Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q9BY76 (adipokine)
 3,147 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The researchers' view regarding the role of white adipose tissue (WAT) in inflammation has been greatly transformed over the last 10 years. WAT is now considered as an active organ producing many crucial molecules called adipokines. Resistin is a recently discovered cysteine-rich adipokine that has emerged during this decade as a promising inflammatory marker in various diseases. It is synthesized either from adipocytes or from immune cells, and exerts a pro-inflammatory profile in a variety of different experimental settings. Inflammatory bowel disease (IBD) is characterized by anorexia, malnutrition, altered body composition and the development of mesenteric WAT hypertrophy. The study by Konrad-Zerna et al. in this issue of the journal demonstrates an increased serum resistin in IBD patients, this being in agreement with previous IBD studies in mesenteric WAT and serum. Interesting aspects like the true validity of resistin as a marker of disease activity, the role of its different molecular isoforms, the cells that predominantly produce this molecule, and the possible use of resistin as a guide for therapeutic interventions, arise.
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PMID:Resistin: another rising biomarker in inflammatory bowel disease? 1799 23

Chronic inflammation, which is widely seen in long-term dialysis patients, is associated with malnutrition, atherosclerosis and an increased mortality risk. The relationship between inflammation and nutrition is certainly bidirectional with inflammation affecting nutritional status and dietary factors influencing the state of inflammation. Cytokines, such as IL-6 and TNF-alpha, interfere with the satiety center inducing loss of appetite, delayed gastric emptying and catabolism of skeletal muscle protein. High adipokine levels may also contribute to the development of malnutrition. On the other hand, dietary factors may interfere directly or indirectly with inflammatory activity. For example, dietary AGEs intake may aggravate inflammation while natural antioxidants, such as polyphenolic flavones or vitamin C from fruits and vegetables may even decrease inflammatory activity. Although there is a lack of good prospective nutritional studies in CKD patients, the individual patient should be advised to follow a more Mediterranean-style diet, restrain from broiling meats in order to avoid dietary AGEs, and take multivitamins regularly.
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PMID:Potential interplay between nutrition and inflammation in dialysis patients. 1845 61

Profound loss of adipose and other tissues is a hallmark of cancer cachexia, a debilitating condition associated with increased morbidity and mortality. Fat loss cannot be attributable to reduced appetite alone as it precedes the onset of anorexia and is much more severe in experimental models of cachexia than in food restriction. Morphological examination has shown marked remodelling of adipose tissue in cancer cachexia. It is characterised by the tissue containing shrunken adipocytes with a major reduction in cell size and increased fibrosis in the tissue matrix. The ultrastructure of 'slimmed' adipocytes has revealed severe delipidation and modifications in cell membrane conformation. Although the molecular mechanisms remain to be established, evidence suggests that altered adipocyte metabolism may lead to adipose atrophy in cancer cachexia. Increased lipolysis appears to be a key factor underlying fat loss, while inhibition of adipocyte development and lipid deposition may also contribute. Both tumour and host-derived factors are implicated in adipose atrophy. Zinc-alpha2-glycoprotein (ZAG), which is overexpressed by certain malignant tumours, has been identified as a novel adipokine. ZAG transcripts and protein expression in adipose tissue are up regulated in cancer cachexia but reduced with adipose tissue expansion in obesity. Studies in vitro demonstrate that recombinant ZAG stimulates lipolysis. ZAG may therefore act locally, as well as systemically, to promote lipid mobilisation in cancer cachexia. Further elucidation of ZAG function in adipose tissue may lead to novel targets for preventing adipose atrophy in malignancy.
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PMID:New insights into adipose tissue atrophy in cancer cachexia. 1971 94

Puberty in mammals is associated with important physical and psychological changes due to the increase in sex steroids and growth hormone (GH). Indeed, an increase in growth velocity and the attainment of sexual maturity for future reproductive function are the hallmark changes during this stage of life. Both growth and reproduction consume high levels of energy, requiring suitable energy stores to face these physiological functions. During the last two decades our knowledge concerning how peptides produced in the digestive tract (in charge of energy intake) and in adipose tissue (in charge of energy storage) provide information regarding metabolic status to the central nervous system (CNS) has increased dramatically. Moreover, these peptides have been shown to play an important role in modulating the gonadotropic axis with their absence or an imbalance in their secretion being able to disturb pubertal onset or progression. In this article we will review the current knowledge concerning the role played by leptin, the key adipokine in energy homeostasis, and ghrelin, the only orexigenic and growth-promoting peptide produced by the digestive tract, on sexual development. The normal evolutionary pattern of these peripherally produced metabolic signals throughout human puberty will be summarized. The effect of two opposite situations of chronic malnutrition, obesity and anorexia, on these signals and how they influence the course of puberty will also be discussed. Finally, we will briefly mention other peptides derived from the digestive tract (such as PYY) that may be involved in the regulatory link between energy homeostasis and sexual development.
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PMID:Metabolic signals in human puberty: effects of over and undernutrition. 2002 79

In patients with end-stage renal disease (ESRD), inflammation, and protein energy wasting (PEW) are two highly prevalent and interconnected entities, jointly exerting a deleterious effect on multiple other ESRD-specific pathological processes and eventually on patient outcome. With respect to the pathophysiology underlying this strong association, knowledge has been actively expanded over the past few years. As such, it is nowadays recognized that inflammation acts via direct, as well as indirect, pathways in its contribution to PEW. Directly, inflammation causes alterations in amino acid utilization, translating into increased catabolism and decreased anabolism of muscle tissue. Indirectly, inflammation may act via altered ghrelin and adipokine metabolism, adipose tissue distribution, and pathological neuroendocrine signaling, as well as coexistent depression in inducing anorexia and PEW. In addition, two relatively new inflammatory markers (pentraxin-3 and TNF-like weak inducer of apoptosis) have gained attention with respect to their roles in this specific context. The current review deals with recent updates in the literature on the aforementioned pathways connecting inflammation to PEW and subsequent mortality.
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PMID:Recent insights in inflammation-associated wasting in patients with chronic kidney disease. 2162

Although adipose tissue metabolism in obesity has been widely studied, there is limited research on the anorexic state, where the endocrine system is disrupted by reduced adipose tissue mass and there are depot-specific changes in adipocyte type and function. Stress exposure at different stages of life can alter the balance between energy intake and expenditure and thereby contribute to the pathogenesis of anorexia nervosa. This review integrates information from human clinical trials to describe endocrine, genetic and epigenetic aspects of adipose tissue physiology in the anorexic condition. Changes in the hypothalamus-pituitary-thyroid, -adrenal, and -gonadal axes and their relationships to appetite regulation and adipocyte function are discussed. Because of the role of stress in triggering or magnifying anorexia, and the dynamic but also persistent nature of environmentally-induced epigenetic modifications, epigenetics is likely the link between stress and long-term changes in the endocrine system that disrupt homoeostatic food intake and adipose tissue metabolism. Herein, we focus on the adipocyte and changes in its function, including alterations reinforced by endocrine disturbance and dysfunctional adipokine regulation. This information is critical because of the poor understanding of anorexic pathophysiology, due to the lack of suitable research models, and the complexity of genetic and environmental interactions.
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PMID:Chronic stress and adipose tissue in the anorexic state: endocrine and epigenetic mechanisms. 3277 66