Importance of the nutritional status for the interpretation of nuclear medicine examinations

Malnutrition is very prevalent in the Third World, but still in developing Countries and is found in certain communities in developed Countries. Several laboratories examinations are affected by malnutrition. Recently, gestational or neonatal malnutrition were considered to contribute to the development of chronic diseases in adulthood, this phenomena was named programming or metabolic imprinting. Similar consideration were suggested for Nuclear Medicine examinations. Here we review the literature about this aspect and present our own data showing changes in biodistribution of a radiopharmaceutical compound in different animal models of adult malnutrition or caused by maternal malnutrition programming.<br>A desnutrição é muito prevalente em países do Terceiro Mundo, mas ainda o é em países em desenvolvimento e em certas comunidades de países desenvolvidos. Diversos exames laboratoriais são afetados pela desnutrição. Recentemente, demonstrou-se que a desnutrição no período gestacional ou neonatal contribui para o surgimento de doenças crônicas na idade adulta. Este fenômeno foi denominado de programação ou impressão metabólica. Considera-se, de forma similar, que os exames de Medicina Nuclear poderiam ser afetados pela desnutrição ou programação. Neste artigo revisamos a literatura a este respeito, incluindo nossos próprios dados que mostram modificações na biodistribuição de um radiofarmaco em diferentes modelos animais de desnutrição em adultos ou causada por programação

Hyperphagia and hyperleptinemia induced by low-protein, high-carbohydrate diet is reversed at a later stage of development in rats

Abstract This study investigated whether increased food intake after 15 days of low-protein, high-carbohydrate (LPHC) and its normalization in the later period of development change the content of key proteins related to leptin or adiponectin signaling in the hypothalamus. Male rats were divided into five groups: Control groups received a control diet (17% protein, 63% carbohydrate) for 15 (C15) or 45 (C45) days; LPHC groups received an LPHC diet (6% protein, 74% carbohydrate) for 15 (LPHC15) or 45 (LPHC45) days; and Reverse group (R): received LPHC diet for 15 days followed by control diet for another 30 days. The LPHC15 group showed increased adiposity index, leptin level, and adiponectin level, as well as decreased the leptin receptor (ObRb) and pro-opiomelanocortin (POMC) content in the hypothalamus compared with the C15 group. LPHC diet for 45 days or diet reversion (R group) rescued these alterations, except the adiponectin level in LPHC45 rats, which was higher. In summary, LPHC diet reduced hypothalamic leptin action by diminishing ObRb and POMC levels, leading to hyperphagia and adiposity body. Medium-term administration of LPHC diet or reverting to control diet restored the levels of these proteins, thereby improving body lipid mass rearrangement in adulthood

The long-lasting shadow of litter size in rodents: litter size is an underreported variable that strongly determines adult physiology.

BACKGROUND/PURPOSE: Litter size is a biological variable that strongly influences adult physiology in rodents. Despite evidence from previous decades and recent studies highlighting its major impact on metabolism, information about litter size is currently underreported in the scientific literature. Here, we urge that this important biological variable should be explicitly stated in research articles. RESULTS/CONCLUSION: Below, we briefly describe the scientific evidence supporting the impact of litter size on adult physiology and outline a series of recommendations and guidelines to be implemented by investigators, funding agencies, editors in scientific journals, and animal suppliers to fill this important gap

Comportamento alimentar de ratos adultos submetidos à restrição protéica cujas mães sofreram desnutrição durante a lactação Feeding behavior of adult rats submitted to protein malnutrition whose mothers received protein restricted diets during lactation

Foi avaliado o consumo alimentar de animais adultos submetidos à restrição protéica, cujas mães receberam dieta hipoprotéica ou hipocalórica na lactação: controle (C) ração normal com 23% de proteína; restrição protéica (RP) 8% de proteína; restrição energética (RE) 23% de proteína, em quantidade restrita à ingerida pelo grupo restrição protéica. Após o desmame todos os filhotes receberam ração normal até 60 dias e nesta época foram submetidos, por 21 dias, ao seguinte tratamento: (C/C)-filhotes de mães C recebendo ração normal; (restrição protéica/controle)-filhotes de mães Controle, recebendo ração hipoprotéica; (C/RP)-filhotes de mães RP recebendo ração normal; (RP/RP)-filhotes de mães RP recebendo ração hipoprotéica; (C/RE)-filhotes de mães RE recebendo ração normal; (RP/RE)-filhotes de mães RE recebendo ração hipoprotéica. Os filhotes de mães RP consumiram menos ração até 57 dias (p<0,01), enquanto os filhotes de mães RE normalizaram a ingestão aos 37 dias. Aos 81 dias, os animais submetidos à restrição protéica consumiram menos ração (p<0,01). A dieta materna na lactação modificou o consumo alimentar e o peso corporal da prole na vida adulta, estando, possivelmente, a restrição protéica associada a uma alteração permanente no controle hipotalâmico da seleção de nutrientes da prole.<br>This study evaluated food intake of adult animals whose mothers received protein- or energy-restricted diets during lactation as follows: control (C)- 23% of protein; protein-restricted (PR) - 8% of protein; energy-restricted (ER) - 23% of protein, restricted in quantity. After weaning all pups received the control diet until 60 days, when they were separated into groups, with free access to the following diets during 21 days: (C/C)- pups of control dams fed control diet; (PR/C)-pups of control dams fed protein-restricted diet; (C/PR)- pups of protein-restricted dams fed control diet; (PR/PR)-pups of protein-restricted dams fed protein-restricted diet; (C/ER)-pups of energy-restricted dams fed control diet; (PR/ER)-pups of energy-restricted dams fed protein-restricted diet. Pups of protein-restricted dams consumed less food until day 57 (p<0.01), while pups of energy-restricted dams normalized their ingestion at 37 days. At 81 days, all malnourished animals consumed less food than the control (p<0.01). The kind of diet consumed in the lactation period changed the food intake and the body weight of the offspring in the adulthood. So, the protein restriction can possibly be associated with a permanent alteration in the hypothalamic control of nutrients selection of the offspring

Cross-fostering reduces obesity induced by early exposure to monosodium glutamate in male rats

Maternal obesity programmes a range of metabolic disturbances for the offspring later in life. Moreover, environmental changes during the suckling period can influence offspring development. Because both periods significantly affect long-term metabolism, we aimed to study whether cross-fostering during the lactation period was sufficient to rescue a programmed obese phenotype in offspring induced by maternal obesity following monosodium L-glutamate (MSG) treatment. Obesity was induced in female Wistar rats by administering subcutaneous MSG (4&nbsp;mg/g body weight) for the first 5&nbsp;days of postnatal life. Control and obese female rats were mated in adulthood. The resultant pups were divided into control second generation (F2) (CTLF2), MSG-treated second generation (F2) (MSGF2), which suckled from their CTL and MSG biological dams, respectively, or CTLF2-CR, control offspring suckled by MSG dams and MSGF2-CR, MSG offspring suckled by CTL dams. At 120 days of age, fat tissue accumulation, lipid profile, hypothalamic leptin signalling, glucose tolerance, glucose-induced, and adrenergic inhibition of insulin secretion in isolated pancreatic islets were analysed. Maternal MSG-induced obesity led to an obese phenotype in male offspring, characterized by hyperinsulinaemia, hyperglycaemia, hyperleptinaemia, dyslipidaemia, and impaired leptin signalling, suggesting central leptin resistance, glucose intolerance, impaired glucose-stimulated, and adrenergic inhibition of insulin secretion. Cross-fostering normalized body weight, food intake, leptin signalling, lipid profiles, and insulinaemia, but not glucose homeostasis or insulin secretion from isolated pancreatic islets. Our findings suggest that alterations during the lactation period can mitigate the development of obesity and prevent the programming of adult diseases