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

Children and adolescents with obesity face stigmatization and discrimination in many areas of their lives, and it has been assumed that their psychological well-being will be compromised as a result. This chapter examines the most recent empirical evidence on the relationship between childhood obesity and body dissatisfaction, self-esteem and depression. Studies of clinical samples typically report poorer psychological well-being in treatment seekers when compared with population-based obese and normal weight controls. However, research in community samples suggests that despite moderate levels of body dissatisfaction, few obese children are depressed or have low self-esteem. A number of important moderators and mediators of the association between obesity and well-being have emerged, with females, Caucasians and adolescents being particularly at risk. Implications for treatment and future research priorities are suggested.
Best Pract Res Clin Endocrinol Metab 2005 Sep
PMID:The impact of obesity on psychological well-being. 1615 Mar 84

Childhood obesity is a complex disease with different genetic, metabolic, environmental and behavioural components that are interrelated and potentially confounding, thus making causal pathways difficult to define. Given the tracking of obesity and the associated risk factors, childhood is an important period for prevention. To date, evidence would support preventative interventions that encourage physical activity and a healthy diet, restrict sedentary activities and offer behavioural support. However, these interventions should involve not only the child but the whole family, school and community. If the current global obesity epidemic is to be halted, further large-scale, well-designed prevention studies are required, particularly within settings outside of the USA, in order to expand the currently limited evidence base upon which clinical recommendations and public health approaches can be formulated. This must be accompanied by enhanced monitoring of paediatric obesity prevalence and continued support from all stakeholders at global, national, regional and local levels.
Best Pract Res Clin Endocrinol Metab 2005 Sep
PMID:Prevention of childhood obesity. 1615 Mar 85

The prevalence of child and adolescent overweight and obesity is rapidly increasing and is associated with morbidity, both medical and psychosocial. Obesity is unlikely to resolve spontaneously. It is important that health professionals can assess obesity and initiate an action plan. The evidence base for what works best in the management of child and adolescent overweight and obesity is limited. It is uncertain whether protocols from clinical research trials can be translated into primary care. Dietary change, with an emphasis on lower fat intake and smaller portion size, should be commenced. There should be an increase in physical activity and a decrease in sedentary behaviours, combined with behavioural change and parental involvement. These are the elements of a lifestyle intervention. In the severely obese adolescent with obesity-related co-morbidity, the use of very low-energy diets and anti-obesity agents could be considered. Bariatric surgery may be indicated in carefully selected, older, severely obese adolescents.
Best Pract Res Clin Endocrinol Metab 2005 Sep
PMID:Childhood obesity. Treatment options. 1615 Mar 86

Release of fatty acids (FAs) from adipose tissue through lipolysis in fat cells is a key event in many processes. FAs are not only energy substrates but also signalling molecules and substrates for lipoprotein production by the liver. Fat cells consist of>95% triglycerides that are hydrolysed during lipolysis to glycerol and FAs. The major rate-limiting factor for lipolysis is hormone-sensitive lipase, but additional lipases such as adipose tissue triglyceride lipase may also play a role. The regulation of human fat cell lipolysis is, in many ways, species unique. Only catecholamines, insulin and natriuretic peptides have pronounced acute effects. Catecholamines influence lipolysis through four different adrenoceptor subtypes, in contrast to rodents where only one subtype (beta(3)) is of major importance. There are regional variations in adipocyte lipolysis leading to more release of FAs from the visceral than subcutaneous adipose tissue during hormone stimulation (insulin, catecholamines). Since, only visceral fat is linked to the liver (by the portal vein), alterations in visceral adipocyte tissue lipolysis have direct effects on the liver through portal FA release. The regional variations in lipolysis are further enhanced in obesity and polycystic ovarian syndrome, and are of importance for dyslipidaemia, hyperinsulinaemia and glucose intolerance in these conditions. There is a marked elevation of circulating FA levels among the obese, which may be due to enhanced production of tumour necrosis factor alpha in adipose tissue. This cytokine stimulates lipolysis through so-called MAP kinases. Pharmacological agents in clinical practice such as nicotinic acid and glitazones exert lipid-lowering and glucose-lowering effects, respectively, by decreasing FA output from the adipose tissue. This review covers the biochemistry, regulation and clinical aspects of human fat cell lipolysis.
Best Pract Res Clin Endocrinol Metab 2005 Dec
PMID:Human fat cell lipolysis: biochemistry, regulation and clinical role. 1631 Dec 12

Obesity and lipoatrophy are major risks for insulin resistance, non-insulin-dependent diabetes and cardiovascular disease. In the past three decades, significant advances have been made in delineating the key transcription factors of adipogenesis, as well as extracellular effectors and intracellular signalling pathways that regulate fat cell formation. This review focuses on in vitro models of adipocyte differentiation, and on the balance between pro- and anti-adipogenic factors that drive the adipocyte differentiation process. Full understanding of the mechanisms of adipose tissue differentiation represents a major issue to develop a comprehensive strategy to prevent and treat obesity.
Best Pract Res Clin Endocrinol Metab 2005 Dec
PMID:Adipogenesis: cellular and molecular aspects. 1631 Dec 13

In recent years, the thiazolidinediones (e.g. rosiglitazone, pioglitazone) have emerged as an exciting novel class of therapeutic agent for the treatment of type 2 diabetes mellitus and the human metabolic syndrome. At first glance, the use of these high-affinity peroxisome proliferator-activated receptor gamma (PPARgamma) agonists, that promote adipogenesis, to treat a group of disorders that typically have their origins in obesity seems counter-intuitive. However, to view PPARgamma simply as a regulator of fat mass, and adipocytes themselves as passive vessels for energy storage, is to ignore an extensive body of data that speaks of the diverse roles of both this receptor and adipose tissue in the maintenance of normal metabolic homeostasis. This article highlights the important clinical and laboratory observations made in human subjects harbouring genetic variations in PPARgamma that have confirmed its pivotal role in the regulation of adipocyte endocrine function, and thus our metabolic response to the environment.
Best Pract Res Clin Endocrinol Metab 2005 Dec
PMID:Peroxisome proliferator-activated receptor gamma and the regulation of adipocyte function: lessons from human genetic studies. 1631 Dec 14

With the growing prevalence of obesity, scientific interest in the biology of adipose tissue has been extended to the secretory products of adipocytes, since they are increasingly shown to affect several aspects in the pathogenesis of obesity-related diseases. The cloning of the ob gene is consistent with this concept and suggests that body fat content in adult rodents is regulated by a negative feedback loop centred in the hypothalamus. In recent years, a number of additional signalling molecules secreted by adipose tissue have been discovered, commonly referred to as 'adipocytokines'. Among these, adiponectin is perhaps the most interesting and promising compound for the clinician since it has profound protective actions in the pathogenesis of diabetes and cardiovascular disease. Adiponectin is low in obese subjects and, in particular, insulin-resistant patients. In contrast, resistin seems to be of greater relevance in relation to the immune stress response than in the regulation of glucose homeostasis. However, inflammatory processes have recently been connected with the development of atherosclerosis. Finally, little is known regarding the clinical relevance of visfatin. Recent research has revealed many functions of adipocytokines extending far beyond metabolism, such as immunity, cancer and bone formation. This report aims to review some of the recent topics of adipocytokine research that may be of particular importance.
Best Pract Res Clin Endocrinol Metab 2005 Dec
PMID:Adipocytokines: leptin--the classical, resistin--the controversical, adiponectin--the promising, and more to come. 1631 Dec 15

Adipose tissue is a highly active organ. In addition to storing calories as triglycerides, it also secretes a large variety of proteins, including cytokines, chemokines and hormone-like factors, such as leptin, adiponectin and resistin. Intriguingly, many, if not most, of these adipose-derived proteins have dual actions; cytokines have both immunomodulatory functions and act as systemic or auto-/paracrine regulators of metabolism, while proteins such as leptin and adiponectin are regulators of both metabolism and inflammation. The production of pro-atherogenic chemokines by adipose tissue is of particular interest since their local secretion, e.g. by perivascular adipose depots, may provide a novel mechanistic link between obesity and the associated vascular complications.
Best Pract Res Clin Endocrinol Metab 2005 Dec
PMID:Adipose tissue: a regulator of inflammation. 1631 Dec 16

Obesity is strongly associated with arterial hypertension. A positive correlation between obesity and plasma aldosterone levels has been observed by different investigators, suggesting that an abnormal secretion of aldosterone in obesity contributes to the development of arterial hypertension in obese subjects. The mechanisms proposed to explain this abnormal aldosterone production mainly involve the adipose renin-angiotensin system, an indirect effect of increased fatty acids, and direct adrenal stimulation by adipocyte secretory products. Indeed, adipose mineralocorticoid-stimulating activity was recently observed in isolated human adipocytes, suggesting a hitherto unknown direct involvement of adipose tissue in the regulation of blood pressure in obesity.
Best Pract Res Clin Endocrinol Metab 2005 Dec
PMID:Mineralocorticoid-stimulating activity of adipose tissue. 1631 Dec 17

Nutrients regulate metabolic fluxes and homeostasis through transcriptional and translational control of enzyme concentrations and allosteric modulation of enzyme activity. Dietary omega-3 polyunsaturated fatty acids (PUFAs) have been shown to exert a variety of beneficial health effects such as reducing adiposity and increasing insulin sensitivity in rodents. It is now clear that PUFAs regulate fundamental adipose cell and liver functions through modulation of activity and abundance of key transcription factors that act as nutrient sensors, including peroxisome proliferator-activated receptors (PPARalpha/delta/gamma), sterol regulatory element binding proteins (SREBP-1/2), and liver X receptors (LXRalpha/beta). However, in the state of obesity, where adipose tissue shows elevated storage of triglycerides, many lipogenic genes that are essential for adipose cell function including PPARgamma, SREBP-1c, CCAAT-enhancer binding protein alpha and stearoyl-CoA desaturase-1 are downregulated, apparently due to desensitization of the very same crucial nutrient sensors. This chapter will summarize recent studies of PUFA- and obesity-induced changes in gene expression in white adipose tissue.
Best Pract Res Clin Endocrinol Metab 2005 Dec
PMID:Nutrition-/diet-induced changes in gene expression in white adipose tissue. 1631 Dec 19


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