Archives of medical research · 2026
Symbiotic (L. acidophilus and Agave Inulin) Prevents Cognitive Impairment in High-Fat Diet/STZ Rats.
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Romo-Araiza Alejandra, Márquez Luis A, Rocha-Botello Gabriela, Galván Emilio J, Ponce-Lopez Teresa, Fernández-Presas Ana María, Jasso-Chávez Ricardo, Cueto Macarena Fuentes-Fernández, Bustamante-Laguna Diego, Alfaro-González Andrés, Pérez-Arreola Aranza, Aguirre-Rivera Carlos, Mejía Iván Ignacio, Ibarra-Garcia Andrea P, García-Vences Elisa, Rodriguez-Barrera Roxana, Cruz-Martinez Yolanda, Albores-Méndez Exsal Manuel, Vargas Marco Antonio, Rodriguez-Serrano Luis Miguel, Ibarra Antonio
Аннотация
BACKGROUND: Type 2 diabetes has been linked to oxidative stress, inflammation, and an imbalance in the gut microbiota, all of which contribute to neuroinflammation and cognitive decline. Gut microbiota influence inflammation and produce various substances, including butyrate, a short-chain fatty acid that promotes brain-derived neurotrophic factor (BDNF), which is essential for memory. This study investigated whether prebiotics, probiotics, or a combination of both (symbiotics) could improve memory in diabetic rats.
METHODS: Male Wistar rats were divided into five groups: control; diabetic and obese (induced by a high-fat diet and streptozotocin); diabetic and obese with prebiotics (inulin); diabetic and obese with probiotics (Lactobacillus acidophilus); and diabetic and obese with symbiotics (inulin + L. acidophilus). Treatments lasted 42 d. Memory performance was evaluated using the Morris water maze (spatial memory) and the Eight-arm radial maze (working memory). After testing, hippocampal tissue was analyzed for inflammatory markers (TNF-α, IL-10), BDNF, and butyric acid.
RESULTS: Diabetes impaired memory and increased neuroinflammatory markers. All supplemented groups showed improved memory. The symbiotic group exhibited the most pronounced benefits, with higher levels of BDNF, IL-10, and butyric acid, and reduced TNF-α. Electrophysiological recordings revealed that diabetes reduced the firing frequency of CA1 pyramidal cells and decreased the synaptic strength in the hippocampus. Symbiotic supplementation preserved these neuronal and synaptic functions.
CONCLUSION: Symbiotic treatment effectively countered diabetes-induced cognitive deficits by reducing neuroinflammation, increasing neurotrophic support, and maintaining synaptic plasticity. These results imply that altering the gut microbiota through symbiotic supplementation may be an effective approach to prevent or mitigate diabetes-associated cognitive decline.
METHODS: Male Wistar rats were divided into five groups: control; diabetic and obese (induced by a high-fat diet and streptozotocin); diabetic and obese with prebiotics (inulin); diabetic and obese with probiotics (Lactobacillus acidophilus); and diabetic and obese with symbiotics (inulin + L. acidophilus). Treatments lasted 42 d. Memory performance was evaluated using the Morris water maze (spatial memory) and the Eight-arm radial maze (working memory). After testing, hippocampal tissue was analyzed for inflammatory markers (TNF-α, IL-10), BDNF, and butyric acid.
RESULTS: Diabetes impaired memory and increased neuroinflammatory markers. All supplemented groups showed improved memory. The symbiotic group exhibited the most pronounced benefits, with higher levels of BDNF, IL-10, and butyric acid, and reduced TNF-α. Electrophysiological recordings revealed that diabetes reduced the firing frequency of CA1 pyramidal cells and decreased the synaptic strength in the hippocampus. Symbiotic supplementation preserved these neuronal and synaptic functions.
CONCLUSION: Symbiotic treatment effectively countered diabetes-induced cognitive deficits by reducing neuroinflammation, increasing neurotrophic support, and maintaining synaptic plasticity. These results imply that altering the gut microbiota through symbiotic supplementation may be an effective approach to prevent or mitigate diabetes-associated cognitive decline.