Maternal Roux-en-Y gastric bypass impairs insulin action and endocrine pancreatic function in male F1 offspring

Autor(es)

Pietrobon, Carla Bruna ^[1] ; Bertasso, Iala Milene ^[1] ; Ribeiro, Rosane Aparecida ^[2] ; Paiva Alegre-Maller, Ana Claudia ^[1] ; Lubaczeuski, Camila ^[3] ; Boschero, Antonio Carlos ^[3] ; Faria Araujo, Allan Cezar ^[4] ; Balbo, Sandra Lucinei ^[1] ; Bonfleur, Maria Lucia ^[1]

Afiliação do(s) autor(es)

^[1] Univ Estadual Oeste Parana UNIOESTE, Ctr Ciencias Biol & Saude, Lab Fisiol Endocrina & Metab LAFEM, BR-85811911 Cascavel, PR - Brazil

^[2] Univ Fed Rio de Janeiro, Campus UFRJ Macae, Macae, RJ - Brazil

^[3] Univ Estadual Campinas, Inst Biol, Dept Biol Estrutural & Func, Lab Pancreas Endocrino & Metab, UNICAMP, Campinas, SP - Brazil

^[4] Univ Estadual Oeste Parana, Ctr Ciencias Med & Farmaceut, Cascavel, PR - Brazil

• Tipo de documento: Artigo Científico
• Fonte: EUROPEAN JOURNAL OF NUTRITION; v. 59, n. 3, p. 1067-1079, APR 2020.
• Citações Web of Science: 3

Resumo

Purpose Obesity is predominant in women of reproductive age. Roux-en-Y gastric bypass (RYGB) is the most common bariatric procedure that is performed in obese women for weight loss and metabolic improvement. However, some studies suggest that this procedure negatively affects offspring. Herein, using Western diet (WD)-obese female rats, we investigated the effects of maternal RYGB on postnatal body development, glucose tolerance, insulin secretion and action in their adult male F1 offspring. Methods Female Wistar rats consumed a Western diet (WD) for 18 weeks, before being submitted to RYGB (WD-RYGB) or SHAM (WD-SHAM) operations. After 5 weeks, WD-RYGB and WD-SHAM females were mated with control male breeders, and the F1 offspring were identified as: WD-RYGB-F1 and WD-SHAM-F1. Results The male F1 offspring of WD-RYGB dams exhibited decreased BW, but enhanced total nasoanal length gain. At 120 days of age, WD-RYGB-F1 rats displayed normal fasting glycemia and glucose tolerance but demonstrated reduced insulinemia and higher glucose disappearance after insulin stimulus. In addition, these rodents presented insulin resistance in the gastrocnemius muscle and retroperitoneal fat, as judged by lower Akt phosphorylation after insulin administration, but an increase in this protein in the liver. Finally, the islets from WD-RYGB-F1 rats secreted less insulin in response to glucose and displayed increased beta-cell area and mass. Conclusions RYGB in WD dams negatively affected their F1 offspring, leading to catch-up growth, insulin resistance in skeletal muscle and white fat, and beta-cell dysfunction. Therefore, our data are the first to demonstrate that the RYGB in female rats may aggravate the metabolic imprinting induced by maternal WD consumption, in their male F1 descendants. However, since we only used male F1 rats, further studies are necessary to demonstrate if such effect may also occur in female F1 offspring from dams that underwent RYGB operation. (AU)

• Processo FAPESP: 15/12611-0 - Mecanismos moleculares envolvidos na disfunção e morte de células beta pancreáticas no Diabetes mellitus: estratégias para a inibição desses processos e para a recuperação da massa insular
• Beneficiário: Antonio Carlos Boschiero
• Modalidade de apoio: Auxílio à Pesquisa - Temático