RSS-Feed abonnieren
DOI: 10.1055/s-0034-1382035
Inflammatory Status is Different in Relationship to Insulin Resistance in Severely Obese People and Changes after Bariatric Surgery or Diet-induced Weight Loss
Publikationsverlauf
received 15. März 2014
first decision 17. Mai 2014
accepted 28. Mai 2014
Publikationsdatum:
08. Juli 2014 (online)
![](https://www.thieme-connect.de/media/eced/201410/lookinside/thumbnails/10.1055-s-0034-1382035-1.jpg)
Abstract
Aim: To assess if insulin resistance is related to a different inflammatory status (especially lymphocyte subpopulations) in severely obese people and to evaluate changes after weight loss either following a very-low calorie diet (VLCD) or bariatric surgery.
Research Methods & Procedures: Severely obese patients were consecutively recruited in our Obesity Unit. Blood lymphocyte subpopulations and inflammatory parameters were measured baseline, after a VLCD during 6 weeks and one year after biliopancreatic diversion. Insulin resistance was evaluated by Homeostasis Model Assessment (HOMA) index.
Results: After excluding diabetic patients, 58 patients were studied. HOMA index classified 63.8% of them as insulin resistant (IR). Serum baseline levels of inflammatory cytokines were not significantly different between IR and insulinsensitive (IS) patients but, regarding lymphocyte subpopulations, Natural Killer (NK) cells were higher in IR patients [(305.0 (136.7) vs. 235.0 (80.7) cells/µL, p=0.047]. NK cells showed a significant positive correlation with HOMA index (r=0.484, p=0.000) and with the carbohydrate content of the diet (r=0.420, p=0.001). After VLCD, NK cells significantly decreased, but only in IR patients and in those losing more than 10% of their initial weight. After biliopancreatic diversion, total and CD8 T Lymphocytes, B lymphocytes and NK cells also decreased but only in IR individuals.
Conclusion: NK cells are significantly increased in IR severely obese people in respect to IS, suggesting a slightly different immune status in these patients with a probable dietary relationship. Weight loss could reverse this increase either after VLCD or after bariatric surgery.
-
References
- 1 Hardy OT, Czech MP, Corvera S. What causes the insulin resistance underlying obesity? Current Opinion in Endocrinology. Diabetes and Obesity 2012; 19: 81-87 10.1097/MED.1090b1013e3283514e3283513
- 2 Sell HHC, Eckel J. Adaptive immunity in obesity and insulin resistance. Nat Rev Endocrinol 2012; 8: 709-716
- 3 Hotamisligil G. Inflammation and metabolic disorders. Nature 2006; 444: 860-867
- 4 Lasselin J, Magne E, Beau C et al. Adipose Inflammation in Obesity: Relationship With Circulating Levels of Inflammatory Markers and Association With Surgery-Induced Weight Loss. The Journal of Clinical Endocrinology & Metabolism 2014; 99: E53-E61
- 5 Anderson EK, Gutierrez DA, Hasty AH. Adipose tissue recruitment of leukocytes. Current Opinion in Lipidology 2010; 21: 172-177 110.1097/MOL.1090b1013e3283393867
- 6 Caspar-Bauguil S, Cousin B, Galinier A et al. Adipose tissues as an ancestral immune organ: Site-specific change in obesity. FEBS letters 2005; 579: 3487-3492
- 7 Caspar-Bauguil SCB, Bour S, Casteilla L et al. Adipose tissue lymphocytes: types and roles. J Physiol Biochem 2009; 65: 423-436
- 8 O’Rourke RWMM, White AE, Madala A et al. Depot-specific differences in inflammatory mediators and a role for NK cells and IFN-gamma in inflammation in human adipose tissue. Int J Obes (Lond) 2009; 33: 978-990
- 9 To VT, Hüttl TP, Lang R et al. Changes in Body Weight, Glucose Homeostasis, Lipid Profiles, and Metabolic Syndrome after Restrictive Bariatric Surgery. Exp Clin Endocrinol Diabetes 2012; 120: 547-552
- 10 Bachmayer C, Lammert A, Hasenberg T et al. Healthy Obese and Post Bariatric Patients – Metabolic and Vascular Patterns. Exp Clin Endocrinol Diabetes. 2013; 121: 483-487
- 11 Ascaso JFPS, Real JT, Lorente RI et al. Diagnosing insulin resistance by simple quantitative methods in subjects with normal glucose metabolism. Diabetes Care. 2003; 26: 3320-3325
- 12 van der Weerd K, Dik WA, Schrijver B et al. Morbidly Obese Human Subjects Have Increased Peripheral Blood CD4+ T Cells With Skewing Toward a Treg- and Th2-Dominated Phenotype. Diabetes 2012 61: 401-408
- 13 Nishimura SMI, Nagasaki M, Eto K et al. CD8+ effector T cells contribute to macrophage recruitment and adipose tissue inflammation in obesity. Nat Med 2009; 15: 914-920
- 14 Kirwan SE, Burshtyn DN. Regulation of natural killer cell activity. Current Opinion in Immunology. 2007; 19: 46-54
- 15 Chmelar JCK, Chavakis T. The role of innate immune cells in obese adipose tissue inflammation and development of insulin resistance. Thromb Haemost 2013; 109: 3
- 16 Lynch LAOCJ, Kwasnik AK, Cawood TJ et al. Are natural killer cells protecting the metabolically healthy obese patient?. Obesity (Silver Spring) 2009; 17: 601-605
- 17 Kelley DSDP, Branch LB, Johnson HL et al. Energy restriction decreases number of circulating natural killer cells and serum levels of immunoglobulins in overweight women. Eur J Clin Nutr 1994; 48: 9-18
- 18 Guo H, Xu B, Gao L et al. High frequency of activated natural killer and natural killer T-cells in patients with new onset of type 2 diabetes mellitus. Experimental Biology and Medicine 2012; 237: 556-562
- 19 Martínez-Rodríguez JE, Munné-Collado J, Rasal R et al. Expansion of the NKG2C+ Natural Killer – Cell Subset Is Associated With High-Risk Carotid Atherosclerotic Plaques in Seropositive Patients for Human Cytomegalovirus. Arteriosclerosis, Thrombosis, and Vascular Biology 2013 33: 2653-2659
- 20 Wu L, Van Kaer L. Contribution of lipid-reactive natural killer T cells to obesity-associated inflammation and insulin resistance. Adipocyte 2013; 2: 12-16
- 21 Moulin CMMI, Peron JP, Halpern A et al. Bariatric surgery reverses natural killer (NK) cell activity and NK-related cytokine synthesis impairment induced by morbid obesity. Obesity Surgery. 2011; 21: 112-118