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

Adipose tissue cells express and secrete numerous proteins influencing the signal transduction pathways of insulin receptor by auto-, para- and endocrine manner. Several cytokines, tumor necrosis factor-alpha and its soluble receptor forms, sTNFR1 and sTNFR2, resistin, retinol-binding protein 4, plasminogen activator inhibitor, lipocain 1 inhibit the signalization of insulin receptor causing insulin resistance in target tissues, mainly in adipose, liver and muscle, brain, endothelial as well as in pancreatic beta-cells. However, many other proteins produced by the fat tissue, such as adiponectin, visfatin, vaspin, apelin, omentin and chemerin enhance the signal transmission of the receptor. Recently discovered common mechanisms leading to insulin and cytokine resistance in obesity and type 2 diabetes mellitus, e.g. protein family of suppressor of cytokine signaling (SOCS) are also discussed.
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PMID:[Molecular mechanisms and correlations of insulin resistance, obesity, and type 2 diabetes mellitus]. 1972 6

Cardiovascular diseases are currently the most frequent cause of death in Poland and their incidence continually rises. This is related to the high incidence of obesity associated with insulin resistance, which is present in type 2 diabetes mellitus. Adipose tissue produces multiple cytokines(TNF-alpha, IL-6, PAI-1, CRP, angiotensinogen, leptin, adiponectin, visfatin, apelin, resistin)which decrease insulin sensitivity and induce inflammatory processes, endothelial dysfunction,and atherosclerosis. This article presents the link between obesity, insulin resistance, and type 2 diabetes mellitus according to studies conducted in vitro and in animal models. In human studies, the influence of resistin on the development of insulin resistance is controversial. The article underlines the role of resisitin in the development of inflammatory processes and endothelial dysfunction in humans. In clinical studies, resistin was shown to be a predictive factor of coronary artery disease and mortality connected with cardiovascular diseases.
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PMID:[Resistin: a pathogenic factor or a biomarker of metabolic disorders and inflammation?]. 1994 Mar 27

Nonalcoholic fatty liver disease (NAFLD), one of the most common forms of chronic liver disease, is closely associated with obesity and insulin resistance. Recent studies suggest that apelin, a newly described adipokine, is associated with hyperinsulinemia and inflammation. The aim of the study was to investigate plasma apelin concentrations in biopsy-proven NAFLD patients who had no metabolic confounders and also to search for the association of apelin with adiponectin, body mass index (BMI), and insulin sensitivity. Fifty male patients with NAFLD and 30 healthy male controls were enrolled. Apelin was measured along with BMI, lipids, glucose, insulin, adiponectin, and homeostasis model assessment (HOMA) of insulin resistance indexes. Plasma apelin levels were significantly higher and adiponectin levels were lower in NAFLD patients when compared with the controls (P < .001 and P = .013, respectively). In multivariate analysis adjusted for BMI and HOMA indexes, the differences in apelin and adiponectin disappeared in the 2 groups (P = .3 and P = .1, respectively). In addition, apelin levels were positively correlated with BMI (r = 0.29, P = .05) and HOMA indexes (r = 0.4, P = .008) in subjects with NAFLD. The results of this preliminary study suggest that plasma apelin levels are not altered in nondiabetic and normotensive male subjects with NAFLD.
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PMID:Plasma apelin levels in subjects with nonalcoholic fatty liver disease. 2004 53

The last two decades brings many data about white adipose tissue capacity to secrete hormones, named adipokines, which could mediate the relationship between obesity and lung diseases. In this paper we presented some data about adipokines involvement on pulmonary function, with special emphasis on leptin, adiponectin, tumor necrosis factor alpha, vascular endothelial growth factor, resistin, hepatocyte growth factor, interleukin-6, angiotensinogen and apelin.
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PMID:Adipokines involvement in lung function. 2020 Dec 59

Apelin, an adipocyte-secreted factor upregulated by insulin, is increased in adipose tissue (AT) and plasma with obesity. Apelin was recently identified as a new player in the control of glucose homeostasis. However, the regulation of apelin and APJ (apelin receptor) expression in skeletal muscle in relation to insulin resistance or type 2 diabetes is not known. Thus we studied apelin and APJ expression in AT and muscle in different mice models of obesity and in type 2 diabetic patients. In insulin-resistant high-fat (HF)-fed mice, apelin and APJ expression were increased in AT compared with control. This was not the case in AT of highly insulin-resistant db/db mice. In skeletal muscle, apelin expression was similar in control and HF-fed mice and decreased in db/db mice. APJ expression was decreased in both HF-fed and db/db mice. Control subjects and type 2 diabetic patients were subjected to a hyperinsulinemic-euglycemic clamp, and tissues biopsies were obtained before and at the end of the clamp. There was no significant difference in basal apelin and APJ expression in AT and muscle between control and diabetic patients. However, apelin plasma levels were significantly increased in diabetic patients. During the clamp, hyperinsulinemia increased apelin and APJ expression in AT of control but not in diabetic subjects. In muscle, only APJ mRNA levels were increased in control but also in diabetic patients. Taken together, these data show that apelin and APJ expression in mice and humans is regulated in a tissue-dependent manner and according to the severity of insulin resistance.
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PMID:Apelin and APJ regulation in adipose tissue and skeletal muscle of type 2 diabetic mice and humans. 2023 41

Recent studies have shown the ability of apelin to restore glucose tolerance in obese and insulin-resistant mice. Eicosapentaenoic acid (EPA) is a polyunsaturated fatty acid (PUFA) from the omega-3 family that has many beneficial effects in obesity-linked disorders. The aim of this study was to examine in vitro the effects of EPA on apelin secretion and gene expression in mature 3T3-L1 adipocytes. Treatment with EPA (100 and 200 microM) significantly increased basal (p<0.01) and insulin-stimulated (p<0.001) apelin secretion and gene expression in adipocytes. EPA also stimulated Akt phosphorylation, a down-stream target of phosphatidylinositol 3-kinase (PI3K), in 3T3-L1 adipocytes. Moreover, treatment with the PI3K inhibitor LY294002 completely blocked EPA-stimulatory action on apelin mRNA gene expression (p<0.001), but not modified the stimulatory effect of EPA on basal apelin secretion. Furthermore, the stimulatory effect of EPA on basal apelin release was also observed in the presence of Actinomycin D and Cycloheximide, suggesting that EPA might also regulate apelin secretion by via post-transcriptional mechanisms. These findings suggest that the mechanisms mediating EPA-induced apelin synthesis and/or secretion are complex, involving steps that are PI3K dependent and steps that are PI3K independent.
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PMID:Eicosapentaenoic acid up-regulates apelin secretion and gene expression in 3T3-L1 adipocytes. 2035 20

Adipokines play key roles in the regulation of bone growth, obesity, diabetes mellitus type 2, and HIV infection. As a newly discovered hormone in the adipokine family, the precise role of apelin on articular cartilage metabolism is not yet clear. The aim of this study was to evaluate the role of apelin on articular cartilage. In vitro, we examined the effects of apelin on normal chondrocyte proliferation and gene expression of metalloproteinases (MMPs) and interleukin-1beta (IL-1beta). In vivo, by intra-articular injection with apelin, we examined MMP-3, -9, collagen II and IL-1beta at both gene and protein levels. Furthermore, we measured the messenger RNA (mRNA) expression of ADAMTS-4 and -5 (a disintegrin and metalloproteinase with thrombospondin motifs 4 and 5) and the proteoglycan content in articular cartilage. Apelin stimulated the proliferation of chondrocytes and significantly increased mRNA levels of MMP-1, -3, -9 and IL-1beta in vitro. Intra-articular injection with apelin in vivo up-regulated the expression of MMP-3, -9, and IL-1beta as well as decreased the level of collagen II. Additionally, after treatment with apelin, mRNA levels of ADAMTS-4 and -5 markedly increased and depletion of proteoglycan in articular cartilage was found by histological assessment. These findings suggest that apelin plays a catabolic role in cartilage metabolism and is a risk factor in the pathophysiology of osteoarthritis.
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PMID:Apelin plays a catabolic role on articular cartilage: in vivo and in vitro studies. 2066 51

Cumulative evidence suggests that the origins of obesity may occur during fetal development. In this respect, the concept of "developmental programming" was introduced and supported by experimental and epidemiological data. This concept supports the idea that the nutritional and hormonal status during pregnancy could irreversibly interfere in metabolism control. The mechanisms responsible for this developmental programming remain poorly documented. However, recent research indicates that adipocytokines may play a critical role in this process. Thus, leptin, adiponectin, and the recently identified resistin, visfatin, and apelin, all exert effects on fat, muscle, and liver cells early in life. The aforementioned adipocytokines are secreted by adipocytes and human placenta during fetal life and may play a major role in the etiopathogenesis of the metabolic syndrome. This review will focus on the intrauterine expression of adipocytokines, their contribution to the hormonal control of fetal growth, and their role in restricted and exaggerated intrauterine growth.
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PMID:The role of adipocytokines in fetal growth. 2084 Feb 57

Obesity, the most common nutritional disorder in industrialized countries, is associated with an increased mortality and morbidity of cardiovascular disease (CVD). Obesity is primarily considered to be a disorder of energy balance, and it has recently been suggested that some forms of obesity are associated with chronic low-grade inflammation. The present paper focuses on the current status of our knowledge regarding chronic inflammation, a link between obesity and CVDs, including heart diseases, vascular disease and atherosclerosis. The paper discusses the methods of body fat evaluation in humans, the endocrinology and distribution of adipose tissue in the genders, the pathophysiology of obesity, the relationship among obesity, inflammation, and CVD, and the adipose tissue-derived cytokines known to affect inflammation. Due to space limitations, this paper focuses on C-reactive protein, serum amyloid A, leptin, adiponectin, resistin, visfatin, chemerin, omentin, vaspin, apelin, and retinol binding protein 4 as adipokines.
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PMID:Inflammation, a link between obesity and cardiovascular disease. 2084 13

The initial discovery of leptin, an appetite-suppressing hormone originating from fat tissue, substantially supported the idea that fat-borne factors act on the brain to regulate food intake and energy expenditure. Since then, a growing number of cytokines have been found to be released from adipose tissue, thus acting in an endocrine manner. These adipocytokines include not only, e.g., adiponectin, apelin, resistin, and visfatin, but also inflammatory cytokines and steroid hormones such as estrogens and glucocorticoids. They are secreted from their adipose depots and differ in terms of release stimuli, downstream signaling, and their action on the brain. Clearly, adipocytokines play a prominent role in the central control of body weight, and the deregulation of this circuit may lead to the development of obesity and related disorders. In this chapter, we will focus on crosstalk mechanisms and the deregulation of adipocytokines at the expression level and/or sites of central action that eventually will lead to the development and perpetuation of obesity and diabetes.
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PMID:Adipocyte-brain: crosstalk. 2086 82


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