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Day-restricted feeding during pregnancy and lactation programs glucose intolerance and impaired insulin secretion in male rat offspring

de Almeida Faria, J. ; de Araújo, T. M. F. ; Mancuso, R. I. ; Meulman, J. ; da Silva Ferreira, D. ; Batista, T. M. ; Vettorazzi, J. F. ; da Silva, P. M. R. ; Rodrigues, S. C. ; Kinote, A. ; Carneiro, E. M. ; Bordin, S. ; Anhê, G. F.

Acta Physiologica, 2016-07, Vol.217 (3), p.240-253 [Periódico revisado por pares]

England: Blackwell Publishing Ltd

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  • Título:
    Day-restricted feeding during pregnancy and lactation programs glucose intolerance and impaired insulin secretion in male rat offspring
  • Autor: de Almeida Faria, J. ; de Araújo, T. M. F. ; Mancuso, R. I. ; Meulman, J. ; da Silva Ferreira, D. ; Batista, T. M. ; Vettorazzi, J. F. ; da Silva, P. M. R. ; Rodrigues, S. C. ; Kinote, A. ; Carneiro, E. M. ; Bordin, S. ; Anhê, G. F.
  • Assuntos: Animals ; Calcium - metabolism ; Caloric Restriction - adverse effects ; Energy Metabolism - physiology ; Female ; Glucose Intolerance - metabolism ; In Vitro Techniques ; Insulin - metabolism ; Insulin Secretion ; Islets of Langerhans - metabolism ; lactation ; Lactation - physiology ; Male ; metabolic programming ; MicroRNAs - biosynthesis ; MicroRNAs - genetics ; NADP - metabolism ; out-of-phase feeding ; Pregnancy ; Pregnancy, Animal - metabolism ; Rats ; Rats, Wistar ; Syntaxin 1 - biosynthesis ; Syntaxin 1 - genetics
  • É parte de: Acta Physiologica, 2016-07, Vol.217 (3), p.240-253
  • Notas: National Council of Research (CNPq)
    istex:4719F0D640E136A8C18D6D1A8516DEB423E3AAF9
    ark:/67375/WNG-69BGFJSK-R
    ArticleID:APHA12684
    Figure S1. Number of pups per litter born to AL and DF mothers (a) and the male:female ratio per litter (b).Figure S2. Weekly measurements of body weight (a) and body weight gain (b) of male rates belonging to the AL/AL off (n = 19), AL/DF off (n = 13), DF/AL off (n = 13) and DF/DF off (n = 9) between the 4th and the 11th weeks of life. Weekly measurements of body weight (c) and body weight gain (d) of female rates belonging to the AL/AL off (n = 13), AL/DF off (n = 11), DF/AL off (n = 26) and DF/DF off (n = 7) between the 4th and the 11th weeks of life. Data are presented as the mean ± S.E. (N). *indicating P < 0.05 for AL/AL off vs. age-matched AL/DF off, DF/AL off and DF/DF off; #indicating P < 0.05 for AL/AL off vs. AL/DF off, DF/AL off and DF/DF off (One-way anova).
    Research Foundation of the State of Sao Paulo (FAPESP)
    ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-2
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  • Descrição: Aim The maternal environment during pregnancy and lactation plays a determining role in programming energy metabolism in offspring. Among a myriad of maternal factors, disruptions in the light/dark cycle during pregnancy can program glucose intolerance in offspring. Out‐of‐phase feeding has recently been reported to influence metabolism in adult humans and rodents; however, it is not known whether this environmental factor impacts offspring metabolism when applied during pregnancy and lactation. This study aims to determine whether maternal day‐restricted feeding (DF) influences energy metabolism in offspring. Methods Pregnant and lactating Wistar rats were subjected to ad libitum (AL) or DF during pregnancy and lactation. The offspring born to the AL and DF dams were intra‐ and interfostered, which resulted in 4 group types. Results The male offspring born to and breastfed by the DF dams (DF/DF off) were glucose intolerant, but without parallel insulin resistance as adults. Experiments with isolated pancreatic islets demonstrated that the male DF/DF off rats had reduced insulin secretion with no parallel disruption in calcium handling. However, this reduction in insulin secretion was accompanied by increased miRNA‐29a and miRNA34a expression and decreased syntaxin 1a protein levels. Conclusion We conclude that out‐of‐phase feeding during pregnancy and lactation can lead to glucose intolerance in male offspring, which is caused by a disruption in insulin secretion capacity. This metabolic programming is possibly caused by mechanisms dependent on miRNA modulation of syntaxin 1a.
  • Editor: England: Blackwell Publishing Ltd
  • Idioma: Inglês

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