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The insulin-like growth factor (IGF) system is altered with intra-uterine growth retardation and in adult metabolic disease. The aim of the present study was to observe effects of continued protein restriction on the IGF-I system and body composition in offspring of mothers fed a low-protein (LP) diet. Offspring from Wistar dams fed either a 20 % (CON) or 8 % (LP) protein diet during gestation and lactation were studied at birth, 10 d, weaning and at 12 weeks after maintenance on either the 8 % (lp) or 20 % (con) protein diet from weaning. LP offspring had reduced weaning weights (P < 0·05) and reduced serum insulin (P < 0·005). Serum IGF-I (P < 0·001) and acid-labile subunit (ALS) (P < 0·0001) were reduced at 10 and 21 d. Hepatic expression of IGF-I (P < 0·05) and ALS (P < 0·005) were reduced at 10 and 21 d. IGF binding protein (IGFBP)-1 hepatic expression was elevated at 10 d (P < 0·001) but not at 21 d. Adult LP-con offspring had reduced body weight (P < 0·05), lean (P < 0·0001) and bone (P < 0·0001) but not fat (P = 0·6) mass with no persistent effects on IGF-I, ALS and IGFBP-1.Postnatal lp feeding reduced lean mass (P < 0·0001) and bone mass (P < 0·0001) in CON and LP animals. Percentage fat (LP P = 0·04; CON P = 0·6) and IGFBP-1 (LP P = 0·01; CON P = 0·2) were increased in LP-lp but not CON-lp offspring. This suggests that postnatal nutrition is important in the effects of maternal protein restriction on adult body composition and that IGFBP-1 may be involved. [ABSTRACT FROM PUBLISHER]

We apply nutritional geometry, a framework for modelling the interactive effects of nutrients on animals, to help understand the role of modern environments in the obesity pandemic. Evidence suggests that humans regulate the intake of protein energy (PE) more strongly than non-protein energy (nPE), and consequently will over- and under-ingest nPE on diets with low or high PE, respectively. This pattern of macronutrient regulation has led to the protein leverage hypothesis, which proposes that the rise in obesity has been caused partly by a shift towards diets with reduced PE:nPE ratios relative to the set point for protein regulation. We discuss potential causes of this mismatch, including environmentally induced reductions in the protein density of the human diet and factors that might increase the regulatory set point for protein and hence exacerbate protein leverage. Economics--the high price of protein compared with fats and carbohydrates--is one factor that might contribute to the reduction of dietary protein concentrations. The possibility that rising atmospheric CO₂ levels could also play a role through reducing the PE:nPE ratios in plants and animals in the human food chain is discussed. Factors that reduce protein efficiency, for example by increasing the use of ingested amino acids in energy metabolism (hepatic gluconeogenesis), are highlighted as potential drivers of increased set points for protein regulation. We recommend that a similar approach is taken to understand the rise of obesity in other species, and identify some key gaps in the understanding of nutrient regulation in companion animals.