Inflammation Insulin Resistance
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Peer Reviewed Scientific Research Reports.
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1. IRS1-independent defects define major nodes of insulin resistance.
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Insulin resistance is a common disorder caused by a wide variety of physiological insults, some of which include poor diet, inflammation, anti-inflammatory steroids, hyperinsulinemia, and dyslipidemia. The common link between these diverse insults and insulin resistance is widely considered to involve impaired insulin signaling, particularly at the level of the insulin receptor substrate (IRS). To test this model, we utilized a heterologous system involving the platelet-derived growth factor (PDGF) pathway that recapitulates many aspects of insulin action independently of IRS. We ... Read More »
» Published in Cell Metab. 2008 May;7(5):421-33.
2. The dual function of hepatic SOCS3 in insulin resistance in vivo.
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Inflammation associates with insulin resistance, which dysregulates nutrient homeostasis and leads to diabetes. The suppressor of cytokine signaling 3 (SOCS3), which is induced by pro-inflammatory cytokines, such as TNFalpha and IL-6, has been implicated in inflammation-mediated insulin resistance in the liver and adipocytes. However, no genetic evidence has been provided for the involvement of SOCS3 on insulin resistance. Here, we generated hepatocyte-specific SOCS3-deficient (L-SOCS3 cKO) mice and examined insulin sensitivity. Being consistent with a previous idea, the loss of SOCS3 in the ... Read More »
» Published in Genes Cells. 2007 Feb;12(2):143-54.
3. Macrophages, inflammation, and insulin resistance.
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Obesity induces an insulin-resistant state in adipose tissue, liver, and muscle and is a strong risk factor for the development of type 2 diabetes mellitus. Insulin resistance in the setting of obesity results from a combination of altered functions of insulin target cells and the accumulation of macrophages that secrete proinflammatory mediators. At the molecular level, insulin resistance is promoted by a transition in macrophage polarization from an alternative M2 activation state maintained by STAT6 and PPARs to a classical M1 activation state driven by NF-kappaB, AP1, and other signal ... Read More »
» Published in Annu Rev Physiol. 2010 Mar 17;72:219-46.
4. Molecular mechanisms involved in obesity-associated insulin resistance: therapeutical approach.
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Insulin resistance is an important contributor to the pathogenesis of T2D and obesity is a risk factor for its development. It has been demonstrated that these obesity-related metabolic disorders are associated with a state of chronic low-intensity inflammation. Several mediators released from adipocytes and macrophages, such as the pro-inflammatory cytokines TNF-alpha and IL-6, have been suggested to impair insulin action in peripheral tissues, including fat and skeletal muscle. Such insulin resistance can initially be compensated by increased insulin secretion, but the prolonged presence of ... Read More »
» Published in Arch Physiol Biochem. 2009 Oct;115(4):227-39.
5. Infliximab and insulin resistance.
Match Strength: 9.533
Insulin resistance is the most important pathophysiologic feature of obesity, type 2 diabetes mellitus and prediabetic states. TNF-alpha, a proinflammatory cytokine, plays a pivotal role in the pathogenesis of inflammation-associated insulin resistance during the course of rheumatic diseases. Therapies aimed at neutralizing TNF-alpha, such as the monoclonal antibody infliximab, represent a novel approach for the treatment of rheumatic diseases and allow to obtain significant results in terms of control of the inflammatory process. In this article we reviewed the scientific evidence published ... Read More »
» Published in Autoimmun Rev. 2010 Jun;9(8):536-9. Epub 2010 Jan 7.
6. Inflammation and insulin resistance: an old story with new ideas.
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Years before insulin was discovered, anti-inflammatory sodium salicylate was used to treat diabetes in 1901. Intriguingly for many years that followed, diabetes was viewed as a disorder of glucose metabolism, and then it was described as a disease of dysregulated lipid metabolism. The diabetes research focused on the causal relationship between obesity and insulin resistance, a major characteristic of type 2 diabetes. It is only within the past 20 years when the notion of inflammation as a cause of insulin resistance began to surface. In obesity, inflammation develops when macrophages ... Read More »
» Published in Korean Diabetes J. 2010 Jun;34(3):137-45. Epub 2010 Jun 30.
7. Berberine Inhibits Inflammatory Response and Ameliorates Insulin Resistance in Hepatocytes.
Match Strength: 9.137
Berberine, a major isoquinoline alkaloid present in Chinese herb Rhizoma coptidis, is a potent inhibitor of inflammation and has anti-diabetic activity. This study aims to investigate effects of berberine on ameliorating insulin resistance and molecular mechanisms involved in HepG2 cells. Inflammatory responses and insulin resistance were induced by palmitate (PA) stimulation for 24 h. Treatment of berberine enhanced insulin-mediated glycogen synthesis and restored insulin inhibition of triglyceride secretion. Stimulation of PA resulted in IL-6 and TNF-a production in HepG2 cells, and ... Read More »
» Published in Inflammation. 2010 Nov 26.
8. Inflammation and insulin resistance.
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Over a hundred years ago, high doses of salicylates were shown to lower glucose levels in diabetic patients. This should have been an important clue to link inflammation to the pathogenesis of type 2 diabetes (T2D), but the antihyperglycemic and antiinflammatory effects of salicylates were not connected to the pathogenesis of insulin resistance until recently. Together with the discovery of an important role for tissue macrophages, these new findings are helping to reshape thinking about how obesity increases the risk for developing T2D and the metabolic syndrome. The evolving concept of ... Read More »
» Published in J Clin Invest. 2006 Jul;116(7):1793-801.
9. Is there evidence of separate inflammatory or metabolic forms of preeclampsia?
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OBJECTIVES: To examine whether high insulin resistance versus high inflammation identifies subtypes of preeclampsia. METHODS: A cytokine panel, glucose and insulin were measured in 37 preeclampsia plasma samples. Wilcoxon rank sum assessed median concentration of HOMA(IR) by pro-inflammatory:anti-inflammatory ratio. Regression stratifying by BMI and preterm birth was conducted. RESULTS: There was no difference in median HOMA(IR) by the pro-inflammatory:anti-inflammatory ratio (p = 0.16). No subsets scatterplot clusters emerged. A positive correlation between HOMAlog and the ratio was ... Read More »
» Published in Hypertens Pregnancy. 2011;30(1):1-10. Epub 2010 May 12.
10. Anti-tumor necrosis factor-alpha blockade improves insulin resistance in patients with rheumatoid arthritis.
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OBJECTIVE: Systemic inflammation, insulin resistance, and endothelial dysfunction have been implicated in the development of cardiovascular disease in rheumatoid arthritis (RA). Since insulin resistance can promote endothelial dysfunction and anti-TNF-alpha blockade yield a rapid improvement of endothelial function, we have sought to assess whether TNF-alpha blockade may also result in a reduction of insulin serum levels and improvement of insulin resistance in RA patients who require this therapy because of severe and refractory disease. METHODS: We recruited patients with RA seen over a ... Read More »
» Published in Clin Exp Rheumatol. 2006 Jan-Feb;24(1):83-6.
11. Influence of TNF-alpha and IL-6 infusions on insulin sensitivity and expression of IL-18 in humans.
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Inflammation is associated with insulin resistance, and both tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 may affect glucose uptake. TNF induces insulin resistance, whereas the role of IL-6 is controversial. High plasma levels of IL-18 are associated with insulin resistance in epidemiological studies. We investigated the effects of TNF and IL-6 on IL-18 gene expression in skeletal muscle and adipose tissue. Nine human volunteers underwent three consecutive interventions, receiving an infusion of recombinant human (rh)IL-6, rhTNF, and saline. Insulin sensitivity was assessed by ... Read More »
» Published in Am J Physiol Endocrinol Metab. 2006 Jul;291(1):E108-14. Epub 2006 Feb 7.
12. Luteolin inhibits inflammatory response and improves insulin sensitivity in the endothelium.
Match Strength: 8.345
Endothelial insulin resistance is tightly associated with diabetic cardiovascular complication, and it is well known that inflammation plays an important role in the development of insulin resistance. Luteolin, a flavonoid abundant in some medical and eatable plants, is a potent inhibitor of inflammation. It is also reported that luteolin exhibited some chemoprotection capability to the endothelial integrity. This study aims to clarify whether the anti-inflammatory potency of luteolin contributes to amelioration of insulin resistance in the endothelium. Palmitate (PA) stimulation markedly ... Read More »
» Published in Biochimie. 2011 Mar;93(3):506-12. Epub 2010 Nov 21.
13. C-reactive protein impairs hepatic insulin sensitivity and insulin signaling in rats: role of mitogen-activated protein kinases.
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Plasma C-reactive protein (CRP) concentration is increased in the metabolic syndrome, which consists of a cluster of cardiovascular disease risk factors, including insulin resistance. It is not known, however, whether CRP is merely a marker of accompanying inflammation or whether it contributes causally to insulin resistance. The objective of this study is to investigate the role that CRP may play in the development of insulin resistance. We examined the effect of single-dose intravenous administration of purified human (h)CRP on insulin sensitivity in Sprague-Dawley rats using the euglycemic, ... Read More »
» Published in Hepatology. 2011 Jan;53(1):127-35. doi: 10.1002/hep.24011. Epub 2010 Oct 21.
14. Interleukin-6 depletion selectively improves hepatic insulin action in obesity.
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Obesity and insulin resistance are considered chronic inflammatory states, in part because circulating IL-6 is elevated. Exogenous IL-6 can induce hepatic insulin resistance in vitro and in vivo. The importance of endogenous IL-6, however, to insulin resistance of obesity is unresolved. To test the hypothesis that IL-6 contributes to the inflammation and insulin resistance of obesity, IL-6 was depleted in Lep(ob) mice by injection of IL-6-neutralizing antibody. In untreated Lep(ob) mice, signal transducer and activator of transcription-3 (STAT3) activation was increased compared with that in ... Read More »
» Published in Endocrinology. 2005 Aug;146(8):3417-27. Epub 2005 Apr 21.
15. Activin in glucose metabolism.
Match Strength: 7.944
Activins, members of the TGF-ß family, are multifunctional growth and differentiation factors. Activins regulate glucose/energy metabolism by promoting the differentiation of insulin-producing and -responsive cells, and regulating function of the differentiated cells. In the pancreas, activins stimulate the differentiation of ß cells and secretion of insulin, which enables the cells to respond to glucose uptake efficiently. By contrast, in the liver, skeletal muscle and white adipose tissue, activins exert negative regulation on organogenesis, which leads to impaired insulin sensitivity. ... Read More »
» Published in Vitam Horm. 2011;85:217-34.
16. Decreased AMP-activated protein kinase activity is associated with increased inflammation in visceral adipose tissue and with whole-body insulin resistance in morbidly obese humans.
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Inflammation and infiltration of immune cells in white adipose tissue have been implicated in the development of obesity-associated insulin resistance. Likewise, dysregulation of the fuel-sensing enzyme AMP-activated protein kinase (AMPK) has been proposed as a pathogenetic factor for these abnormalities based on both its links to insulin action and its anti-inflammatory effects. In this study, we examined the relationships between AMPK activity, the expression of multiple inflammatory markers in visceral (mesenteric and omental) and abdominal subcutaneous adipose tissue, and whole-body ... Read More »
» Published in Biochem Biophys Res Commun. 2011 Jan 7;404(1):382-7. Epub 2010 Dec 3.
17. Grape powder extract attenuates tumor necrosis factor a-mediated inflammation and insulin resistance in primary cultures of human adipocytes.
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Grapes are rich in phenolic phytochemicals that possess anti-oxidant and anti-inflammatory properties. However, the ability of grape powder extract (GPE) to prevent inflammation and insulin resistance in human adipocytes caused by tumor necrosis factor a (TNFa), a cytokine elevated in plasma and white adipose tissue (WAT) of obese, diabetic individuals, is unknown. Therefore, we examined the effects of GPE on markers of inflammation and insulin resistance in primary cultures of newly differentiated human adipocytes treated with TNFa. We found that GPE attenuated TNFa-induced expression of ... Read More »
» Published in J Nutr Biochem. 2011 Jan;22(1):89-94. Epub 2010 Apr 10.
18. High molecular weight adiponectin correlates with insulin sensitivity in patients with hepatitis C genotype 3, but not genotype 1 infection.
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BACKGROUND: Obesity is recognized as a cofactor in hepatitis C (HCV) liver injury. Adipokines may be the link between increasing body mass index (BMI) and disease progression in HCV. Adiponectin is an anti-inflammatory adipokine that is present in serum in a range of multimeric forms that appear to have different metabolic functions. METHODS: We studied 30 male patients with untreated chronic HCV (15 each with genotypes 1 and 3) and 12 controls. The three groups were matched for age and BMI. Total adiponectin and high (HMW) and low (LMW) molecular weight adiponectin multimers were measured. ... Read More »
» Published in Am J Gastroenterol. 2005 Dec;100(12):2717-23.
19. Indomethacin activates peroxisome proliferator-activated receptor ? to improve insulin resistance in cotton pellet granuloma model.
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Inflammation is involved in the development of insulin resistance and diabetes. However, the effectiveness of anti-inflammatory drugs in diabetic therapy remains obscure. In the present study, the possible mechanisms of indomethacin, one of the nonsteroidal anti-inflammatory drugs, in the improvement of insulin resistance were investigated. Indomethacin treatment significantly decreased cotton pellet implantation induced white blood cell count elevation and immune cells infiltration in epididymal white adipose tissue. Also, cotton pellet implantation induced impaired glucose utilization and ... Read More »
» Published in Horm Metab Res. 2010 Oct;42(11):775-80. Epub 2010 Jul 27.
20. Deficiency of haematopoietic-cell-derived IL-10 does not exacerbate high-fat-diet-induced inflammation or insulin resistance in mice.
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AIMS/HYPOTHESIS: Recent work has identified the important roles of M1 pro-inflammatory and M2 anti-inflammatory macrophages in the regulation of insulin sensitivity. Specifically, increased numbers of M2 macrophages and a decrease in M1 macrophages within the adipose tissue are associated with a state of enhanced insulin sensitivity. IL-10 is an anti-inflammatory cytokine and is a critical effector molecule of M2 macrophages. METHODS: In the present study, we examined the contribution of haematopoietic-cell-derived IL-10 to the development of obesity-induced inflammation and insulin resistance ... Read More »
» Published in Diabetologia. 2011 Apr;54(4):888-99. Epub 2011 Jan 6.
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