Your browser doesn't support javascript.
loading
Distinct alterations of gut morphology and microbiota characterize accelerated diabetes onset in nonobese diabetic mice.
Simon, Marie-Christine; Reinbeck, Anna Lena; Wessel, Corinna; Heindirk, Julia; Jelenik, Tomas; Kaul, Kirti; Arreguin-Cano, Juan; Strom, Alexander; Blaut, Michael; Bäckhed, Fredrik; Burkart, Volker; Roden, Michael.
Afiliación
  • Simon MC; Institute for Clinical Diabetology, German Diabetes Center, D-40225 Düsseldorf, Germany.
  • Reinbeck AL; German Center for Diabetes Research (DZD), D-85764 München-Neuherberg, Germany.
  • Wessel C; Wallenberg Laboratory and Sahlgrenska Center for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, University of Gothenburg, S-41348 Gothenburg, Sweden.
  • Heindirk J; Institute for Clinical Diabetology, German Diabetes Center, D-40225 Düsseldorf, Germany.
  • Jelenik T; German Center for Diabetes Research (DZD), D-85764 München-Neuherberg, Germany.
  • Kaul K; Institute for Clinical Diabetology, German Diabetes Center, D-40225 Düsseldorf, Germany.
  • Arreguin-Cano J; German Center for Diabetes Research (DZD), D-85764 München-Neuherberg, Germany.
  • Strom A; Institute for Clinical Diabetology, German Diabetes Center, D-40225 Düsseldorf, Germany.
  • Blaut M; German Center for Diabetes Research (DZD), D-85764 München-Neuherberg, Germany.
  • Bäckhed F; Institute for Clinical Diabetology, German Diabetes Center, D-40225 Düsseldorf, Germany.
  • Burkart V; German Center for Diabetes Research (DZD), D-85764 München-Neuherberg, Germany.
  • Roden M; Institute for Clinical Diabetology, German Diabetes Center, D-40225 Düsseldorf, Germany.
J Biol Chem ; 295(4): 969-980, 2020 01 24.
Article en En | MEDLINE | ID: mdl-31822562
The rising prevalence of type 1 diabetes (T1D) over the past decades has been linked to lifestyle changes, but the underlying mechanisms are largely unknown. Recent findings point to gut-associated mechanisms in the control of T1D pathogenesis. In nonobese diabetic (NOD) mice, a model of T1D, diabetes development accelerates after deletion of the Toll-like receptor 4 (TLR4). We hypothesized that altered intestinal functions contribute to metabolic alterations, which favor accelerated diabetes development in TLR4-deficient (TLR4-/-) NOD mice. In 70-90-day-old normoglycemic (prediabetic) female NOD TLR4+/+ and NOD TLR4-/- mice, gut morphology and microbiome composition were analyzed. Parameters of lipid metabolism, glucose homeostasis, and mitochondrial respiratory activity were measured in vivo and ex vivo Compared with NOD TLR4+/+ mice, NOD TLR4-/- animals showed lower muscle mass of the small intestine, higher abundance of Bacteroidetes, and lower Firmicutes in the large intestine, along with lower levels of circulating short-chain fatty acids (SCFA). These changes are associated with higher body weight, hyperlipidemia, and severe insulin and glucose intolerance, all occurring before the onset of diabetes. These mice also exhibited insulin resistance-related abnormalities of energy metabolism, such as lower total respiratory exchange rates and higher hepatic oxidative capacity. Distinct alterations of gut morphology and microbiota composition associated with reduction of circulating SCFA may contribute to metabolic disorders promoting the progression of insulin-deficient diabetes/T1D development.
Asunto(s)
Palabras clave

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Tracto Gastrointestinal / Diabetes Mellitus Experimental / Microbioma Gastrointestinal Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: J Biol Chem Año: 2020 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Tracto Gastrointestinal / Diabetes Mellitus Experimental / Microbioma Gastrointestinal Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: J Biol Chem Año: 2020 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Estados Unidos