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Peer Reviewed Scientific Research Reports.
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1. IRS1-independent defects define major nodes of insulin resistance.
Match Strength: 10.373
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. Marked insulin resistance in pregnancy: a case report and literature review.
Match Strength: 9.695
Pregnancy is usually accompanied by insulin resistance; however, severe insulin resistance in pregnancy requiring massive doses of insulin is rare. We report a case of a 14-year-old with acanthosis nigricans and a strong family history of Type 2 diabetes who exhibited marked insulin resistance during pregnancy. Her treatment included terbutaline for pre-term labor and dexamethasone for fetal lung maturity. Shortly after these interventions, her insulin requirements escalated to 130 units per hour. Multiple insulin regimens were used in her treatment. Investigations were negative for ... Read More »
» Published in Tenn Med. 2006 Oct;99(10):35-7.
3. The dual function of hepatic SOCS3 in insulin resistance in vivo.
Match Strength: 9.601
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.
4. Molecular mechanisms involved in obesity-associated insulin resistance: therapeutical approach.
Match Strength: 9.216
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: 9.116
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. Macrophages, inflammation, and insulin resistance.
Match Strength: 8.999
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.
7. Berberine Inhibits Inflammatory Response and Ameliorates Insulin Resistance in Hepatocytes.
Match Strength: 8.584
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. Inflammatory signaling in skeletal muscle insulin resistance: green signal for nutritional intervention?
Match Strength: 8.458
PURPOSE OF REVIEW: To review the evidence implying a role of inflammatory signaling pathways, specifically nuclear factor-?B and c-Jun NH2-terminal kinase, in fatty acid-induced skeletal muscle insulin resistance and to discuss the potential of dietary interventions to interfere with these processes. RECENT FINDINGS: Fatty acids can induce skeletal muscle insulin resistance via inflammatory signaling after binding Toll-like receptors at the cell membrane of muscle cells or after accumulating as intramyocellular lipid metabolites. In both processes, activation of intracellular inflammatory ... Read More »
» Published in Curr Opin Clin Nutr Metab Care. 2010 Nov;13(6):647-55.
9. Inflammation and insulin resistance: an old story with new ideas.
Match Strength: 8.387
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.
10. Serum concentrations of cortisol, interleukin 6, leptin and adiponectin predict stress induced insulin resistance in acute inflammatory reactions.
Match Strength: 8.301
INTRODUCTION: Inflammatory stimuli are causative for insulin resistance in obesity as well as in acute inflammatory reactions. Ongoing research has identified a variety of secreted proteins that are released from immune cells and adipocytes as mediators of insulin resistance; however, knowledge about their relevance for acute inflammatory insulin resistance remains limited. In this study we aimed for a clarification of the relevance of different insulin resistance mediating factors in an acute inflammatory situation. METHODS: Insulin resistance was measured in a cohort of 37 non-diabetic ... Read More »
» Published in Crit Care. 2008;12(6):R157. Epub 2008 Dec 17.
11. Anti-tumor necrosis factor-alpha blockade improves insulin resistance in patients with rheumatoid arthritis.
Match Strength: 8.215
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.
12. Effects of infliximab treatment on insulin resistance in patients with rheumatoid arthritis and ankylosing spondylitis.
Match Strength: 8.194
BACKGROUND: Tumour necrosis factor alpha (TNFalpha) may be an important mediator of insulin resistance. Infliximab is a chimeric monoclonal, high affinity antibody against the soluble and transmembrane TNFalpha, which can reduce markedly the biological activity of circulating and tissue TNFalpha and is used to treat various autoimmune disorders. OBJECTIVE: To assess the effects of infliximab infusions on insulin sensitivity in patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). METHODS: 45 patients (28 with RA, 17 with AS) aged 19-74 years were studied. All patients were ... Read More »
» Published in Ann Rheum Dis. 2005 May;64(5):765-6. Epub 2004 Sep 30.
13. Insulin resistance in the HIV-infected population: the potential role of mitochondrial dysfunction.
Match Strength: 8.141
Insulin resistance is accepted as the underlying fundamental defect that predates and ultimately leads to the development of type 2 (adult onset) diabetes mellitus in the general non-human immunodeficiency virus (HIV)-infected population. Insulin resistance is also a major component of the metabolic syndrome that, in association with other factors such as hypertension, hypercholesterolemia, and central obesity, defines a pre-diabetic atherogenic state that leads to adverse cardiovascular events. Growing evidence now suggests that mitochondrial dysfunction in skeletal muscle may be the ... Read More »
» Published in Curr Drug Targets Infect Disord. 2005 Sep;5(3):255-62.
14. Adiponectin and its potential in the treatment of obesity, diabetes and insulin resistance.
Match Strength: 8.075
Adiponectin is a protein hormone produced exclusively by adipocytes. Its circulating levels are decreased in individuals with obesity, atherosclerosis and insulin resistance, suggesting that its deficiency may have a causal role in the etiopathogenesis of these diseases. Studies have shown that adiponectin administration in rodents has insulin-sensitizing, anti-atherogenic and anti-inflammatory effects and under certain settings also decreases body weight. Therefore, adiponectin replacement in humans may represent a promising approach to prevent and/or treat obesity, insulin resistance and ... Read More »
» Published in Curr Opin Investig Drugs. 2005 Oct;6(10):988-93.
15. Influence of TNF-alpha and IL-6 infusions on insulin sensitivity and expression of IL-18 in humans.
Match Strength: 8.074
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.
16. Dioscorea opposita reverses dexamethasone induced insulin resistance.
Match Strength: 8.015
The effects of Dioscorea opposita (huai shan yao, HSY) on dexamethasone-induced insulin resistance were investigated in vitro and in vivo. D. opposita extract reduced significantly the blood insulin and glucose levels in dexamethasone-induced diabetic rats. In vitro, HSY significantly enhanced insulin-stimulated glucose uptake in 3T3-L1 adipocytes. Moreover, HSY increase the mRNA expression of GLUT4 glucose transporter in 3T3-L1 adipocytes. These data suggest that D. opposita has insulin sensitivity that is associated with the regulation of GLUT4 expression ... Read More »
» Published in Fitoterapia. 2007 Jan;78(1):12-5. Epub 2006 Sep 23.
17. Insulin resistance, endocrine function and adipokines in type 2 diabetes patients at different glycaemic levels: potential impact for glucotoxicity in vivo.
Match Strength: 8.007
OBJECTIVE: To evaluate the interplay between hyperglycaemia, insulin resistance, hormones and adipokines in patients with type 2 diabetes mellitus (T2DM). DESIGN AND METHODS: Ten patients with T2DM with good glycaemic control (G), 10 with poor control (P) and 10 nondiabetic control subjects (C) were matched for sex (M/F 6/4), age and body mass index. A hyperinsulinaemic, euglycaemic clamp was performed and cytokines and endocrine functions, including cortisol axis activity were assessed. RESULTS: Patients with diabetes were more insulin resistant than group C, and group P exhibited the highest ... Read More »
» Published in Clin Endocrinol (Oxf). 2006 Sep;65(3):301-9.
18. C-reactive protein impairs hepatic insulin sensitivity and insulin signaling in rats: role of mitogen-activated protein kinases.
Match Strength: 7.974
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.
19. Interleukin-6 depletion selectively improves hepatic insulin action in obesity.
Match Strength: 7.942
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.
20. Aspirin inhibits serine phosphorylation of insulin receptor substrate 1 in growth hormone treated animals.
Match Strength: 7.827
In this study, we demonstrate that pretreatment with aspirin inhibits GH-induced insulin resistance. GH was observed to lead to serine phosphorylation of IRS-1, a phenomenon which was reversed by aspirin in liver, muscle and WAT in parallel with a reduction in JNK activity. In addition, our data show an impairment of insulin activation in the IR/IRS/PI(3)kinase pathway and a reduction in IRS-1 protein levels in rats treated with GH, which was also reversed in the animals pretreated with aspirin. Overall, these results provide new insights into the mechanism of GH-induced insulin resistance ... Read More »
» Published in FEBS Lett. 2005 Jun 6;579(14):3152-8.
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