Low protein

About: Low protein is a research topic. Over the lifetime, 8139 publications have been published within this topic receiving 213225 citations.

Social inequality and child malnutrition in four Andean countries

Abstract: Objective. To analyze the effects of socioeconomic, regional, and ethnic conditions on chronic malnutrition in four Andean countries of South America: Bolivia, Colombia, Ecuador, and Peru. Methods. The study was based on Demographic and Health Surveys (DHS) for Colombia (1995), Peru (1996), and Bolivia (1997), and on a Living Standard Measurement Survey for Ecuador (1998). We developed an index of household socioeconomic status using categorical principal components analysis. We broke down the prevalence of stunting by socioeconomic status (SES), ethnicity, place of residence (large cities, small cities, towns, and countryside), and region (highland region versus other areas of the country). We applied smoothed regression curves and linear functions to analyze SES effects on stunting, with specific models for Bolivia, Ecuador, and Peru. Results. Bolivia, Ecuador, and Peru have similar characteristics, with high stunting prevalences overall; higher stunting prevalences in their highland areas, particularly among indigenous populations; and strong socioeconomic disparities. Colombia, in contrast, has a lower stunting prevalence and smaller regional disparities. The socioeconomic gradient of stunting is strong in all four countries, with prevalence rates in the poorest deciles at least three times as high as those in the top decile. Discussion. The sharp contrast between the conditions found in Bolivia, Ecuador, and Peru and those in Colombia may be the result of specific ethnic factors affecting indigenous groups; a particular diet profile in the highland areas, with low protein and micronutrient intake; and differences in the long-term economic and social development paths that the countries have taken. Along with the strong socioeconomic gradient in all the countries, the weight of ethnic and regional factors suggests the need to reduce inequality as well as to comprehensively improve education and housing, better target health and nutrition programs, and implement participatory programs integrated into indigenous cultures.

Amphibian neural crest cell migration on purified extracellular matrix components: a chondroitin sulfate proteoglycan inhibits locomotion on fibronectin substrates.

Abstract: The ability of purified extracellular matrix components to promote the initial migration of amphibian neural crest (NC) cells was quantitatively investigated in vitro. NC cells migrated avidly on fibronectin (FN), displaying progressively more extensive dispersion at increasing amounts of material incorporated in the substrate. In contrast, dispersion on laminin substrates was optimal at low protein concentrations but strongly reduced at high concentrations. NC cells were unable to migrate on substrates containing a high molecular mass chondroitin sulfate proteoglycan (ChSP). When proteolytic peptides, representing isolated functional domains of the FN molecule, were tested as potential migration substrates, the cell binding region of the molecule (105 kD) was found to be as active as the intact FN. A 31-kD heparin-binding fragment also stimulated NC cell migration, whereas NC cells dispersed to a markedly lower extent on the isolated collagen-binding domain (40 kD), or the latter domain linked to the NH2-terminal part of the FN molecule. Migration on the intact FN was partially inhibited by antibodies directed against the 105- and 31-kD fragments, respectively; dispersion was further decreased when the antibodies were used in combination. Addition of the ChSP to the culture medium dramatically perturbed NC cell migration on substrates of FN, as well as of 105- or 31-kD fragments. However, preincubation of isolated cells or substrates with ChSP followed by washing did not affect NC cell movement. The use of substrates consisting of different relative amounts of ChSP and the 105-kD peptide revealed that ChSP counteracted the motility-promoting activity of the 105-kD FN fragment in a concentration-dependent manner also when bound to the substrate. Our results indicate that NC cell migration on FN involves two separate domains of the molecule, and that ChSP can modulate the migratory behavior of NC cells moving along FN-rich pathways and may therefore influence directionally and subsequent localization of NC cells in the embryo.

Protein restriction during gestation and/or lactation causes adverse transgenerational effects on biometry and glucose metabolism in F1 and F2 progenies of rats.

Abstract: Substantial evidence suggests that poor intrauterine milieu elicited by maternal nutritional disturbance may programme susceptibility in the fetus to later development of chronic diseases, such as obesity, hypertension, cardiovascular disease and diabetes. One of the most interesting features of fetal programming is the evidence from several studies that the consequences may not be limited to the first-generation offspring and that it can be passed transgenerationally. In the present study, female rats (F0) were fed either a normal-protein diet [control diet (C); 19 g of protein/100 g of diet] or a low-protein diet [restricted diet (R); 5 g of protein/100 g of diet]. The offspring were termed according to the period and the types of diet the dams were fed, i.e. CC, RC, CR and RR (first letter indicates the diet during gestation and the second the diet during lactation). At 3 months of age, F1 females were bred to proven males, outside the experiment, to produce F2 offspring. At weaning, F2 offspring were divided by gender. RC1 offspring (with the number indicating the filial generation) were born with low birthweight, but afterwards they had catch-up growth, reaching the weight of the CC1 offspring. The increased glycaemia in RC1 offspring was associated with insulin resistance. CR1 and RR1 offspring had impaired growth with no changes in glucose metabolism. RC2 offspring had high BM (body mass) at birth, which was sustained over the whole experiment in male offspring. The F2 generation had more alteration in glucose metabolism than the F1 generation. CR2 and RC2 offspring had hyperglycaemia accompanied by hyperinsulinaemia and insulin resistance in both genders. CR2 offspring had an increase in body adiposity with hyperleptinaemia. In conclusion, low protein during gestation improves BM, fat mass and growth rate in F1 rats, but has adverse effects on glucose and leptin metabolism, resulting in insulin resistance in adult F1 and F2 offspring. Low protein during lactation has adverse effects on glucose, insulin and leptin metabolism, resulting in insulin resistance in adult F2 offspring. These findings suggest that low protein during gestation and/or lactation can be passed transgenerationally to the second generation.