while still present in KD mice. IL-6 was similar between the groups, however TNF-a was elevated in KD mice (841 pg/mL) compared to CD mice (534 pg/mL, p=0.03) after LPS. A 10-fold increase in hepatic NFkB mRNA was observed in CD mice after LPS, with a 5-fold increase in KD mice relative to CD mice after saline (p=0.001).

Conclusion: Mice fed KD normalized blood glucose while mice fed CD developed hypoglycemia from endotoxin sepsis. The switch to fat-based metabolism induced by KD may prevent hypoglycemia by maintaining hepatic glycogen, increasing insulin resistance, and decreasing inflammatory signaling.

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