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

The proinflammatory cytokine Interleukin 1 beta (IL-1beta) is elevated in obese individuals and rodents and it is implicated in impaired insulin secretion, decreased cell proliferation and apoptosis of pancreatic beta cells. In this study we describe the therapeutic effects by an IL-1beta antibody to improve glucose control in hyperglycemic mice with diet-induced obesity. After 13 weeks of treatment the IL-1beta antibody treated group showed reduced glycated hemoglobin (( *)P=0.049), reduced serum levels of proinsulin (( *)P=0.015), reduced levels of insulin and smaller islet size (( *)P=1.65E-13) relative to the control antibody treated group. Neutralization of IL-1beta also significantly reduced serum amyloid A (SAA) which is an indicator of inflammation-induced acute phase response (( *)P=0.024). While there was no improvement of obesity, a significant improvement of glycemic control and of beta cell function is achieved by this pharmacological treatment which may slow/prevent disease progression in Type 2 Diabetes.
Cytokine 2008 Oct
PMID:Treatment with an Interleukin 1 beta antibody improves glycemic control in diet-induced obesity. 1872 71

Cytokines are considered to be involved in obesity-related metabolic diseases. Study objectives are to determine the heritability of circulating cytokine levels, to investigate pleiotropy between cytokines and obesity traits, and to present genome scan results for cytokines in 1030 Hispanic children enrolled in VIVA LA FAMILIA Study. Cytokine phenotypes included monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-alpha), leptin, adiponectin, soluble intercellular adhesion molecule-1 (sICAM-1), transforming growth factor beta 1 (TGF-beta1), C-reactive protein (CRP), regulated upon activation, normal T-cell expressed and secreted (RANTES) and eotaxin. Obesity-related phenotypes included body mass index (BMI), fat mass (FM), truncal FM and fasting serum insulin. Heritabilities ranged from 0.33 to 0.97. Pleiotropy was observed between cytokines and obesity traits. Positive genetic correlations were seen between CRP, leptin, MCP-1 and obesity traits, and negative genetic correlations with adiponectin, ICAM-1 and TGF-beta1. Genome-wide scan of sICAM-1 mapped to chromosome 3 (LOD=3.74) between markers D3S1580 and D3S1601, which flanks the adiponectin gene (ADIPOQ). Suggestive linkage signals were found in other chromosomal regions for other cytokines. In summary, significant heritabilities for circulating cytokines, pleiotropy between cytokines and obesity traits, and linkage for sICAM-1 on chromosome 3q substantiate a genetic contribution to circulating cytokine levels in Hispanic children.
Cytokine 2008 Nov
PMID:A genetic contribution to circulating cytokines and obesity in children. 1884 81

Inflammatory cytokines have been linked to obesity-related insulin resistance. To investigate the effect of TNF-alpha, an inflammatory cytokine, on insulin action, C57BL/6J mice were treated with TNF-alpha for 7 days after which we examined the in vivo effects of TNF-alpha on glucose tolerance and insulin sensitivity with IV glucose tolerance tests and hyperinsulinemic-euglycemic clamps. In addition, we analyzed the in vivo effect of TNF-alpha on several metabolism-related genes and adipocytokines implicated in the development of insulin resistance. TNF-alpha treatment resulted in markedly increased fasting blood glucose, insulin and free fatty acids (FFA) levels and reduced glucose tolerance. During the clamps, the rates insulin-stimulated whole body (G(Rd)) and skeletal muscle glucose uptake (MGU) and insulin's ability to suppress hepatic glucose production (HGP) were decreased in TNF-alpha treated animals, indicating insulin resistance. In addition, both PPARgamma and ATGL mRNA expression in adipose tissues as well as ATGL protein levels in plasma were downregulated. Moreover, adipose mRNA expression and plasma protein levels of adiponectin and visfatin were significantly down-regulated. We conclude that the alterations of PPARgamma, ATGL, adiponectin and visfatin may contribute to the development of insulin resistance mediated by TNF-alpha.
Cytokine 2009 Jan
PMID:The adipose triglyceride lipase, adiponectin and visfatin are downregulated by tumor necrosis factor-alpha (TNF-alpha) in vivo. 1902 57

The prevalence of overweight and obesity is rapidly increasing world wide. Numerous epidemiological studies have shown that obesity is a risk factor for postmenopausal breast cancer and relapse. However, the biological factors that drive the growth and progression of these tumors and how obesity contributes to the tumor microenvironment are poorly understood. Tumor development and metastasis are dependent on the process of angiogenesis or the formation of new blood vessels. More importantly, a ready supply of adipose tissue-derived angiogenic adipokines, notably VEGF and leptin, and the production of inflammatory cytokines by infiltrating macrophages that occurs in adipose tissues with obesity, promotes the paracrine stimulation of vascular endothelial cell growth needed for adipogenesis, while maintaining a microenvironment that is favorable for breast tumorigenesis.
Cytokine Growth Factor Rev 2009 Jun
PMID:Angiogenesis, adipokines and breast cancer. 1952 May 99

Flavonoids are functional constituents of many fruits and vegetables. Procyanidins are flavonoids with an oligomeric structure, and it has been shown that they can improve the pathological oxidative state of a diabetic situation. To evaluate whether procyanidins can modulate inflammation, an event strongly associated with obesity, diabetes and insulin resistance states, we used human adipocytes (SGBS) and macrophage-like (THP-1) cell lines and administered an extract of grape-seed procyanidins (GSPE). THP-1 and SGBS cells pre-treated with GSPE showed a reduction of IL-6 and MCP-1 expression after an inflammatory stimulus. GSPE stimuli alone modulate adipokine (APM1 and LEP) and cytokine (IL-6 and MCP-1) gene expression. GSPE partially inhibited NF-kappaB translocation to the nucleus in both cell lines. These preliminary findings demonstrate that GSPE reduces the expression of IL-6 and MCP-1 and enhances the production of the anti-inflammatory adipokine adiponectin suggesting that may have a beneficial effect on low-grade inflammatory diseases such obesity and type 2 diabetes.
Cytokine 2009 Aug
PMID:Grape-seed procyanidins modulate inflammation on human differentiated adipocytes in vitro. 1956 Sep 35

Bone morphogenetic proteins (BMPs) regulate many processes in embryonic development as well as in the maintenance of normal tissue function later in adult life. However, the role of this family of proteins in formation of adipose tissue has been underappreciated in the field of developmental biology. With the growing epidemic of obesity, improved knowledge of adipocyte development and function is urgently needed. Recently, there have been significant advances in understanding the role of different members of the BMP superfamily in control of adipocyte differentiation and systemic energy homeostasis. This review summarizes recent progress in understanding how BMPs specify adipose cell fate in stem/progenitor cells and their potential role in energy metabolism. We propose that BMPs provide instructive signals for adipose cell fate determination and regulate adipocyte function. These findings have opened up exciting opportunities for developing new therapeutic approaches for the treatment of obesity and its many associated metabolic disorders.
Cytokine Growth Factor Rev
PMID:Emerging role of bone morphogenetic proteins in adipogenesis and energy metabolism. 1989 88

Obesity is the presence of either abnormal absolute amount or relative proportion of body fat. Contrary to gluteal obesity, visceral obesity is associated with different metabolic alterations including insulin resistance (IR). A relatively new adipocytokine visfatin is shown to be expressed predominantly in visceral fat and exhibit insulin-mimicking effects in rodents. It is still unclear whether serum visfatin levels are associated with increased total or visceral fat mass in humans. The aim of our study was to investigate the relation between visfatin and obesity parameters namely body mass index (BMI) and waist circumference (WaC) and IR in healthy female subjects. Eighty one female subjects 20 years of age, having no diagnosis of glucose intolerance or diabetes, hypertension and dyslipidemia were chosen. The patients were divided into four groups according to their BMI and WaC values. Serum visfatin and HOMA-IR levels did not differ among groups. No correlation was detected between serum visfatin levels and obesity and metabolic parameters. In conclusion, we demonstrated that body fat distribution did not affect serum visfatin levels in healthy female subjects. Further studies are needed to clarify the exact factors influencing and determining serum visfatin levels and its clinical reflections.
Cytokine 2010 Mar
PMID:Body fat distribution has no effect on serum visfatin levels in healthy female subjects. 2004 51

Obesity is an important background of metabolic syndrome progression. Our previous study demonstrated that chemokine CCL2 expression was suppressed in liver of obese mice that were highly susceptible to Listeria monocytogenes infection. We investigated the role of adiponectin in CCL2 expression in obese mice after L. monocytogenes infection. When leptin-deficient obese ob/ob mice were infected intraperitoneally with L. monocytogenes, the elimination of bacteria from spleen, liver, mesenteric lymph nodes and adipose tissue was inhibited in ob/ob mice compared with their heterozygote littermates, ob/? mice. CCL2 expression in the adipose tissue of ob/? mice was enhanced by L. monocytogenes infection, different from ob/ob mice. Similarly, adiponectin expression was not observed in the adipose tissue of ob/ob mice. When mouse adipocyte 3T3-F442A-derived adipocytes were infected with L. monocytogenes, CCL2 expression was transiently up-regulated, following up-regulation of adiponectin expression. Up-regulation of CCL2 in adipocytes by L. monocytogenes infection was suppressed by knocked-down of adiponectin expression and supplementation of recombinant adiponectin partially recovered CCL2 expression. These results suggest that adiponectin is required for appropriate expression of CCL2 that is important for macrophage recruitment in response to bacterial infection.
Cytokine 2010 May
PMID:Adiponectin is required for enhancement of CCL2 expression in adipose tissue during Listeria monocytogenes infection. 2004 52

A prompt and regulated interferon (IFN) system is critical for host defense against infectious pathogens. Although increased susceptibility to infection has been observed in subjects with diabetes or obesity, little is known about the relationship between metabolic disorders and increased susceptibility to infection. In order to evaluate the association between immune function and metabolic parameters, we examined the relationship between capacity of IFN-alpha production and metabolic parameters including fasting plasma glucose (FPG), lipids, uric acid, body mass index (BMI), and blood pressure in 575 healthy subjects. Linear regression analysis showed that log(IFN-alpha production) was positively correlated with log(triglyceride) (r = 0.088, P = 0.03) and uric acid (r = 0.091, P = 0.03), and negatively correlated with age (r = -0.158, P = 0.0001) and FPG (r = -0.088, P = 0.03). Multiple regression analysis showed that log(IFN-alpha production) was independently determined by age (beta = -0.148, P < 0.0001), sex (beta = -0.240, P = 0.0003), and FPG (beta = -0.096, P = 0.0209), suggesting that lesser degrees of hyperglycemia also affect IFN-alpha production. We conclude that hyperglycemia but not BMI, hypertension, or hyperlipidemia may be associated with decreased capacity of IFN-alpha production and glycemic control is critical even for both subjects without any medication for diabetes and subjects under the diagnosis of diabetes on infectious diseases.
J Interferon Cytokine Res 2010 Jun
PMID:Association between capacity of interferon-alpha production and metabolic parameters. 2023 27

Visfatin (NAMPT formerly known as PBEF1) is an adipokine that is strongly expressed in visceral fat and has caused much debate among researchers, regarding its involvement in glucose homeostasis and insulin resistance. It was initially isolated from bone marrow cells, and its involvement in inflammatory procedures such as sepsis and acute lung inflammation is now evident. Several studies have also reported an association of plasma visfatin levels with obesity. We undertook an evaluation of the involvement of the NAMPT gene in the development of type 2 diabetes (T2DM) in the Greek population. We studied 178 patients with T2DM and 177 controls that were matched for sex, age and body mass index. We genotyped three tagging SNPs selected from the HapMap II CEPH European population as reference for the Greek population. These three SNPs tag another 12 SNPs over the entire NAMPT gene with a mean r(2) of 0.92. No indications of association with disease status were found with any of the tested variants or the inferred haplotypes. Results were also negative when the quantitative traits of weight and BMI were tested. Although our study covers common variants across the NAMPT gene, the possible involvement of rare variants in T2DM etiology cannot be ruled out and will require the investigation of very large numbers of cases and controls.
Cytokine 2010 Jul
PMID:Genetic variation in the visfatin (PBEF1/NAMPT) gene and type 2 diabetes in the Greek population. 2045 5


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