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Ensayo controlado aleatorizado2022Solo mecanismos

Intermittent fasting activates markers of autophagy in mouse liver, but not muscle from mouse or humans

Chaudhary R, Liu B, Bensalem J, Sargeant TJ, Page AJ, Wittert GA, Hutchison AT, Heilbronn LK

Nutrition (Burbank, Los Angeles County, Calif.) · 27 citas

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Cómo se estudió

Diseño
Ensayo controlado aleatorizado (indexado por PubMed)
Estudiado en
Personas, más trabajo en animales o laboratorio
Resultado principal
Solo mecanismos

Quién lo pagó

Financiación
Financiación independiente
Gobierno
National Health and Medical Research Council
Subvenciones
National Health and Medical Research Council (1023401)

Según 1 financiador declarado.

Publicación

Publicado
2022-03-25 · Nutrition · vol. 101 · pág. 111662
Editorial
Elsevier BV
Citado
37 citas · más que el 95% de estudios similares · 3.7× el promedio de su campo
Impacto
Entre el 10 % más citado de su campo
Referencias
44 trabajos
Acceso
De pago
Áreas de investigación
Dietary Effects on Health · Autophagy in Disease and Therapy · Genetics, Aging, and Longevity in Model Organisms
Palabras clave
intermittent fasting, autophagy, liver, skeletal muscle, LC3, Beclin-1, p62, LAMP1, high-fat diet, fasting, weight loss, autophagy markers
MeSH
muscle, skeletal, liver, animals, mice, inbred c57bl, humans, mice, microtubule-associated proteins, rna, messenger, fasting, autophagy, female, male, lysosomal-associated membrane protein 1, biomarkers, sequestosome-1 protein, beclin-1

8 autores

  • Rajesh Chaudhary🇦🇺South Australian Health and Medical Research Institute; The University of Adelaide
  • Bo Liu🇦🇺South Australian Health and Medical Research Institute; The University of Adelaide
  • Julien Bensalem🇦🇺South Australian Health and Medical Research Institute
  • Timothy J. Sargeant🇦🇺South Australian Health and Medical Research Institute; The University of Adelaide
  • Amanda J. Page🇦🇺South Australian Health and Medical Research Institute; The University of Adelaide
  • Gary Wittert🇦🇺South Australian Health and Medical Research Institute; The University of Adelaide
  • Amy T. Hutchison🇦🇺South Australian Health and Medical Research Institute; The University of Adelaide
  • Leonie Kaye Heilbronn🇦🇺 · autor de correspondenciaSouth Australian Health and Medical Research Institute; The University of Adelaide

Resumen

El texto original del estudio, en el idioma en que se publicó.

Objectives

Intermittent fasting (IF) activates autophagy in cardiac muscle and pancreatic islets. We examined the effect of IF on markers of autophagy in liver and skeletal muscle in mice and in humans.

Methods

Ten-wk-old C57 BL/6 J male mice were ad libitum (AL) fed a high-fat diet (HFD) or chow diet for 8 wk, before randomization to AL or IF (24-h fast, 3 non-consecutive days per week) for 8 wk (8-16 per group). Tissue was collected in the fed or 22-h fasted state. Fifty women (51 ± 2 y, 31.8 ± 4.3 kg/m2) were randomly assigned to one of two IF protocols (24-hfast, 3 non-consecutive days per week) and fed at 70% (IF70) or 100% (IF100) of energy requirements for 8 wk. Vastus lateralis muscle was collected at 0800 after 12- and 24-h fasts. Microtubule-associated protein light chain 1 (Map1 lc3 b), Beclin1 (Becn1), Sequestosome 1 (Sqstm1/p62), and Lysosomal associated membrane protein 2 (Lamp2) were assessed by quantitative polymerase chain reaction and LC3, BECLIN1 and LAMP1 protein content by immunoblotting.

Results

Fasting increased hepatic LC3 I protein and Map1 lc3 b mRNA levels in IF mice fed chow or HFD. LAMP1 protein and Beclin1 mRNA levels in liver were also increased by fasting, but only in chow-fed mice. IF did not activate markers of autophagy in mouse muscle. In humans, a 24-h fast increased SQSTM1. BECLIN1, SQSTM1 and LAMP2 mRNA levels were decreased in IF70 after a 12-h overnight fast .

Conclusion

Markers of autophagy in liver, but not in muscle, were elevated in response to IF in mice. In humans, autophagy markers in muscle were reduced, likely in response to weight loss.

Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial.

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