Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Under- and over-nutrition in children in KwaZulu-Natal, South Africa was investigated comparing data collected from primary school children in a rural district (643 children aged 8-11 years in 1994) with secondary data from the National Schools Study (16,179 children, 4-11 years in 1994), the Vitamin A Consultative Group Study (408 children, 2-5 years in 1994) and the Income Dynamics Study (1,593 children, 2-11 years in 1998). Stunting and wasting (WHO/NCHS guidelines) and overweight and obesity (International Obesity Task Force guidelines) were retrospectively analysed from these studies and compared in the children aged 4-5 and 8-11 years. There was moderate stunting in 10-25%, wasting in 1-6%, 5-24% were overweight and 1-10% obese. Girls in the National Schools Study (p<0.005) and in the primary datasets (p=0.02) had a significantly higher prevalence of overweight than boys; girls (1.4%) were also more obese than boys (0.9%) in the Schools Study (p=0.002), and the boys significantly more stunted (p<0.005) and wasted (p<0.005). An increasing prevalence of overweight and obesity was seen in both the 4-5- and 8-11-year age-groups. The finding that moderate stunting co-exists with overweight and obesity suggests that patterns of under- and over-nutrition in South African children are changing and might indicate the early stages of a complex nutritional transition. Action is required to prevent the future risk of non-communicable diseases.
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PMID:Changing patterns of under- and over-nutrition in South African children-future risks of non-communicable diseases. 1581 43

Oleoyl-estrone (OE) decreases appetite, induces adipose tissue wasting and resets the ponderostat setting, sparing glucose and protein. The beta3-adrenergic agonists increase energy expenditure and lipolysis. We studied the combination of both treatments to enhance fat mobilization. Overweight male rats received oral OE for 10 days; they were compared with controls and rats receiving a beta3-adrenergic agonist, CL316,243 (B3A); another group received both OE and B3A. Serum 3-hydroxybutyrate, NEFA, triacylglycerols and glucose showed only slight changes in all groups vs. controls; OE-treated rats showed lower cholesterol. OE decreased food intake and B3A increased energy expenditure. OE rats lost about 15%, B3A 24%, and those receiving both compounds lost 39% of their initial total body energy. In all cases, most of this energy imbalance was accounted for by the loss of body lipid. The combined treatment of OE and B3A reduced food intake, nevertheless maintaining a high energy expenditure. The combination of a beta3-adrenergic agonist with OE may help compensate the short-lived effects of the agonist and enhance the lipid mobilization action of OE. The eventual combination of both compounds should be explored as a way to obtain faster and more effective ways to treat obesity.
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PMID:Combined effects of oleoyl-estrone and a beta3-adrenergic agonist (CL316,243) on lipid stores of diet-induced overweight male Wistar rats. 1593 2

Although traditional risk factors for cardiovascular disease are common in dialysis patients, they alone cannot explain the unacceptably high prevalence of vascular disease in this patient group. Much recent interest has therefore focused on the role of various nontraditional cardiovascular risk factors, such as inflammation, wasting, obesity, vascular calcification, and oxidative stress. In addition, genetic factors such as single nucleotide polymorphisms (SNPs) may significantly influence the immune response, the levels of inflammatory markers and body composition, as well as the prevalence of vascular calcification in this patient group. While genetic variations in the tumor necrosis factor (TNF)-alpha-308 and interleukin (IL)-10 -1082 SNPs seem to be consistently associated with adverse clinical outcome in end-stage renal disease (ESRD) patients, the results regarding genetic variations in the IL-6 gene have been conflicting. To elucidate the respective role of DNA polymorphisms in the IL-6 and C-reactive protein (CRP) genes, as well as genes that encode vascular calcification inhibitors (such as fetuin-A, matrix Gla protein, and osteoprotegerin), sufficiently powered studies are needed in which both the protein product and the specific phenotype are determined. In addition, polymorphisms in genes related to body composition may be excellent candidates for analysis in the ESRD population, since nutritional parameters are strongly associated with adverse events in these patients. It seems conceivable that in the future, prognostic or predictive multigene DNA assays (which allow a simultaneous and rapid assessment of multiple genetic variants) will provide nephrologists with a more precise approach for the identification of "high-risk" ESRD patients and the development of accurate individualized treatment strategies.
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PMID:Gene polymorphism association studies in dialysis: the nutrition-inflammation axis. 1607 56

We have developed a primary skeletal muscle cell culture model derived from normal prepubertal children to investigate the effects of insulin-like growth factor-I (IGF-I), insulin-like growth factor binding protein-3 (IGFBP-3) and tumour necrosis factor alpha (TNFalpha) on growth, differentiation and metabolism. Cells of myoblast lineage were characterized morphologically by desmin staining and differentiated successfully into multinucleated myotubes. Differentiation was confirmed biochemically by an increase in creatine kinase (CK) activity and IGFBP-3 secretion over time. IGF-I promoted whilst TNFalpha inhibited myoblast proliferation, differentiation and IGFBP-3 secretion. IGF-I partially rescued the cells from the inhibiting effects of TNFalpha. Compared to adult myoblast cultures, children's skeletal muscle cells demonstrated higher basal and day 7 CK activities, increased levels of IGFBP-3 secretion, diminished IGF-I/TNFalpha action and absence of the inhibitory effect of exogenous IGFBP-3 on differentiation. Additional studies demonstrated that TNFalpha increased basal glucose transport via GLUT1, nitric oxide synthase and p38MAPK-dependent mechanisms. These studies provide baseline data to study the interactivity effects of growth factors and cytokines on differentiation and metabolism in muscle in relation to important metabolic disorders such as obesity, type II diabetes or chronic wasting diseases.
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PMID:Isolation and validation of human prepubertal skeletal muscle cells: maturation and metabolic effects of IGF-I, IGFBP-3 and TNFalpha. 1608 85

Whereas the most powerful stimuli for bone formation is supposed to be a stretching of muscles, Frost HM classified the effect of muscle on bone mineral density (BMD) into various types: 1. age-related loss of bone mineral density (BMD) is partly due to loss of muscular wasting, 2. the increase of BMD in obesity is due to the increase in muscular power to support the increased body weight and 3. the decrease of BMD in chronic wasting disease is partly due to the decrease in muscular power. Likewise, the decrease in BMD in mandibular alveolar bones will be partly due to the decrease in the power of masticating muscles, if such exists. A case report of mitochondrial encephalo-myopathy associated with impaired function of cranial nerves involving trigeminus nerves and impaired function of masticating muscles and dysphagia. This patient showed decrease in alveolar BMD and atrophy of mandibular.
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PMID:[Muscular power of masticating muscles and mandibular osteoporosis]. 1646 28

The coexistence of child malnutrition and maternal overweight in the same households typifies rapid nutrition transition in developing countries (DCs). It is reportedly less common in Africa than in Latin America or Asia, but the phenomenon is still little documented. The purpose of our study in poor urban neighbourhoods of the capital city of Benin (West Africa) was to assess the magnitude of the overlap of child protein-energy malnutrition (PEM) and maternal overweight within households, and to compare these households with other nutritional phenotypes in terms of socio-economic circumstances and diet quality. Our hypothesis was that both child PEM and maternal overweight could stem from poor socio-economic conditions, including lack of sanitation, and poor diet quality. Food diversity was used as an index of diet quality, or the qualitative dimension of food security. A random sample of 148 households that included a least the biological mother, one child between 6 and 59 months of age and a second one between 5 and 11 years was selected in two poor neighbourhoods of the capital city of Cotonou to assess the prevalence of "double burden" households and of other nutritional phenotypes of households: with PEM only in at least one child; with maternal overweight only; and without PEM or overweight. Body weights and heights of mothers and of the two targeted children were measured. As long as one child had low weight-for-height or height-for-age (z-score <-2.0), the household came under the "PEM" type. In mothers, overweight was defined as body mass index (BMI) > or = 25, obesity > or = 30 and chronic energy deficiency <18.5. We retained 126 households for interviews with mothers on socio-economic circumstances and food diversity. A socio-economic status (SES) score was constructed on the basis of household amenities and maternal education. Food insecurity was based on reported shortage of food in the last year in the household. Based on the frequency of consumption of 13 different food groups in the previous week, a food diversity score was computed. Overall 35.5% of children were malnourished, and school-age children had a worse nutritional status than under-5 children: 41% and 30% PEM (chronic or acute or both), respectively. The rate of maternal overweight was 39.1% including 15.5% of obesity. Child PEM coexisted with maternal overweight or obesity in 16.2% of the households; 27.7% of households had PEM only, 23% overweight only, 20.3% showed no malnutrition or overweight, and 12.8% had an underweight mother. Maternal BMI status was significantly associated with both children's weight-for-height z-score, particularly the elder one. The rate of child malnutrition, particularly wasting, was significantly higher among underweight mothers and lower in overweight mothers . Underweight mothers were merged with mothers with BMI < or = 25 for the remaining analyses. Households with overweight mothers tended to enjoy relatively better socio-economic conditions--higher SES, higher maternal education, less food insecurity, better household sanitation; they also tended to have a more diversified diet. This is in contrast with PEM households. Dual burden households shared several socio-economic features with the PEM households, except for a higher (not significant) SES score. Dual burden households also had the lowest food diversity score of all household types. Logistical regression models revealed that a relatively higher SES level was associated with a higher likelihood of maternal overweight in PEM households, whereas poor household sanitation increased the odds of PEM among maternal overweight households. Food diversity appeared significantly associated with a lower likelihood of dual burden in all types of households. The study highlights the importance of addressing the double burden of malnutrition and overweight even in poor areas of low income countries of West Africa. It suggests that prevention efforts should be aimed at improving diet quality and sanitation in poor urban households.
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PMID:[Child malnutrition and maternal overweight in same households in poor urban areas of Benin]. 1647 7

Since the earliest reports of human immunodeficiency virus (HIV) disease, undernutrition has been associated with HIV infection, typically with the late stages of the disease (namely acquired immunodeficiency syndrome), and may advance to severe wasting and cachexia. Specific micronutrient deficiencies are also recognized to occur with HIV infection, but their actual effect on the clinical course of the disease is hard to assess. The studies reviewed provide more insight into the complex interface between undernutrition and, in some cases, obesity and HIV/acquired immunodeficiency syndrome and highlight the possibility of alleviating or curing undernutrition by means of simple and comparatively inexpensive dietary adjustments.
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PMID:Nutritional and metabolic abnormalities in pre-AIDS HIV infection. 1670 57

Ghrelin, an acylated upper gastrointestinal peptide, is the only known orexigenic hormone. Considerable evidence implicates ghrelin in mealtime hunger and meal initiation. Circulating levels decrease with feeding and increase before meals, achieving concentrations sufficient to stimulate hunger and food intake. Preprandial ghrelin surges occur before every meal on various fixed feeding schedules and also among individuals initiating meals voluntarily without time- or food-related cues. Ghrelin injections stimulate food intake rapidly and transiently, primarily by increasing appetitive feeding behaviors and the number of meals. Preprandial ghrelin surges are probably triggered by sympathetic nervous output. Postprandial suppression is not mediated by nutrients in the stomach or duodenum, where most ghrelin is produced. Rather, it results from post-ingestive increases in lower intestinal osmolarity (information probably relayed to the foregut via enteric nervous signaling), as well as from insulin surges. Consequently, ingested lipids suppress ghrelin poorly compared with other macronutrients. Beyond a probable role in meal initiation, ghrelin also fulfills established criteria for an adiposity-related hormone involved in long-term body-weight regulation. Ghrelin levels circulate in relation to energy stores and manifest compensatory changes in response to body-weight alterations. Ghrelin crosses the blood-brain barrier and stimulates food intake by acting on several classical body-weight regulatory centers, including the hypothalamus, hindbrain, and mesolimbic reward system. Chronic ghrelin administration increases body weight via diverse, concerted actions on food intake, energy expenditure, and fuel utilization. Congenital ablation of the ghrelin or ghrelin-receptor gene causes resistance to diet-induced obesity, and pharmacologic ghrelin blockade reduces food intake and body weight. Ghrelin levels are high in Prader-Willi syndrome and low after gastric bypass surgery, possibly contributing to body-weight alterations in these settings. Extant evidence favors roles for ghrelin in both short-term meal initiation and long-term energy homeostasis, making it an attractive target for drugs to treat obesity and/or wasting disorders.
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PMID:Ghrelin and the short- and long-term regulation of appetite and body weight. 1685 20

HIV has classically been a wasting disease. However, in the United States, obesity is increasingly common among HIV-infected individuals receiving effective antiviral treatment. The risks of obesity are unclear in HIV, although the increased prevalence of diabetes and cardiovascular disease in the presence or absence of obesity causes growing concern. This study aimed to assess the effects of weight loss (through energy restriction combined with aerobic and resistance exercise) on body composition, body fat distribution, resting energy expenditure, quality of life (QOL), strength and fitness, and metabolic risk factors in obese, HIV-infected women. Eighteen HIV-infected women with a body mass index of 30 or more completed a 12-week weight loss program. Before and after the intervention, body composition and fat distribution by dual energy x-ray absorptiometry and whole-body magnetic resonance imaging, resting energy expenditure by indirect calorimetry, QOL, strength, and fitness were measured. Insulin sensitivity by intravenous glucose tolerance test and circulating cardiovascular risk factors (including lipids, tissue plasminogen activator, and plasminogen activator inhibitor 1) were measured in a subset (n = 9). Daily food intake and total body weight decreased (mean +/- SD) by 3195 +/- 477 kJ and 6.7 +/- 4.2 kg, respectively. Weight lost was 95.5% fat by dual energy x-ray absorptiometry or 6.2 L of subcutaneous adipose tissue, 0.7 L visceral adipose tissue, and 0.8 L skeletal muscle by magnetic resonance imaging. Resting energy expenditure fell approximately 419 kJ, strength and fitness increased by 28.9% +/- 18.5% and 36.8% +/- 41.6%, respectively, and QOL improved in 11 of 13 dimensions. There was significant insulin resistance in the subset with metabolic measurements at baseline, and at follow-up there was no improvement in fasting glucose, insulin, or insulin sensitivity, nor was there any change in fasting lipids, tissue plasminogen activator, or plasminogen activator inhibitor 1. There was no significant change in CD4 count or HIV viral load. In conclusion, moderate weight loss achieved by a short-term program of diet and exercise in obese HIV-positive women appears safe and induces loss of adiposity in both the subcutaneous adipose tissue and visceral adipose tissue regions. Despite reduced food intake, weight and fat loss, as well as improvements in strength, fitness, and QOL, the lack of improvement in metabolic parameters suggests that additional interventions may be necessary to reduce the risk of diabetes and cardiovascular disease in this population.
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PMID:Body composition and metabolic effects of a diet and exercise weight loss regimen on obese, HIV-infected women. 1697 3

The 350,000 maintenance hemodialysis (MHD) patients in the United States have an unacceptably high mortality rate of >20%/year. Almost half of all deaths are assumed to be cardiovascular. Markers of kidney disease wasting (KDW) such as hypoalbuminemia, anorexia, body weight and fat loss, rather than traditional cardiovascular risk factors, appear to be the strongest predictors of early death in these patients. The KDW is closely related to oxidative stress (SOX). Such SOX markers as serum myeloperoxidase are associated with pro-inflammatory cytokines and poor survival in MHD patients. Identifying the conditions that modulate the KDW/SOX-axis may be the key to improving outcomes in MHD patients. Dysfunctional lipoproteins such as a higher ratio of the high-density lipoprotein inflammatory index (HII) may engender or aggravate the KDW, whereas functionally intact or larger lipoprotein pools, as in hypercholesterolemia and obesity, may mitigate the KDW in MHD patients. Hence, a reverse epidemiology or "bad-gone-good" phenomenon may be observed. Diet and gene and their complex interaction may lead to higher proportions of pro-inflammatory or oxidative lipoproteins such as HII, resulting in the aggravation of the SOX and inflammatory processes, endothelial dysfunction, and subsequent atherosclerotic cardiovascular disease and death in MHD patients. Understanding the factors that modulate the KDW/SOX complex and their associations with genetic polymorphism, nutrition, and outcomes in MHD patients may lead to developing more effective strategies to improve outcomes in this and the 20 to 30 million Americans with chronic disease states such as individuals with chronic heart failure, advanced age, malignancies, AIDS, or cachexia.
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PMID:The kidney disease wasting: inflammation, oxidative stress, and diet-gene interaction. 1701 6


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