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Young adult obese subjects with and without insulin resistance: what is the role of chronic inflammation and how to weigh it non-invasively?

Giovanni Tarantino1*, Patrizia Colicchio1, Paolo Conca1, Carmine Finelli1, Matteo Nicola Dario Di Minno1, Marianna Tarantino2, Domenico Capone3 and Fabrizio Pasanisi1

Author Affiliations

1 Department of Clinical and Experimental Medicine, Federico II University Medical School of Naples, Italy

2 Department of Biomorphological and Functional Sciences, Federico II University Medical School of Naples, Italy

3 Department of Neurosciences, Unit of Clinical Pharmacology, Federico II University Medical School of Naples, Italy

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Journal of Inflammation 2009, 6:6  doi:10.1186/1476-9255-6-6

Published: 16 March 2009

Abstract

Background

Obesity is a leading risk factor for metabolic syndrome whose further expression is non-alcoholic fatty liver disease. Metabolic syndrome is associated with a proinflammatory state that contributes to insulin resistance. Finally, a "metabolically benign obesity" that is not accompanied by insulin resistance has recently been postulated to exist.

Aim

To find whether any inflammation markers were independently associated with the presence of insulin resistance, evaluating specific anthropometric, ultrasonographic and laboratory parameters in a population of young adult obese subjects.

Methods

Of forty two young individuals, divided into two groups (with or without insulin resistance), were studied serum C-reactive protein and fibrinogen as indexes of chronic pro-inflammatory status. Body mass index, waist circumference and metabolic syndrome presence were assessed as part of the metabolic evaluation. Ultrasonography weighted visceral and subcutaneous abdominal fat thickness, spleen size as longitudinal diameter and liver hyperechogenicity.

Results and Discussion

Serum C-reactive protein and fibrinogen as well as spleen longitudinal diameter were significantly increased in the obese young with insulin resistance compared to non-insulin resistance group. Insulin resistance was significantly associated with hepatic steatosis score at sonography (r = 0.33, P = 0.03), spleen longitudinal diameter (r = 0.35, P = 0.02) and C-reactive protein (r = 0.38, P = 0.01), but not with body mass index, visceral or subcutaneous abdominal adipose tissue, waist circumference and fibrinogen (P = 0.18, 0.46, 0.33, 0.37 and 0.4, respectively). Steatosis score at sonography was well associated with spleen volume (rho = 0.40, P = 0.01) and C-reactive protein levels (rho = 0.49, P = 0.002). Metabolic syndrome was much more frequent in obese patients with insulin resistance. These findings show that in young adults the only abdominal adiposity without insulin resistance, plays a scarce role in determining hepatic steatosis as well as metabolic syndrome.

Conclusion

Increases in spleen size and CRP levels represent a reliable tool in diagnosing insulin resistance.