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Obesity Insulin Resistance
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1. Molecular mechanisms involved in obesity-associated insulin resistance: therapeutical approach.
Match Strength: 13.619

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.

2. Adiponectin and its potential in the treatment of obesity, diabetes and insulin resistance.
Match Strength: 12.794

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.

3. Macrophages, inflammation, and insulin resistance.
Match Strength: 12.671

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. Interleukin-6 depletion selectively improves hepatic insulin action in obesity.
Match Strength: 12.060

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.

5. Variants of the interleukin-10 promoter gene are associated with obesity and insulin resistance but not type 2 diabetes in caucasian italian subjects.
Match Strength: 11.925

Interleukin (IL)-10 is a major anti-inflammatory cytokine that has been associated with obesity and type 2 diabetes. The three polymorphisms -1082G/A, -819C/T, and -592C/A in the IL10 promoter were reported to influence IL10 transcription. We investigated whether these polymorphisms were associated with type 2 diabetes and related traits in a cohort of Italian Caucasians comprising 551 type 2 diabetic and 1,131 control subjects. The -819C/T and -592C/A polymorphisms were in perfect linkage disequilibrium (r(2) = 1.0). The -1082G/A polymorphism was not associated with type 2 diabetes or related ... Read More »
» Published in Diabetes. 2006 May;55(5):1529-33.

6. Inflammation and insulin resistance: an old story with new ideas.
Match Strength: 11.675

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. Beyond obesity: the diagnosis and pathophysiology of metabolic syndrome.
Match Strength: 11.645

Metabolic syndrome (MSX) identifies clinical symptoms and lab results, including abdominal obesity, insulin resistance, hyperglycemia, hyperlipidemia, and hypertension, that lead to an increased risk of cardiovascular disease (CVD). Obesity typically results in insulin and leptin resistance and a shift from expansion of subcutaneous fat to deposition of abdominal and ectopic fat. These conditions cause metabolic dysregulation, elevated fatty acids (FFA), and increased secretion of pro-inflammatory "adipokines". Left untreated, these conditions cause lipotoxicity, chronic inflammation, ... Read More »
» Published in Clin Lab Sci. 2010 Winter;23(1):51-61; quiz 62-5.

8. The role of inflammation and macrophage accumulation in the development of obesity-induced type 2 diabetes mellitus and the possible therapeutic effects of long-chain n-3 PUFA.
Match Strength: 11.551

The WHO estimate that >1 x 10(6) deaths in Europe annually can be attributed to diseases related to excess body weight, and with the rising global obesity levels this death rate is set to drastically increase. Obesity plays a central role in the metabolic syndrome, a state of insulin resistance that predisposes patients to the development of CVD and type 2 diabetes mellitus. Obesity is associated with low-grade chronic inflammation characterised by inflamed adipose tissue with increased macrophage infiltration. This inflammation is now widely believed to be the key link between obesity and ... Read More »
» Published in Proc Nutr Soc. 2010 May;69(2):232-43. Epub 2010 Feb 17.

9. Infliximab and insulin resistance.
Match Strength: 11.509

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.

10. Neutralization of osteopontin inhibits obesity-induced inflammation and insulin resistance.
Match Strength: 11.445

OBJECTIVE: Obesity is associated with a state of chronic low-grade inflammation mediated by immune cells that are primarily located to adipose tissue and liver. The chronic inflammatory response appears to underlie obesity-induced metabolic deterioration including insulin resistance and type 2 diabetes. Osteopontin (OPN) is an inflammatory cytokine, the expression of which is strongly upregulated in adipose tissue and liver upon obesity. Here, we studied OPN effects in obesity-induced inflammation and insulin resistance by targeting OPN action in vivo. RESEARCH DESIGN AND METHODS: C57BL/6J ... Read More »
» Published in Diabetes. 2010 Apr;59(4):935-46. Epub 2010 Jan 27.

11. The dual function of hepatic SOCS3 in insulin resistance in vivo.
Match Strength: 11.427

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.

12. Adiponectin and its gene variants as risk factors for insulin resistance, the metabolic syndrome and cardiovascular disease.
Match Strength: 11.309

The increasing prevalence of obesity and metabolic syndrome/insulin resistance has attracted considerable interest due to their identification as risk factors for cardiovascular disease and, hence, targets for cardiovascular disease prevention. This review focuses on adiponectin, the most profusely secreted protein from adipose tissue, which itself is being increasingly recognised as an important and very active endocrine organ, secreting a wide range of biologically active substances known as adipokines or adipocytokines. Adiponectin has been demonstrated to have insulin sensitising effects, ... Read More »
» Published in Atherosclerosis. 2006 Oct;188(2):231-44. Epub 2006 Apr 3.

13. The metabolic syndrome: metabolic changes with vascular consequences.
Match Strength: 11.044

Despite criticism regarding its clinical relevance, the concept of the metabolic syndrome improves our understanding of both the pathophysiology of insulin resistance and its associated metabolic changes and vascular consequences. Free fatty acids (FFA) and tumour necrosis factor-alpha (TNF-alpha) play prominent roles in the development of insulin resistance by impairing the intracellular insulin signalling transduction pathway. Obesity is an independent risk factor for cardiovascular disease and strongly related to insulin resistance. In case of obesity, FFAs and TNF-alpha are produced in ... Read More »
» Published in Eur J Clin Invest. 2007 Jan;37(1):8-17.

14. Characterization of alterations in carbohydrate metabolism in children with Prader-Willi syndrome.
Match Strength: 10.804

OBJECTIVE: To study carbohydrate metabolism and insulin sensitivity and secretion in children and adolescents with Prader-Willi syndrome (PWS) compared with multifactorial obesity (MO) controls. PATIENTS AND METHODS: Seventy-five patients with PWS and 395 controls with MO were studied by oral glucose tolerance test. Insulin resistance (IR) and beta-cell function were assessed by homeostasis model assessment (HOMA), insulin glucose index, fasting insulin and insulin sensitivity index. RESULTS: The incidence of diabetes mellitus was 0% in PWS and 1.5% in MO, while carbohydrate intolerance was 9 ... Read More »
» Published in J Pediatr Endocrinol Metab. 2006 Jul;19(7):911-8.

15. Hereditary postprandial hypertriglyceridemic rabbit exhibits insulin resistance and central obesity: a novel model of metabolic syndrome.
Match Strength: 10.779

OBJECTIVE: We have established a hereditary postprandial hypertriglyceridemic (PHT) rabbit. The present study was designed to define whether this rabbit model represents both insulin resistance and central obesity. METHODS AND RESULTS: Body weight, abdominal circumference, visceral fat weight, and glucose tolerance were compared between PHT and Japanese white (JW) rabbit. Plasma levels of triglycerides (TG), total cholesterol (TC), glucose, and insulin were measured before and after feeding. Abdominal circumference of PHT rabbit was larger than that of JW rabbit, with no difference in body ... Read More »
» Published in Arterioscler Thromb Vasc Biol. 2006 Dec;26(12):2752-7. Epub 2006 Sep 21.

16. Is the use of resveratrol in the treatment and prevention of obesity premature?
Match Strength: 10.728

Obesity is a multi-faceted disease, predisposing sufferers to numerous co-morbidities such as epithelial dysfunction and insulin resistance which ultimately result in CVD. Visceral adipose tissue in particular is associated with inflammation due to the release of pro-inflammatory cytokines by adipocytes. Inflammation seems to be rather central in causing damage to endothelial cells as well as exerting negative effects on glucose metabolism, ultimately leading to insulin resistance. Resveratrol is a naturally occurring phenolic substance which has been found to display anti-inflammatory, ... Read More »
» Published in Nutr Res Rev. 2009 Dec;22(2):111-7.

17. Role of adiponectin and PBEF/visfatin as regulators of inflammation: involvement in obesity-associated diseases.
Match Strength: 10.512

Obesity and obesity-related disorders play an important role in clinical medicine. Adipose tissue, with its soluble mediators called adipocytokines, has emerged as a major endocrine organ. These adipocytokines comprise many mediators such as adiponectin, PBEF (pre-B-cell-enhancing factor)/visfatin, leptin, resistin, retinol-binding protein-4 and others. They play major roles in key aspects of metabolism, such as insulin resistance, fatty acid oxidation, inflammation and immunity. Adiponectin, a prototypic adipocytokine, is of importance in the regulation of insulin resistance, as circulating ... Read More »
» Published in Clin Sci (Lond). 2008 Feb;114(4):275-88.

18. Obesity and inflammation: lessons from bariatric surgery.
Match Strength: 10.363

BACKGROUND: Obesity is associated with a series of comorbid conditions that are characterized by an inflammatory state. The purpose of this review is to update knowledge about obesity, adipose tissue, and inflammation. METHODS: Review of the published literature using search terms of adipose, inflammation, obesity, and insulin resistance in combinations. RESULTS: Adipose tissue elaborates proinflammatory cytokines such as interleukin-6 and tumor necrosis factor-alpha, with greater secretion from the stromal vascular fraction than from adipocytes and with greater secretion from visceral than ... Read More »
» Published in JPEN J Parenter Enteral Nutr. 2008 Nov-Dec;32(6):645-7.

19. Insulin facilitates monocyte migration: a possible link to tissue inflammation in insulin-resistance.
Match Strength: 10.302

Mononuclear cells (MNCs) are the primary cell type involved in the pro-inflammatory state of obesity-linked insulin-resistance, and atherosclerosis. Increased serum levels of MMP-9 are reported in insulin-resistant type 2 diabetic patients. Here we demonstrate insulin facilitating human monocytic THP-1 cell chemotaxis via prolonged Erk1/2-dependent induction of MMP-9. In vivo, significantly increased serum levels of MMP-9 were found in obesity-induced hyperinsulinemic C57BL/J6 mice, which were diminished by treatment with the anti-diabetic PPARgamma-ligand pioglitazone. In line with this, ... Read More »
» Published in Biochem Biophys Res Commun. 2008 Jan 18;365(3):503-8. Epub 2007 Nov 20.

20. Determinants of insulin resistance in renal transplant recipients.
Match Strength: 10.256

BACKGROUND: Insulin resistance is considered to play an important role in the development of cardiovascular disease, which limits long-term renal transplant survival. Renal transplant recipients are more insulin-resistant compared with healthy controls. It is not known to date which factors relate to this excess insulin resistance. Therefore, we investigated which factors are related to insulin resistance long-term after renal transplantation. METHODS: All renal transplant recipients at our outpatient clinic with a functioning graft for more than one year were invited to participate. We ... Read More »
» Published in Transplantation. 2007 Jan 15;83(1):29-35.

 << Prev 20  Showing results 1 to 20 of 215 Next 20 >>

* All information on is for educational purposes only. These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease. Before changing your diet, or adding supplements to your diet, or beginning an exercise program, everyone should consult a qualified and licensed health practitioner; a physician, dietician or similar professional.

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