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

Since the discovery of IL-15 and its role in T-cell proliferation in 1994, different studies on the effects of the cytokine on metabolic effects have been performed. These studies have mainly been involved with the metabolic pathways involved in lipid and protein metabolism. The present review summarises the metabolic effects of IL-15 at different target tissues and the possibilities and potential for therapeutic interventions based on the cytokine's roles in obesity and wasting.
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PMID:Therapeutic potential of interleukin-15: a myokine involved in muscle wasting and adiposity. 1904 16

Nutrition transition is one of the driving forces of the upcoming global epidemic of diabetes mellitus and cardiovascular diseases. We hypothesized that in previously deprived rapidly changing regions, the progress of the obesity epidemic is clustered per community and that screening with anthropometric school surveys can detect the negative effects of the nutrition transition in its early stages. In 16 different rural and urban communities in Binh Thuan Province, southern Vietnam, anthropometric surveys were conducted in local primary schools. Anthropometry of 2613 children showed a significant difference of the prevalence of wasting, stunting, and overweight between urban and rural communities. During the transition from high stunting rates to overweight, communities pass through an episode with dual burden of both conditions at different pace. Anthropometry of primary school children can reveal inter-community differences and identify the early stages of the nutrition transition.
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PMID:Regional clustering of anthropometric dimensions of primary school children in rural and suburban Vietnam. 1911 97

Observational studies in chronic kidney disease (CKD) populations consistently have shown the strong mortality-predictability of such markers of protein-energy wasting (PEW) as hypoalbuminemia, low serum cholesterol levels, low body mass index, and reduced dietary protein intake. Even though the PEW-mortality association data traditionally are reported mostly in maintenance dialysis patients, emerging studies extend the existence of these associations to predialysis stages of CKD. Paradoxic risk factor patterns (reverse epidemiology) for both obesity and cholesterol recently have been reported in predialysis CKD, underscoring the overwhelming impact of PEW, a short-term killer, on reversing the long-term effect of conventional cardiovascular risk factors. Multiple pathophysiologic mechanisms have been suggested to explain the link between PEW and mortality in CKD, including derangements in muscle, adipose tissue, and the gastrointestinal, hematopoietic, and immune systems; complications related to deficiencies of multiple micronutrients; and the maladaptive activation of the inflammatory cascade. In addition to well-described pathophysiologic mechanisms involved in the higher mortality seen with PEW, we also discuss the potential role of novel factors such as circulating actin, gelsolin, and proinflammatory high-density lipoprotein. Whether PEW is causally related to adverse outcomes in CKD needs to be verified in randomized controlled trials of nutritional interventions. The initiation of major clinical trials targeting nutritional interventions with the goal of improving survival in CKD offer the promise of extending the survival of this vulnerable patient population.
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PMID:Why is protein-energy wasting associated with mortality in chronic kidney disease? 1912 69

Insulin resistance often characterizes chronic uremia, and is associated with enhanced morbidity and mortality, because it may contribute to protein-energy wasting (in turn, an independent predictor of reduced survival), atherosclerosis, and cardiovascular death. Causes of insulin resistance in chronic uremia are complex and multifactorial. Obesity is emerging as an independent risk factor for chronic kidney disease, and an expected rise in number of obese uremic patients because of the ongoing worldwide obesity epidemic is likely to increase the prevalence of insulin resistance in chronic uremia in the near future. Similar to the general population, reported associations between obesity and insulin resistance in chronic uremia support a role of adipose tissue and altered adipokine profiles in insulin resistance in obese chronic kidney disease patients. Hormonal imbalances, chronic acidosis, and systemic inflammation and oxidative stress are uremia-associated relevant causes of insulin resistance in nonobese individuals. A further understanding of the causes of insulin resistance in chronic uremia represents a potential important tool in the design of more effective therapeutic strategies to reduce uremia-associated morbidity and mortality.
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PMID:Insulin resistance in chronic uremia. 1912 65

Congenital adrenal hyperplasia (CAH) due to deficiency of the enzyme 21-hydroxylase (21-OH), is distinguished in its classical and nonclassical form and is one of the most common autosomal recessive inherited diseases in humans. The classical form appears between 1:5000 and 1:15000 among the live neonates of North America and Europe, whereas the nonclassical form occurs in approximately 0.2% of the general white populations. Three alleles are associated with the 21-OH locus and can be combined in various ways to individuals who are either unaffected, heterozygote carriers, or affected with the classical or nonclassical disease. Variable signs and symptoms of hyperandrogenism are common to both types of the disorder. In women with CAH, hyperandrogenism may be present, extending from virilization of external genitalia and salt-wasting in classical (C)-CAH cases, to menstrual irregularity, obesity, short stature, infertility or subfertility and skin disorders such as hirsutism, in nonclassical (NC)-CAH cases. These clinical characteristics of NC-CAH cases do not differ unmarkedly from those shown in patients with polycystic ovary syndrome, idiopathic hirsutism, or hyperinsulinemia. The significant advances in molecular biology and gene analysis over the past 2 decades have led to the development of novel sensitive methods of DNA analysis and study, including polymerase chain reaction and Southern blot analysis. Thus it has been revealed that the 21-OH gene (CYP21A2) and its nonfunctional pseudogene (CYP21A1P) are located on chromosome 6 (6p21.3), sharing a high homology of about 98%. Inactivating mutations occur as complete gene deletions, large gene conversions and pseudogene-derived mutations.
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PMID:Congenital adrenal hyperplasia because of 21-hydroxylase deficiency. A genetic disorder of interest to obstetricians and gynecologists. 1922 39

Metabolic syndrome (MetS) is defined as a cluster of risk factors for type 2 diabetes and cardiovascular disease; it is also an independent risk factor for developing chronic kidney disease (CKD) in the general population. Therefore, CKD has many similarities and associations with MetS, and the individual risk factors constituting MetS-especially insulin resistance and glucose intolerance, hypertension, dyslipidemia, and obesity-are also common features of the early stages of CKD. In the later stages of CKD, uremia per se and uremic complications such as fluid retention, protein-energy wasting, inflammation, and oxidative stress further contribute to an increase in the prevalence of MetS in CKD patients. In addition, PD patients exposed to glucose-based PD fluids have an increased risk of developing metabolic complications. The broad use of MetS in clinical research has raised the awareness of the public and of individual patients concerning the value of lifestyle interventions. However, the definition and pathogenesis of MetS are still debated, and no standardized definition nor proven prognostic value has been established for MetS as a cluster of risk factors for diabetes or cardiovascular disease in PD patients. Furthermore, considering the paradoxical associations of some of the risk factors in MetS with decreased mortality, another set of risk factors-those specific to patients with uremia (for example, inflammation and malnutrition)-and the appropriate cut-off levels to individual MetS risk factors should be taken account at the same time. Also, the benefit of interventions targeting these risk factors should be clarified in further clinical studies.
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PMID:Definition of metabolic syndrome in peritoneal dialysis. 1927 Feb 3

Adiponectin may influence the development of chronic heart failure (CHF), but the epidemiological data are scarce. This is due in part to the fact that while higher BMIs are a risk factor for CHF, obesity is a predictor of improved prognoses in patients with CHF since wasting is strongly associated with the increased risk of death in the final stages of CHF. From that standpoint of view, high adiponectin levels are a predictor of mortality in patients with CHF. That paradoxical relationship may exist since high BMI, hence low adiponectin, favors survival in endstage heart failure. We strongly believe that further large-scale clinical studies are warranted to analyze independent prognostic significance of adiponectin levels in patients with CHF.
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PMID:Elevated adiponectin levels in patients with chronic heart failure: an independent predictor of mortality or a marker of cardiac cachexia? 1917 60

Obesity and nutrition-related chronic disorders are fast rising in developing countries. But undernutrition--stunting, underweight, wasting and micronutrient deficiencies--still affect millions of preschool children in both rural and urban settings increasing the risks of morbidity and mortality, impairing cognitive development, reducing productivity and increasing the risk of chronic diseases in later life. In addition undernutrition has a transgenerational effect. Here I review the evidence for a synergistic effect of inadequate nutrition (breastfeeding, complementary feeding), infection, and inappropriate mother-child interactions on growth and nutritional deficiencies. Underlying socioeconomic, environmental and genetic factors are also explored. Finally some perspectives on how urbanization and globalization may affect the prevalence and distribution of undernutrition are discussed. Fighting child under-nutrition is still an urgent necessity and a moral imperative.
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PMID:Postnatal origins of undernutrition. 1934 69

The aims were assessing liver function tests (LFT) in women with congenital adrenal hyperplasia (CAH) on glucocorticoids. Sixty-one women with genetically verified CAH due to 21-hydroxylase deficiency, aged 18-63 years were compared to 61 controls. Serum alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transpeptidase (GGT), anthropometry and fat mass (dual energy X-ray absorptiometry) were measured. ALT and GGT were higher in the entire patient group (p=0.01 and 0.002); AST, GGT and ALP in patients > or =30 years (p=0.007-0.045); all LFT in salt-wasting (p<0.001-0.042); GGT in simple virilizing (p=0.008); ALT, GGT and ALP in Null/Null genotype (p=0.018-0.040); ALT and GGT in I2splice genotype (p<0.001 and 0.011). Using a recently proposed cut-off level for ALT (>0.317 microkat/L), 54% of patients vs 23% of controls had elevated levels (p=0.028). In patients, GGT and ALP correlated with waist circumference and with total body and trunk fat (r=0.274-0.406, p=0.001-0.043). However, ALT, GGT and ALP were increased even in non-obese patients (waist circumference < or =88 cm and body mass index <30 kg/m(2)) (p=0.012-0.045) mainly attributed to the patients > or =30 years who also demonstrated elevated insulin levels and HOMA-indices. In conclusion, compared with controls, women with CAH have higher LFT, in particular patients > or =30 years and those with severe forms, probably reflecting a higher lifetime glucocorticoid exposure. LFT were positively correlated to measurements of body fat. These women might have increased frequency of NAFLD. The finding of higher LFT also in non-obese patients suggests that not only central obesity but also glucocorticoids per se may influence.
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PMID:Increased liver enzymes in adult women with congenital adrenal hyperplasia due to 21-hydroxylase deficiency. 1935 53

Ghrelin, a peptide hormone predominantly produced by the stomach, was isolated as the endogenous ligand for the growth hormone secretagogue receptor. Ghrelin is a potent stimulator of growth hormone (GH) secretion and is the only circulatory hormone known to potently enhance feeding and weight gain and to regulate energy homeostasis following central and systemic administration. Therapeutic intervention with ghrelin in catabolic situations may induce a combination of enhanced food intake, increased gastric emptying and nutrient storage, coupled with an increase in GH thereby linking nutrient partitioning with growth and repair processes. These qualities have fostered the idea that ghrelin-based compounds may have therapeutic utility in treating malnutrition and wasting induced by various sub-acute and chronic disorders. Conversely, compounds that inhibit ghrelin action may be useful for the prevention or treatment of metabolic syndrome components such as obesity, impaired lipid metabolism or insulin resistance. In recent years, the effects of ghrelin on glucose homeostasis, memory function and gastrointestinal motility have attracted considerable amount of attention and revealed novel therapeutic targets in treating a wide range of pathologic conditions. Furthermore, discovery of ghrelin O-acyltransferase has also opened new research opportunities that could lead to major understanding of ghrelin physiology. This review summarizes the current knowledge on ghrelin synthesis, secretion, mechanism of action and biological functions with an additional focus on potential for ghrelin-based pharmacotherapies.
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PMID:Ghrelin in the regulation of body weight and metabolism. 1989 96


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