Premium
Protein malnutrition mitigates the effects of a high‐fat diet on glucose homeostasis in mice
Author(s) -
Branco Renato Chaves Souto,
Camargo Rafael Ludemann,
Batista Thiago Martins,
Vettorazzi Jean Franciesco,
Lubaczeuski Camila,
Bomfim Lucas Henrique Montes,
Silveira Leonardo Reis,
Boschero Antônio Carlos,
Zoppi Cláudio Cesar,
Carneiro Everardo Magalhães
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27361
Subject(s) - medicine , endocrinology , insulin resistance , biology , glucose homeostasis , weaning , low protein diet , amp activated protein kinase , citrate synthase , ampk , protein kinase a , skeletal muscle , insulin , phosphorylation , biochemistry , enzyme
Nutrient malnutrition, during the early stages of development, may facilitate the onset of metabolic diseases later in life. However, the consequences of nutritional insults, such as a high‐fat diet (HFD) after protein restriction, are still controversial. We assessed overall glucose homeostasis and molecular markers of mitochondrial function in the gastrocnemius muscle of protein‐restricted mice fed an HFD until early adulthood. Male C57BL/6 mice were fed a control (14% protein‐control diet) or a protein‐restricted (6% protein‐restricted diet) diet for 6 weeks. Afterward, mice received an HFD or not for 8 weeks (mice fed a control diet and HFD [CH] and mice fed a protein‐restricted diet and HFD [RH]). RH mice showed lower weight gain and fat accumulation and did not show an increase in fasting plasma glucose and insulin levels compared with CH mice. RH mice showed higher energy expenditure, increased citrate synthase, peroxisome‐proliferator‐activated receptor gamma coactivator 1‐alpha protein content, and higher levels of malate and α‐ketoglutarate compared with CH mice. Moreover, RH mice showed increased AMPc‐dependent kinase and acetyl coenzyme‐A (CoA) carboxylase phosphorylation, lower intramuscular triacylglycerol content, and similar malonyl‐CoA levels. In conclusion, protein undernourishment after weaning does not potentiate fat accumulation and insulin resistance in adult young mice fed an HFD. This outcome seems to be associated with increased skeletal muscle mitochondrial oxidative capacity and reduced lipids accumulation.