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Effect of a high‐protein diet on food intake and liver metabolism during pregnancy, lactation and after weaning in mice
Author(s) -
Kuhla Björn,
Kucia Marzena,
Görs Solvig,
Albrecht Dirk,
Langhammer Martina,
Kuhla Siegfried,
Metges Cornelia C.
Publication year - 2010
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.200900789
Subject(s) - lactation , medicine , argininosuccinate synthase , endocrinology , biology , arginine , glutamine , weaning , metabolism , gluconeogenesis , glycogen , catabolism , protein metabolism , amino acid , arginase , biochemistry , pregnancy , genetics
Abstract Major hepatic metabolic pathways are involved in the control of food intake but how dietary proteins affect global metabolism to adjust food intake is incompletely understood, particularly under physiological challenging conditions such as lactation. In order to identify these molecular events, mice were fed a high‐protein (HP) diet from pregnancy, during lactation until after weaning and compared with control fed counterparts. Liver specimens were analyzed for regulated proteins using 2‐DE and MALDI‐TOF‐MS and plasma samples for metabolites. Based on the 26 differentially expressed proteins associated with depleted liver glycogen content, elevated urea and citrulline plasma concentrations, we conclude that HP feeding during lactation leads to an activated amino acid, carbohydrate and fatty acid catabolism while it activates gluconeogenesis. From pregnancy to lactation, plasma arginine, tryptophan, serine, glutamine and cysteine decreased, whereas urea concentrations increased in both groups. Concomitantly, hepatic glycogen content decreased while total fat content remained unaltered in both groups. Consideration of 59 proteins differentially expressed between pregnancy and lactation highlights different strategies of HP and control fed mice to meet energy requirements for lactation by adjusting amino acid degradation, carbohydrate and fat metabolism, citrate cycle, but also ATP‐turnover, protein folding, secretion of proteins and (de)activation of transcription factors.