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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanisms linking intrauterine growth retardation (IUGR) with adulthood obesity and diabetes are unclear. These studies investigated energy homeostasis in 8- and 20-wk-old male and female mice subjected to protein deficiency in utero. Pregnant C57BL/6J female mice were fed a protein-deficient diet (6% protein). Undernourished offspring (UO) and controls (CO) were cross-fostered to lactating dams fed a 20% control diet. The 24-h profiles of energy expenditure, feeding behavior, physical activity, and whole-body substrate preference was assessed using 8-wk UO and CO weaned onto control diet. Blood chemistries, glucose tolerance, and expression of genes involved in hepatic lipid and glucose metabolism were analyzed in 8- and 20-wk-old CO and UO fed control or a high-fat diet. UO exhibited IUGR with catch-up growth at 8 wk of age and increased severity of diet-induced obesity and insulin resistance by 20 wk of age. Therefore, fetal malnutrition in the C57BL/6J mouse increases sensitivity to diet-induced obesity. Abnormal daily rhythms in food intake and metabolism, increased lipogenesis, and inflammation preceded obesity in the UO group. Arrhythmic expression of circadian oscillator genes was evident in brain, liver, and muscle of UO at 8 and 20 wk of age. Expression of the clock-associated nuclear receptor and transcription repressor Rev-erbalpha was reduced in liver and muscle of UO. Altered circadian physiology may be symptomatic of the metabolic dysregulation associated with IUGR, and altered feeding behavior and substrate metabolism may contribute to the obese phenotype.
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PMID:Protein malnutrition during pregnancy in C57BL/6J mice results in offspring with altered circadian physiology before obesity. 2033

Patients who have undergone bariatric surgery are at increased risk of developing nutritional deficiencies from limited food intake and absorption of different nutrients. A systematic review of several database websites (PubMed and ISI Web of Science) was conducted from September 1983 to April 2010 to identify literature related to micronutrient deficiencies occurring after bariatric surgery. Keywords used individually or in various combinations in the search were bariatric surgery, obesity, vitamin/mineral deficiencies, protein deficiency, nutrient absorption and nutrient supplementation. Literature suggests that to prevent or treat nutritional deficiencies resulting from anatomical changes due to surgical techniques nutritional supplementation is usually necessary. The success of oral nutritional supplementation to correct or prevent nutritional deficiencies depends on several factors. Thus, to understand how nutrients can be administered is very important for clinical practice. This review aims to provide help for the best selection of nutrients to ensure an adequate replacement of nutrients in patients who have undergone bariatric surgery.
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PMID:[Bariatric surgery: how and why to supplement]. 2139 Apr 68

A vegetarian diet may be adopted for various reasons that can include ecological, economic, religious, ethical and health considerations. In the latter case they arise from the desire to lose weight, in tackling obesity, improving physical fitness and/or in reducing the risk of acquiring certain diseases. It has been shown that properly applied vegetarian diet is the most effective way of reducing body mass (expressed as BMI), improving the plasma lipid profile and in decreasing the incidence of high arterial blood pressure, cardiovascular disease, stroke, metabolic syndrome and arteriosclerosis. In addition, improved insulin sensitivity together with lower rates of diabetes and cancer has been observed. Some studies have however found that a vegetarian diet may result in changes adversely affecting the body. These could include; hyperhomocysteinaemia, protein deficiency, anaemia, decreased creatinine content in muscles and menstrual disruption in women who undertake increased physical activity. Some of these changes may decrease the ability for performing activities that require physical effort. Nevertheless, on balance it can be reasonably concluded that the beneficial effects of a vegetarian diet significantly, by far, outweigh the adverse ones. It should also be noted that the term 'vegetarian diet' is not always clearly defined in the literature and it may include many dietary variations.
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PMID:Health benefits and risk associated with adopting a vegetarian diet. 2496 73

Malnutrition programs the neuroendocrine axis by disruption of food-intake control, leading to obesity. Taurine (Tau) is neuroprotective and improves anorexigenic actions in the hypothalamus. We evaluated the hypothalamic gene-expression profile and food-intake control in protein-restricted mice submitted to a high-fat diet (HFD) and Tau supplementation. Mice were fed on a control (14 % protein-C) or a protein-restricted diet (6 % protein-R) for 6 weeks. Thereafter, mice received, or not, HFD for 8 weeks (CH and RH) with or without 5 % Tau supplementation (CHT and RHT). Protein restriction led to higher food intake, but calories were matched to controls. Excessive calorie intake occurred in HFD mice and this was prevented by Tau supplementation only in the CH group. Additionally, RH and CH mice developed hypothalamic leptin resistance, which was prevented by Tau. Global alterations in the expressions of genes involved in hypothalamic metabolism, cellular defense, apoptosis and endoplasmic reticulum stress pathways were induced by dietary manipulations and Tau treatment. The orexigenic peptides NPY and AgRP were increased by protein restriction and lowered by the HFD. The anorexigenic peptide Pomc was increased by HFD, and this was prevented by Tau only in CH mice. Thus, food intake was disrupted by dietary protein restriction and obesity. HFD-induced alterations were not enhanced by previous protein deficiency, but the some beneficial effects of Tau supplementation upon food intake were blunted by protein restriction. Tau effects upon feeding behavior control are complex and involve interactions with a vast gene network, preventing hypothalamic leptin resistance.
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PMID:Taurine supplementation preserves hypothalamic leptin action in normal and protein-restricted mice fed on a high-fat diet. 2613 37

Human gut bacterial Na(+)-transporting NADH:ubiquinone reductase (NQR) sequence is associated with Alzheimer disease (AD). Here, Alzheimer disease-associated sequence (ADAS) is further characterized in cultured spore-forming Clostridium sp. Tryptophan and NQR substrate ubiquinone have common precursor chorismate in microbial shikimate pathway. Tryptophan-derived tryptamine presents in human diet and gut microbiome. Tryptamine inhibits tryptophanyl-tRNA synthetase (TrpRS) with consequent neurodegeneration in cell and animal models. Tryptophanyl-tRNA synthetase inhibition causes protein biosynthesis impairment similar to that revealed in AD. Tryptamine-induced TrpRS gene-dose reduction is associated with TrpRS protein deficiency and cell death. In animals, tryptamine treatment results in toxicity, weight gain, and prediabetes-related hypoglycemia. Sequence analysis of gut microbiome database reveals 89% to 100% ADAS nucleotide identity in American Indian (Cheyenne and Arapaho [C&A]) Oklahomans, of which ~93% being overweight or obese and 50% self-reporting type 2 diabetes (T2D). Alzheimer disease-associated sequence occurs in 10.8% of C&A vs 1.3% of healthy American population. This observation is of considerable interest because T2D links to AD and obesity. Alzheimer disease-associated sequence prevails in gut microbiome of colorectal cancer, which linked to AD. Metabolomics revealed that tryptamine, chorismate precursor quinate, and chorismate product 4-hydroxybenzoate (ubiquinone precursor) are significantly higher, while tryptophan-containing dipeptides are lower due to tRNA aminoacylation deficiency in C&A compared with non-native Oklahoman who showed no ADAS. Thus, gut microbial tryptamine overproduction correlates with ADAS occurrence. Antibiotic and diet additives induce ADAS and tryptamine. Mitogenic/cytotoxic tryptamine cause microbial and human cell death, gut dysbiosis, and consequent disruption of host-microbe homeostasis. Present analysis of 1246 participants from 17 human gut metagenomics studies revealed ADAS in cell death diseases.
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PMID:Diet-Related Metabolic Perturbations of Gut Microbial Shikimate Pathway-Tryptamine-tRNA Aminoacylation-Protein Synthesis in Human Health and Disease. 3094 20

Nutritional constraints including not only caloric restriction or protein deficiency, but also energy-dense diets affect metabolic health and frequently lead to obesity and insulin resistance, as well as glucose intolerance and type 2 diabetes. The effects of these environmental factors are often mediated via epigenetic modifiers that target the expression of metabolic genes. More recently, it was discovered that such parentally acquired metabolic changes can alter the metabolic health of the filial and grand-filial generations. In mammals, this epigenetic inheritance can either follow an intergenerational or transgenerational mode of inheritance. In the case of intergenerational inheritance, epimutations established in gametes persist through the first round of epigenetic reprogramming occurring during preimplantation development. For transgenerational inheritance, epimutations persist additionally throughout the reprogramming that occurs during germ cell development later in embryogenesis. Differentially expressed transcripts, genomic cytosine methylations, and several chemical modifications of histones are prime candidates for tangible marks which may serve as epimutations in inter- and transgenerational inheritance and which are currently being investigated experimentally. We review, here, the current literature in support of epigenetic inheritance of metabolic traits caused by nutritional constraints and potential mechanisms in man and in rodent model systems.
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PMID:Nutrition and its role in epigenetic inheritance of obesity and diabetes across generations. 3235 Jun 5

Optimum body composition in terms of higher muscle and bone mass is crucial for balancing metabolic activities for sustainability of healthy human life. Individuals with lesser muscle mass respond poorly to stressed states such as traumatic injury, sepsis and advanced cancers. Most common diseases like obesity, heart disease, cancer and diabetes can be prevented by muscle mass modification. The nutrients like protein, lysine, calcium and vitamin D play a critical role in the maintenance of muscle mass and bone health. Poor dietary protein quality owing to high amounts of cereals and little animal foods have a marked negative impact on health in resource-limited settings. Lysine intake in developing countries is low mainly due to lesser food intake, consumption of cereals as staple diet and processing loss of lysine. Furthermore, lysine intakes have been shown to be marginal in low socio-economic groups which are of even greater concern. Cereal-based diets and cereal-based food subsidy programs offer low quality proteins and pose a risk of quality protein deficiency. Diets lacking in vitamin D contribute to vitamin D deficiency which is prevalent in epidemic proportions in large part of the world. Cereal-based vegetarian diets are responsible for lesser bioaccessibility of calcium as well. For obtaining optimal health, optimal muscle mass should be maintained at a younger age, which can be achieved by improving nutritional quality of diets. Dietary and medicinal supplementation of lysine, calcium and vitamin D may improve the body composition of young adult women in the form of proportionally more muscle mass, bone mass and lesser fat mass, which in turn, may prove helpful in improving general well-being, physical fitness as well as preventing metabolic diseases in developing countries.
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PMID:Protein, lysine and vitamin D: critical role in muscle and bone health. 3329 94


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