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Mitchell A Lazar - One of the best experts on this subject based on the ideXlab platform.
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adenylyl cyclase associated protein 1 is a receptor for human Resistin and mediates inflammatory actions of human monocytes
Cell Metabolism, 2014Co-Authors: Yoowook Kwon, Hanmo Yang, Inhee Mookjung, Junho Chung, Mitchell A LazarAbstract:Summary Human Resistin is a cytokine that induces low-grade inflammation by stimulating monocytes. Resistin-mediated chronic inflammation can lead to obesity, atherosclerosis, and other cardiometabolic diseases. Nevertheless, the receptor for human Resistin has not been clarified. Here, we identified adenylyl cyclase-associated protein 1 (CAP1) as a functional receptor for human Resistin and clarified its intracellular signaling pathway to modulate inflammatory action of monocytes. We found that human Resistin directly binds to CAP1 in monocytes and upregulates cyclic AMP (cAMP) concentration, protein kinase A (PKA) activity, and NF-κB-related transcription of inflammatory cytokines. Overexpression of CAP1 in monocytes enhanced the Resistin-induced increased activity of the cAMP-dependent signaling. Moreover, CAP1-overexpressed monocytes aggravated adipose tissue inflammation in transgenic mice that express human Resistin from their monocytes. In contrast, suppression of CAP1 expression abrogated the Resistin-mediated inflammatory activity both in vitro and in vivo. Therefore, CAP1 is the bona fide receptor for Resistin leading to inflammation in humans.
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human Resistin found in translation from mouse to man
Trends in Endocrinology and Metabolism, 2011Co-Authors: Daniel R Schwartz, Mitchell A LazarAbstract:The discovery of Resistin 10 years ago as a fat cell-secreted factor that modulates insulin resistance suggested a link to the current obesity-associated epidemics of diabetes and cardiovascular disease, which are major human health concerns. Although adipocyte-derived Resistin is indisputably linked to insulin resistance in rodent models, the relevance of human Resistin is complicated because human Resistin is secreted by macrophages rather than adipocytes, and because of the descriptive nature of human epidemiology. In this review, we examine the recent and growing evidence that human Resistin is an inflammatory biomarker and a potential mediator of diabetes and cardiovascular disease.
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macrophage derived human Resistin exacerbates adipose tissue inflammation and insulin resistance in mice
Journal of Clinical Investigation, 2009Co-Authors: Mohammed Qatanani, Rexford S Ahima, Nava Szwergold, David R Greaves, Mitchell A LazarAbstract:Resistin is an adipokine that contributes to insulin resistance in mice. In humans, however, studies investigating the link between Resistin and metabolic disease are conflicting. Further complicating the matter, human Resistin is produced mainly by macrophages rather than adipocytes. To address this important issue, we generated mice that lack adipocyte-derived mouse Resistin but produce human Resistin in a pattern similar to that found in humans, i.e., in macrophages (humanized Resistin mice). When placed on a high-fat diet, the humanized Resistin mice rapidly developed accelerated white adipose tissue (WAT) inflammation, leading to increased lipolysis and increased serum free fatty acids. Over time, these mice accumulated lipids, including diacylglycerols, in muscle. We found that this resulted in increased Pkcq pathway activity, leading to increased serine phosphorylation of Irs-1 and insulin resistance. Thus, although the site of Resistin production differs between species, human Resistin exacerbates WAT inflammation and contributes to insulin resistance.
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loss of Resistin improves glucose homeostasis in leptin deficiency
Diabetes, 2006Co-Authors: Yong Qi, Philipp E Scherer, Mitchell A Lazar, Neel S Singhal, Rexford S AhimaAbstract:Resistin levels are increased in obesity, and hyperResistinemia impairs glucose homeostasis in rodents. Here, we have determined the role of Resistin in ob/ob mice that are obese and insulin resistant because of genetic deficiency of leptin. Loss of Resistin increased obesity in ob/ob mice by further lowering the metabolic rate without affecting food intake. Nevertheless, Resistin deficiency improved glucose tolerance and insulin sensitivity in these severely obese mice, largely by enhancing insulin-mediated glucose disposal in muscle and adipose tissue. In contrast, in C57BL/6J mice with diet-induced obesity but wild-type leptin alleles, Resistin deficiency reduced hepatic glucose production and increased peripheral glucose uptake. Resistin deficiency enhanced Akt phosphorylation in muscle and liver and decreased suppressor of cytokine signaling-3 level in muscle, and these changes were reversed by Resistin replacement. Together, these results provide strong support for an important role of Resistin in insulin resistance and diabetes associated with genetic or diet-induced obesity.
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Resistin is an inflammatory marker of atherosclerosis in humans
Circulation, 2005Co-Authors: Muredach P. Reilly, Mitchell A Lazar, Michael Lehrke, Megan L. Wolfe, Anand Rohatgi, Daniel J. RaderAbstract:Background— Resistin, a plasma protein, induces insulin resistance in rodents. Recent reports suggest that circulating levels of Resistin are elevated in obese and insulin-resistant rodents and humans. Whereas rodent Resistin is made in adipocytes, macrophages are a major source of human Resistin. Given the convergence of adipocyte and macrophage function, Resistin may provide unique insight into links between obesity, inflammation, and atherosclerosis in humans. Methods and Results— We examined whether plasma Resistin levels were associated with metabolic and inflammatory markers, as well as with coronary artery calcification (CAC), a quantitative index of atherosclerosis, in 879 asymptomatic subjects in the Study of Inherited Risk of Coronary Atherosclerosis. Resistin levels were positively associated with levels of inflammatory markers, including soluble tumor necrosis factor-α receptor-2 (P<0.001), interleukin-6 (P=0.04), and lipoprotein-associated phospholipase A2 (P=0.002), but not measures of insul...
S Kumar - One of the best experts on this subject based on the ideXlab platform.
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role of Resistin in obesity insulin resistance and type ii diabetes
Clinical Science, 2005Co-Authors: Christine M Kusminski, P G Mcternan, S KumarAbstract:Resistin is a member of a class of cysteine-rich proteins collectively termed Resistin-like molecules. Resistin has been implicated in the pathogenesis of obesity-mediated insulin resistance and T2DM (Type II diabetes mellitus), at least in rodent models. In addition, Resistin also appears to be a pro-inflammatory cytokine. Taken together, Resistin, like many other adipocytokines, may possess a dual role in contributing to disease risk. However, to date there has been considerable controversy surrounding this 12.5 kDa polypeptide in understanding its physiological relevance in both human and rodent systems. Furthermore, this has led some to question whether Resistin represents an important pathogenic factor in the aetiology of T2DM and cardiovascular disease. Although researchers still remain divided as to the role of Resistin, this review will place available data on Resistin in the context of our current knowledge of the pathogenesis of obesity-mediated diabetes, and discuss key controversies and developments.
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Resistin and type 2 diabetes regulation of Resistin expression by insulin and rosiglitazone and the effects of recombinant Resistin on lipid and glucose metabolism in human differentiated adipocytes
The Journal of Clinical Endocrinology and Metabolism, 2003Co-Authors: P G Mcternan, F Fisher, George Valsamakis, R Chetty, A L Harte, Claire L Mcternan, Penny Clark, Stephen A Smith, Anthony H Barnett, S KumarAbstract:Resistin, an adipocyte secreted factor, has been suggested to link obesity with type 2 diabetes in rodent models, but its relevance to human diabetes remains uncertain. Although previous studies have suggested a role for this adipocytokine as a pathogenic factor, its functional effects, regulation by insulin, and alteration of serum Resistin concentration by diabetes status remain to be elucidated. Therefore, the aims of this study were to analyze serum Resistin concentrations in type 2 diabetic subjects; to determine the in vitro effects of insulin and rosiglitazone (RSG) on the regulation of Resistin, and to examine the functional effects of recombinant human Resistin on glucose and lipid metabolism in vitro. Serum concentrations of Resistin were analyzed in 45 type 2 diabetic subjects and 34 nondiabetic subjects. Subcutaneous human adipocytes were incubated in vitro with insulin, RSG, and insulin in combination with RSG to examine effects on Resistin secretion. Serum Resistin was increased by approximately 20% in type 2 diabetic subjects compared with nondiabetic subjects (P 0.004) correlating with C-reactive protein. No other parameters, including adiposity and fasting insulin levels, correlated with serum Resistin in this cohort. However, in vitro, insulin stimulated Resistin protein secretion in a concentration-dependent manner in adipocytes [control, 1215 87 pg/ml (mean SEM ); 1n M insulin, 1414.0 89 pg/ml; 1 M insulin, 1797 107 pg/ml (P < 0.001)]. RSG (10 nM) reduced the insulin-mediated rise in Resistin protein secretion (1 nM insulin plus RSG, 971 35 pg/ml; insulin, 1 M insulin plus RSG, 1019 28 pg/ml; P < 0.01 vs. insulin alone). Glucose uptake was reduced after treatment with 10 ng/ml recombinant Resistin and higher concentrations (P < 0.05). Our in vitro studies demonstrated a small, but significant, reduction in glucose uptake with human recombinant Resistin in differentiated preadipocytes. In human abdominal sc adipocytes, RSG blocks the insulin-mediated release of Resistin secretion in vitro. In conclusion, elevated serum Resistin in human diabetes reflects the subclinical inflammation prevalent in type 2 diabetes. Our in vitro studies suggest a modest effect of Resistin in reducing glucose uptake, and suppression of Resistin expression may contribute to the insulin-sensitizing and glucose-lowering actions of the thiazolidinediones. (J Clin Endocrinol Metab 88: 6098 – 6106, 2003)
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increased Resistin gene and protein expression in human abdominal adipose tissue
The Journal of Clinical Endocrinology and Metabolism, 2002Co-Authors: P G Mcternan, F Fisher, R Chetty, Claire L Mcternan, Anthony H Barnett, Keely Jenner, Michelle N Lauer, John Crocker, S KumarAbstract:Resistin, a novel signalling molecule isolated in mice has been suggested to be the putative hormone thought to link obesity with type 2 diabetes. The aim of this study was to examine Resistin protein expression in human adipose tissue depots and Resistin secretion in isolated adipose cells, to characterize Resistin expression in human adipose tissue. Both Resistin mRNA and protein expression were analysed from human adipose tissue (n = 5 adipose tissue samples: abdominal subcutaneous (Sc) n = 19, abdominal omental adipose tissue (Om) n = 10, thigh n = 9, breast n = 7). Resistin protein expression levels were similar in both the abdominal Sc and Om adipose tissue depots, and expression in abdominal fat depots were increased compared with thigh (p < 0.001) and breast tissue depots (p < 0.001). These findings were consistent with the mRNA expression studies. Resistin was secreted from both pre-adipocytes and adipocytes cells. Thus, Resistin resides within isolated adipose cells and is expressed and secreted...
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Resistin central obesity and type 2 diabetes
The Lancet, 2002Co-Authors: Claire L Mcternan, P G Mcternan, A L Harte, P L Levick, A H Barnett, S KumarAbstract:Resistin, an adipocyte-derived cytokine, causes insulin resistance and glucose intolerance in mice. We investigated whether Resistin expression was higher in human abdominal adipose tissue than other adipose tissue depots. We extracted RNA from 32 adipose tissue samples (13 subcutaneous abdominal, seven omentum, six thigh, and six breast). Quantitative PCR was used to determine Resistin mRNA expression. Resistin mRNA concentrations were similar in both the subcutaneous abdominal and omental depots. The abdominal depots showed a 418% increase in Resistin mRNA expression compared with the thigh. Increased Resistin expression in abdominal fat could explain the increased risk of type 2 diabetes associated with central obesity.
Rexford S Ahima - One of the best experts on this subject based on the ideXlab platform.
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Resistin in rodents and humans
Diabetes & Metabolism Journal, 2013Co-Authors: Hyeong Kyu Park, Rexford S AhimaAbstract:Obesity is characterized by excess accumulation of lipids in adipose tissue and other organs, and chronic inflammation associated with insulin resistance and an increased risk of type 2 diabetes. Obesity, type 2 diabetes, and cardiovascular diseases are major health concerns. Resistin was first discovered as an adipose-secreted hormone (adipokine) linked to obesity and insulin resistance in rodents. Adipocyte-derived Resistin is increased in obese rodents and strongly related to insulin resistance. However, in contrast to rodents, Resistin is expressed and secreted from macrophages in humans and is increased in inflammatory conditions. Some studies have also suggested an association between increased Resistin levels and insulin resistance, diabetes and cardiovascular disease. Genetic studies have provided additional evidence for a role of Resistin in insulin resistance and inflammation. Resistin appears to mediate the pathogenesis of atherosclerosis by promoting endothelial dysfunction, vascular smooth muscle cell proliferation, arterial inflammation, and formation of foam cells. Indeed, Resistin is predictive of atherosclerosis and poor clinical outcomes in patients with coronary artery disease and ischemic stroke. There is also growing evidence that elevated Resistin is associated with the development of heart failure. This review will focus on the biology of Resistin in rodents and humans, and evidence linking Resistin with type 2 diabetes, atherosclerosis, and cardiovascular disease.
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macrophage derived human Resistin exacerbates adipose tissue inflammation and insulin resistance in mice
Journal of Clinical Investigation, 2009Co-Authors: Mohammed Qatanani, Rexford S Ahima, Nava Szwergold, David R Greaves, Mitchell A LazarAbstract:Resistin is an adipokine that contributes to insulin resistance in mice. In humans, however, studies investigating the link between Resistin and metabolic disease are conflicting. Further complicating the matter, human Resistin is produced mainly by macrophages rather than adipocytes. To address this important issue, we generated mice that lack adipocyte-derived mouse Resistin but produce human Resistin in a pattern similar to that found in humans, i.e., in macrophages (humanized Resistin mice). When placed on a high-fat diet, the humanized Resistin mice rapidly developed accelerated white adipose tissue (WAT) inflammation, leading to increased lipolysis and increased serum free fatty acids. Over time, these mice accumulated lipids, including diacylglycerols, in muscle. We found that this resulted in increased Pkcq pathway activity, leading to increased serine phosphorylation of Irs-1 and insulin resistance. Thus, although the site of Resistin production differs between species, human Resistin exacerbates WAT inflammation and contributes to insulin resistance.
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loss of Resistin improves glucose homeostasis in leptin deficiency
Diabetes, 2006Co-Authors: Yong Qi, Philipp E Scherer, Mitchell A Lazar, Neel S Singhal, Rexford S AhimaAbstract:Resistin levels are increased in obesity, and hyperResistinemia impairs glucose homeostasis in rodents. Here, we have determined the role of Resistin in ob/ob mice that are obese and insulin resistant because of genetic deficiency of leptin. Loss of Resistin increased obesity in ob/ob mice by further lowering the metabolic rate without affecting food intake. Nevertheless, Resistin deficiency improved glucose tolerance and insulin sensitivity in these severely obese mice, largely by enhancing insulin-mediated glucose disposal in muscle and adipose tissue. In contrast, in C57BL/6J mice with diet-induced obesity but wild-type leptin alleles, Resistin deficiency reduced hepatic glucose production and increased peripheral glucose uptake. Resistin deficiency enhanced Akt phosphorylation in muscle and liver and decreased suppressor of cytokine signaling-3 level in muscle, and these changes were reversed by Resistin replacement. Together, these results provide strong support for an important role of Resistin in insulin resistance and diabetes associated with genetic or diet-induced obesity.
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regulation of Resistin expression and circulating levels in obesity diabetes and fasting
Diabetes, 2004Co-Authors: Michael W Rajala, Yong Qi, Hiral R Patel, Nobuhiko Takahashi, Ronadip R Banerjee, Utpal B Pajvani, Madhur K Sinha, Ronald L Gingerich, Philipp E Scherer, Rexford S AhimaAbstract:Resistin was originally reported as an adipose tissue–specific hormone that provided a link between obesity and diabetes. Resistin protein level was elevated in obese mice and decreased by insulin-sensitizing thiazolidinediones. Immunoneutralization of Resistin improved insulin sensitivity in diet-induced obese mice, while the administration of exogenous Resistin induced insulin resistance. More recently, we have shown that ablation of the Resistin gene in mice decreased fasting glucose through impairment of gluconeogenesis, while Resistin treatment in these knockout mice increased hepatic glucose production. However, the link between Resistin and glucose homeostasis has been questioned by studies demonstrating reduced, rather than increased, Resistin mRNA expression in obese and diabetic mice. To better understand the regulation of Resistin, we developed a sensitive and specific RIA Resistin that could accurately measure serum Resistin levels in several mouse models. We show that while Resistin mRNA is indeed suppressed in obese mice, the circulating Resistin level is significantly elevated and positively correlated with insulin, glucose, and lipids. Both Resistin mRNA expression and protein levels in Lep ob/ob mice are suppressed by leptin treatment in parallel with reductions in glucose and insulin. In wild-type mice, serum Resistin increases after nocturnal feeding, concordant with rising levels of insulin. Resistin mRNA and protein levels decline in parallel with glucose and insulin during fasting and are restored after refeeding. We performed clamp studies to determine whether Resistin is causally related to insulin and glucose. Adipose Resistin expression and serum Resistin increased in response to hyperinsulinemia and further in response to hyperglycemia. Taken together, these findings suggest that the nutritional regulation of Resistin and changes in Resistin gene expression and circulating levels in obesity are mediated, at least in part, through insulin and glucose.
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the hormone Resistin links obesity to diabetes
Nature, 2001Co-Authors: Claire M Steppan, Hiral R Patel, Ronadip R Banerjee, Rexford S Ahima, Shannon T Bailey, Savitha Bhat, Elizabeth J Brown, Christopher M Wright, Mitchell A LazarAbstract:Diabetes mellitus is a chronic disease that leads to complications including heart disease, stroke, kidney failure, blindness and nerve damage. Type 2 diabetes, characterized by target-tissue resistance to insulin, is epidemic in industrialized societies and is strongly associated with obesity; however, the mechanism by which increased adiposity causes insulin resistance is unclear. Here we show that adipocytes secrete a unique signalling molecule, which we have named Resistin (for resistance to insulin). Circulating Resistin levels are decreased by the anti-diabetic drug rosiglitazone, and increased in diet-induced and genetic forms of obesity. Administration of anti-Resistin antibody improves blood sugar and insulin action in mice with diet-induced obesity. Moreover, treatment of normal mice with recombinant Resistin impairs glucose tolerance and insulin action. Insulin-stimulated glucose uptake by adipocytes is enhanced by neutralization of Resistin and is reduced by Resistin treatment. Resistin is thus a hormone that potentially links obesity to diabetes.
Martin Haluzik - One of the best experts on this subject based on the ideXlab platform.
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the role of Resistin as a regulator of inflammation implications for various human pathologies
Clinical Immunology, 2009Co-Authors: Mária Filková, Martin Haluzik, Ladislav SenoltAbstract:Resistin was originally described as an adipocyte-secreted peptide that induced insulin resistance in rodents. Increasing evidence indicates its important regulatory roles in various biological processes, including several inflammatory diseases. Further studies have shown that Resistin in humans, in contrast to its production by adipocytes in mice, is synthesized predominantly by mononuclear cells both within and outside adipose tissue. Possible roles for Resistin in obesity-related subclinical inflammation, atherosclerosis and cardiovascular disease, non-alcoholic fatty liver disease, rheumatic diseases, malignant tumors, asthma, inflammatory bowel disease, and chronic kidney disease have already been demonstrated. In addition, Resistin can modulate several molecular pathways involved in metabolic, inflammatory, and autoimmune diseases. In this review, current knowledge about the functions and pathophysiological implications of Resistin in different human pathologies is summarized, although there is a significant lack of firm evidence regarding the specific role Resistin plays in the "orchestra" of the numerous mediators of inflammation.
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Resistin in rheumatoid arthritis synovial tissue synovial fluid and serum
Annals of the Rheumatic Diseases, 2006Co-Authors: Ladislav Senolt, Daniel Housa, Z Vernerova, T Jirasek, R Svobodova, D Veigl, K Anderlova, Ulf Mullerladner, K Pavelka, Martin HaluzikAbstract:BACKGROUND: Resistin is a newly identified adipocytokine which has demonstrated links between obesity and insulin resistance in rodents. In humans, proinflammatory properties of Resistin are superior to its insulin resistance-inducing effects. OBJECTIVES: To assess Resistin expression in synovial tissues, serum and synovial fluid from patients with rheumatoid arthritis, osteoarthritis and spondylarthropathies (SpA), and to study its relationship with inflammatory status and rheumatoid arthritis disease activity. METHODS: Resistin expression and localisation in synovial tissue was determined by immunohistochemistry and confocal microscopy. Serum and synovial fluid Resistin, leptin, interleukin (IL)1beta, IL6, IL8, tumour necrosis factor alpha, and monocyte chemoattractant protein-1 levels were measured. The clinical activity of patients with rheumatoid arthritis was assessed according to the 28 joint count Disease Activity Score (DAS28). RESULTS: Resistin was detected in the synovium in both rheumatoid arthritis and osteoarthritis. Staining in the sublining layer was more intensive in patients with rheumatoid arthritis compared with those with osteoarthritis. In rheumatoid arthritis, macrophages (CD68), B lymphocytes (CD20) and plasma cells (CD138) but not T lymphocytes (CD3) showed colocalisation with Resistin. Synovial fluid Resistin was higher in patients with rheumatoid arthritis than in those with SpA or osteoarthritis (both p<0.001). In patients with rheumatoid arthritis and SpA, serum Resistin levels were higher than those with osteoarthritis (p<0.01). Increased serum Resistin in patients with rheumatoid arthritis correlated with both CRP (r=0.53, p<0.02), and DAS28 (r=0.44, p<0.05), but not with selected (adipo) cytokines. CONCLUSION: The upregulated Resistin at local sites of inflammation and the link between serum Resistin, inflammation and disease activity suggest a role for Resistin in the pathogenesis of rheumatoid arthritis.
Kyong Soo Park - One of the best experts on this subject based on the ideXlab platform.
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Resistin is secreted from macrophages in atheromas and promotes atherosclerosis
Cardiovascular Research, 2006Co-Authors: Hye Seung Jung, Ki Ho Park, Sung Soo Chung, Kyong Soo ParkAbstract:Objective: Resistin belongs to a family of cysteine-rich secreted polypeptides that are mainly produced by monocytes/macrophages in humans. Recently, high concentrations of Resistin were shown to induce vascular endothelial dysfunction and vascular smooth muscle cell proliferation. We examined if Resistin was secreted from macrophages locally in atheromas and if it affected vascular cell function in human. Methods and results: Immunohistochemical staining of human vessels showed that aortic aneurysms exhibited Resistin-positive staining areas along macrophage infiltration, while normal arteries and veins did not. Co-localization of Resistin and CD68 (a marker for macrophages) was observed in immunofluorescent double staining of aneurysms. Resistin mRNA was expressed much higher in cultured monocytes/macrophages than in human vascular smooth muscle cells (VSMCs) and human umbilical venous endothelial cells (HUVECs). This suggested that the Resistin in aneurysms originates from macrophages within the vessels. To determine the effects of Resistin on atherosclerosis, HUVECs and human VSMCs were incubated with Resistin (10–100 ng/mL for 4∼24 h). In HUVECs, plasminogen activator inhibitor (PAI)-1 release was assayed by ELISA, while the PAI-1 and endothelin (ET)-1 mRNA levels were analyzed by Northern blotting. Both were increased significantly with Resistin treatment by factors of 1.3–2.5 ( p <0.05). Migratory activity of VSMCs measured by scratched wound assay also increased significantly (1.6 times, p <0.05). In summary, macrophages infiltrating atherosclerotic aneurysms secrete Resistin, and Resistin affects endothelial function and VSMC migration. Conclusions: Resistin secreted from macrophages may contribute to atherogenesis by virtue of its effects on vascular endothelial cells and smooth muscle cells in humans.
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plasma Resistin concentrations measured by enzyme linked immunosorbent assay using a newly developed monoclonal antibody are elevated in individuals with type 2 diabetes mellitus
The Journal of Clinical Endocrinology and Metabolism, 2004Co-Authors: Byung-soo Youn, Kyong Soo Park, Kangyeol Yu, Hong Je Park, Moon Yeon Youn, Young Joo ParkAbstract:Resistin is an adipocyte-derived peptide that might play a role in obesity and insulin resistance. However, its role in humans is largely unclear. Although many studies have measured the expression of human Resistin in tissues, the circulating concentrations of Resistin and its relation to metabolic parameters in humans are unknown. We developed an ELISA for human Resistin and measured plasma concentrations in aged individuals with or without type 2 diabetes mellitus. To validate the results of plasma Resistin concentrations in our subjects, plasma adiponectin concentrations were also determined, which were higher in nondiabetic subjects than in type 2 diabetic patients and correlated with the homeostasis model assessment for insulin resistance (HOMA-IR). Log-transformed plasma Resistin concentrations (log-Resistin) were higher in diabetic patients compared with normal individuals (0.50 ± 0.39 vs. 0.28 ± 0.51 ng/ml; P < 0.001), and this difference was significant after controlling for gender and body mass...
