Perinatal undernutrition-induced obesity is independent of the developmental programming of feeding

Orozco-Solís, Ricardo; Souza, Sandra Lopes de; Matos, Rhowena Jane Barbosa de; Grit, Isabelle; Bloch, J; Nguyen, Patrick; Castro, Raul Manhães de; Bolaños-Jiménez, Francisco

doi:10.1016/j.physbeh.2008.11.016

Cited by 72 publications

(83 citation statements)

References 68 publications

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“…This compensatory or catch-up growth leads to a more rapid replenishment of fat stores than reconstitution of lean body mass (46). Previous studies have demonstrated that body fat content, rather than body weight alone, is more closely linked with increased risk of obesity-related disorders (47,48). In this context, it is noteworthy that among the extrapancreatic effects of GIP, it promotes adipocyte differentiation and fat accumulation (14).…”

Section: Discussionmentioning

confidence: 99%

Predominant Role of GIP in the Development of a Metabolic Syndrome-like Phenotype in Female Wistar Rats Submitted to Forced Catch-up Growth

et al. 2014

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Catch-up growth has been associated with the appearance of metabolic dysfunctions such as obesity and type 2 diabetes in adulthood. Because the entero-insular axis is critical to glucose homeostasis control, we explored the relevance of the incretins glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) in the development of these pathologies. Offspring of rat dams fed ad libitum (control [C]) or 65% food-restricted during pregnancy and suckling time (undernourished [U]) were weaned onto a high-fat (HF) diet (CHF and UHF, respectively) to drive catch-up growth. Both male and female UHF rats showed an obese phenotype characterized by hyperphagy, visceral fat accumulation, and adipocyte hypertrophy. High-fat diet induced deterioration of glucose tolerance in a sex-dependent manner. Female UHF rats experienced much more severe glucose intolerance than males, which was not compensated by insulin hypersecretion, suggesting insulin resistance, as shown by homeostatic model assessment of insulin resistance values. Moreover, female, but not male, UHF rats displayed enhanced GIP but not GLP-1 secretion during oral glucose tolerance test. Administration of the GIP receptor antagonist (Pro3)GIP to UHF female rats over 21 days markedly reduced visceral fat mass and adipocyte hypertrophy without variations in food intake or body weight. These changes were accompanied by improvement of glucose tolerance and insulin sensitivity. In conclusion, the exacerbated production and secretion of GIP after the catch-up growth seems to represent the stimulus for insulin hypersecretion and insulin resistance, ultimately resulting in derangement of glucose homeostasis. Overall, these data evidence the role of GIP as a critical link between catch-up growth and the development of metabolic disturbances. (Endocrinology 155: 3769 -3780, 2014)

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Section: Discussionmentioning

confidence: 99%

Predominant Role of GIP in the Development of a Metabolic Syndrome-like Phenotype in Female Wistar Rats Submitted to Forced Catch-up Growth

et al. 2014

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“…These experiments showed that the efficiency of the PCR amplification was the same for all the genes and that the expression of b-actin was not influenced either by age or the mother diet. 46 To test for the presence of circadian rhythms, time series data were first analyzed by one-way ANOVA. The existence of a significant effect of time associated with the clustering of the maximum and minimum values for food ingestion or gene expression into two separate time intervals were used as an evidence of the presence of a circadian rhythm.…”

Section: Discussionmentioning

confidence: 99%

“…The C group was fed a control diet containing 20% of protein (200 g protein kg À1 ) whereas the LP group was fed an isocaloric low-protein diet containing 8% of protein (80 g protein kg À1 ).The diets were purchased from Ab Diets (Woerden, The Netherlands) and their composition have been described previously. 35,46 Dams were fed ad libitum and their body weight and daily food intake documented every 4 days during gestation and lactation. The morning on which new born litters were found was designated as P0 and the litter size was adjusted to eight pups per dam maintaining as close to a 1:1, male : female ratio as possible.…”

Section: Methodsmentioning

confidence: 99%

Perinatal nutrient restriction induces long-lasting alterations in the circadian expression pattern of genes regulating food intake and energy metabolism

et al. 2010

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Objective: Several lines of evidence indicate that nutrient restriction during perinatal development sensitizes the offspring to the development of obesity, insulin resistance and cardiovascular disease in adulthood via the programming of hyperphagia and reduced energy expenditure. Given the link between the circadian clock and energy metabolism, and the resetting action of food on the circadian clock, in this study, we have investigated whether perinatal undernutrition affects the circadian expression rhythms of genes regulating food intake in the hypothalamus and energy metabolism in the liver. Design: Pregnant Sprague-Dawley rats were fed ad libitum either a control (20% protein) or a low-protein (8% protein) diet throughout pregnancy and lactation. At weaning, pups received a standard diet and at 17 and 35 days of age, their daily patterns of gene expression were analyzed by real-time quantitative PCR experiments. Results: 17-day-old pups exposed to perinatal undernutrition exhibited significant alterations in the circadian expression profile of the transcripts encoding diverse genes regulating food intake, the metabolic enzymes fatty acid synthase and glucokinase as well as the clock genes BMAL1 and Period1. These effects persisted after weaning, were associated with hyperphagia and mirrored the results of the behavioral analysis of feeding. Thus, perinatally undernourished rats exhibited an increased hypothalamic expression of the orexigenic peptides agouti-related protein and neuropeptide Y. Conversely, the mRNA levels of the anorexigenic peptides pro-opiomelanocortin and cocaine and amphetamine-related transcripts were decreased. Conclusion: These observations indicate that the circadian clock undergoes nutritional programming. The programming of the circadian clock may contribute to the alterations in feeding and energy metabolism associated with malnutrition in early life, which might promote the development of metabolic disorders in adulthood.

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“…On another point of view, research has indicated that the protein restriction during gestation and lactation induces long-lasting alterations in the microstructure of feeding characterised by a delayed appearance of satiety and increased meal size. 44 Corroborating this information, Souza and colls. 45 has shown that protein restriction during perinatal development attenuates the inhibitory action of serotonin (5-HT) on food intake via a reduced sensitivity of 5-HT1B receptors, explaining that the hyperphagia associated with metabolic programming is at least partially related to a reduced regulatory function of 5-HT on food intake.…”

Section: Malnutritionmentioning

confidence: 97%

Malnutrition and experimental epilepsy

Gomes

Oliveira

Castro

2011

J. epilepsy clin. neurophysiol.

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Introduction: Disturbances in intrauterine environment can have harmful effects on the fetus and pathological consequences persisting throughout adolescence and adulthood. Protein restriction during the prenatal period has a significant impact on growth and development of the central nervous system. Food restriction increases the risk of neurological disorders such as epilepsy. Objective: To relate the programming model by malnutrition and its implications in experimental epilepsy. Material and methods: There has been research papers published in the databases Medline, PubMed, CAPES journals, ScienceDirect and Scielo. The keywords selected for the study included epilepsy, Status Epilepticus, pilocarpine, malnutrition, programming. Results and discussion: Several studies in animal models or humans highlights the possible adverse effects of malnutrition at the onset of epileptic seizures. The vulnerability immunological, biochemical and electrolyte abnormalities and hypoglycemia may be the factors responsible for the intensification of the epileptogenic process in malnourished individuals. Conclusion: Malnutrition negatively changes the epileptogenic circuitry.

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Perinatal undernutrition-induced obesity is independent of the developmental programming of feeding

Cited by 72 publications

References 68 publications

Predominant Role of GIP in the Development of a Metabolic Syndrome-like Phenotype in Female Wistar Rats Submitted to Forced Catch-up Growth

Predominant Role of GIP in the Development of a Metabolic Syndrome-like Phenotype in Female Wistar Rats Submitted to Forced Catch-up Growth

Perinatal nutrient restriction induces long-lasting alterations in the circadian expression pattern of genes regulating food intake and energy metabolism

Malnutrition and experimental epilepsy

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