ECE2022 Poster Presentations Diabetes, Obesity, Metabolism and Nutrition (202 abstracts)
Impaired glucose homeostasis in a tau knock-in mouse model
Hamza Benderradji 1 , Sarra Kraiem 2 , Courty Emilie 3 , Sabiha Eddarkaoui 2 , Bourouh Cyril 3 , Faivre Emilie 2 , Rolland Laure 3 , Caron Emilie 1 , Besegher Mélanie 4 , Oger Frederik 5 , Boschetti Theo 4 , Carvalho Kévin 1 , Thiroux Bryan 1 , Gauvrit Thibaut 1 , Nicolas Emilie 6 , Gomez-Murcia Victoria 1 , Bogdanova Anna 1 , Bongiovanni Antonino 7 , Tailleux Anne 6 , Lancel Steve 8 , Bantubungi Kadiombo 6 , Sergeant Nicolas 1 , Annicotte Jean-Sebastien 5 , Buée Luc 1 , Vieau Didier 1 , Blum David 1 & Buée-Scherrer Valérie 1
1Univ. Lille, Inserm, CHU Lille, U1172 LilNCog - Lille Neuroscience & Cognition, Lille, France.; 2Univ. Lille, Inserm, CHU Lille, U1172 LilNCog - Lille Neuroscience & Cognition, Lille, France; 3Univ. Lille, INSERM, CNRS, CHU Lille, Institut Pasteur de Lille, Inserm U1283-UMR8199 - EGID, Lille, France; 4Univ. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, US 41 - UMS 2014 - PLBS, Animal Facility, F-59000 Lille, France.; 5Univ. Lille, INSERM, CNRS, CHU Lille, Institut Pasteur de Lille, Inserm U1283-UMR8199 - EGID, F-59000 Lille, France.; 6Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France., Lille, France; 7Univ. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, US 41 - UMS 2014 - PLBS, BioImaging Center Lille, F-59000 Lille, France, Lille, France; 8Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1167 - RID-AGE - Facteurs de risque et déterminants moléculaires des maladies liées au vieillissement, F-59000 Lille, France., Lille, France
Introduction: Alzheimer disease (AD) is the leading cause of dementia. While impaired glucose homeostasis has been shown to increase AD risk and pathological loss of tau function, the latter has been suggested to contribute to the emergence of the glucose homeostasis alterations observed in AD patients. However, the links between tau impairments and glucose homeostasis, remains unclear.
Objective: In order to better understand the links between tau and glucose homeostasis, the present study aimed at investigating the metabolic phenotype of a new knock-in (KI) mice model.
Method: Males and females Tau KI mice model expressing a human tau protein bearing the P301L mutation under the control of the endogenous mouse Mapt promoter and their non-transgenic littermates (referred as WT) were used. A complete metabolic phenotyping was explored under high fat diet (HFD) versus CHOW diet in both sexes. Also, glucose-stimulated insulin secretion (GSIS) was studied using isolated islets from tau KI and tau knock-out mice and mouse β pancreatic cell line (MIN6).
Results: While under chow diet tau KI mice do not exhibit significant metabolic impairments, we could observe that under HFD male, but not female tau KI animals exhibited glucose homeostasis alterations as compared to control littermates. Interestingly, using immunofluorescence, tau protein was found colocalized with insulin in the β cells of pancreatic islets. Additional experiments performed on isolated islets from tau KI and tau knock-out mice revealed that both exhibit impaired insulin secretion, an effect recapitulated in the mouse β pancreatic cell line (MIN6) following tau knock-down.
Conclusion: Altogether, our data suggest that loss of tau function in pancreatic β cell might favor the development of glucose homeostasis impairment and could contribute to metabolic changes observed in AD.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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