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Mechanism of muscle atrophy in a normal-weight rat model of type 2 diabetes established by using a soft-pellet diet.
Akieda-Asai, Sayaka; Ma, Hao; Han, Wanxin; Nagata, Junko; Yamaguchi, Fumitake; Date, Yukari.
Afiliación
  • Akieda-Asai S; Frontier Science Research Center, University of Miyazaki, Miyazaki, 889-1692, Japan. akieda@med.miyazaki-u.ac.jp.
  • Ma H; Frontier Science Research Center, University of Miyazaki, Miyazaki, 889-1692, Japan.
  • Han W; Frontier Science Research Center, University of Miyazaki, Miyazaki, 889-1692, Japan.
  • Nagata J; Department of Sensory and Motor Organs, Faculty of Medicine, University of Miyazaki, Miyazaki, 889-1692, Japan.
  • Yamaguchi F; Frontier Science Research Center, University of Miyazaki, Miyazaki, 889-1692, Japan.
  • Date Y; Department of Nursing, Faculty of Medicine, University of Miyazaki, Miyazaki, 889-1692, Japan.
Sci Rep ; 14(1): 7670, 2024 04 01.
Article en En | MEDLINE | ID: mdl-38561446
ABSTRACT
Dietary factors such as food texture affect feeding behavior and energy metabolism, potentially causing obesity and type 2 diabetes. We previously found that rats fed soft pellets (SPs) were neither hyperphagic nor overweight but demonstrated glucose intolerance, insulin resistance, and hyperplasia of pancreatic ß-cells. In the present study, we investigated the mechanism of muscle atrophy in rats that had been fed SPs on a 3-h time-restricted feeding schedule for 24 weeks. As expected, the SP rats were normal weight; however, they developed insulin resistance, glucose intolerance, and fat accumulation. In addition, skeletal muscles of SP rats were histologically atrophic and demonstrated disrupted insulin signaling. Furthermore, we learned that the muscle atrophy of the SP rats developed via the IL-6-STAT3-SOCS3 and ubiquitin-proteasome pathways. Our data show that the dietary habit of consuming soft foods can lead to not only glucose intolerance or insulin resistance but also muscle atrophy.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Resistencia a la Insulina / Intolerancia a la Glucosa / Diabetes Mellitus Tipo 2 Límite: Animals Idioma: En Revista: Sci Rep Año: 2024 Tipo del documento: Article País de afiliación: Japón

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Resistencia a la Insulina / Intolerancia a la Glucosa / Diabetes Mellitus Tipo 2 Límite: Animals Idioma: En Revista: Sci Rep Año: 2024 Tipo del documento: Article País de afiliación: Japón