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Akshay Sood, MD, MPH, FCCP; Clifford Qualls, PhD; JeanClare Seagrave, PhD; Christine Stidley, PhD; Tereassa Archibeque, RRT; Marianne Berwick, PhD; Mark Schuyler, MD, FCCP
Author and Funding Information

From the Department of Medicine (Drs Sood and Stidley, Ms Archibeque, and Drs Berwick and Schuyler) and the Clinical Translational Sciences Center (Dr Qualls), University of New Mexico School of Medicine; and the Experimental Toxicology Program (Dr Seagrave), Lovelace Respiratory Research Institute.

Correspondence to: Akshay Sood , MD, MPH, University of New Mexico School of Medicine, Department of Medicine, 1 University of New Mexico, MSC 10 5550, Albuquerque, NM 87131-0001; e-mail: asood@salud.unm.edu


Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Sood has received grants from the University of New Mexico and the National Institutes of Health. The other authors have reported no conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Funding: This work was supported in part by the National Institutes of Health [Grants NCRR M01-RR-00997 and 1 K23 HL 094531-01 A1/A] and Grant UNM-RAC-C-2290.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;137(2):499. doi:10.1378/chest.09-2621
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To the Editor:

We would like to thank Dr Ozol from Ankara, Turkey, for his insightful comments related to the role of adipokines in human asthma in general and to our published article in particular (February 2009).1 Although not well studied, it is possible that specific phases of the menstrual cycle may differentially affect systemic concentrations of specific adipokines in women.2 Therefore, for menstruating women, we limited all study testing within 3 to 14 days following the cessation of menstrual flow1 to minimize the potential effect of the luteal menstrual phase on serum adipokine concentrations.2 However, we were not powered to study the interaction between sex hormones and inhalational allergen challenge on adipokine response in our study.

We also agree with Dr Ozol’s astute observation that our study measured total adiponectin concentrations and not the various isomeric forms.1 Some studies suggest that the high-molecular-weight (HMW) isoform of adiponectin may be the most biologically active form of adiponectin in regulating insulin resistance.3-6 Whether the HMW isoform of adiponectin is more active than other adiponectin isoforms for asthma is currently not known. Our study therefore was unable to assess, for instance, whether subjects with asthma had overall lower diurnal curves of HMW adiponectin isoform compared with controls.

Despite the above limitations, our study successfully met its objective to replicate the relevant mouse experiments by Shore et al7,8 that measured serum adipokine response to allergen challenge in sensitized mice. Of note, these experiments were performed on mice of both sexes, without measurement of either systemic sex hormones or of systemic adiponectin isoforms. These issues nevertheless need additional research in both animal and human asthma in the future. Finally, we could not agree more with Dr Ozol’s conclusions that “considering sex hormones and investigating circulating oligomeric isoforms of adiponectin could help us understand the underlying mechanisms for asthma and adipokines better.”

Sood A, Qualls C, Seagrave J, et al. Effect of specific allergen inhalation on serum adiponectin in human asthma. Chest. 2009;1352:287-294. [CrossRef] [PubMed]
 
Ludwig M, Klein HH, Diedrich K, Ortmann O. Serum leptin concentrations throughout the menstrual cycle. Arch Gynecol Obstet. 2000;2633:99-101. [CrossRef] [PubMed]
 
Hara K, Horikoshi M, Yamauchi T, et al. Measurement of the high-molecular weight form of adiponectin in plasma is useful for the prediction of insulin resistance and metabolic syndrome. Diabetes Care. 2006;296:1357-1362. [CrossRef] [PubMed]
 
Seino Y, Hirose H, Saito I, Itoh H. High molecular weight multimer form of adiponectin as a useful marker to evaluate insulin resistance and metabolic syndrome in Japanese men. Metabolism. 2007;5611:1493-1499. [CrossRef] [PubMed]
 
Seino Y, Hirose H, Saito I, Itoh H. High-molecular-weight adiponectin is a predictor of progression to metabolic syndrome: a population-based 6-year follow-up study in Japanese men. Metabolism. 2009;583:355-360. [CrossRef] [PubMed]
 
Nakashima R, Kamei N, Yamane K, Nakanishi S, Nakashima A, Kohno N. Decreased total and high molecular weight adiponectin are independent risk factors for the development of type 2 diabetes in Japanese-Americans. J Clin Endocrinol Metab. 2006;9110:3873-3877. [CrossRef] [PubMed]
 
Shore SA, Schwartzman IN, Mellema MS, Flynt L, Imrich A, Johnston RA. Effect of leptin on allergic airway responses in mice. J Allergy Clin Immunol. 2005;1151:103-109. [CrossRef] [PubMed]
 
Shore SA, Terry RD, Flynt L, Xu A, Hug C. Adiponectin attenuates allergen-induced airway inflammation and hyperresponsiveness in mice. J Allergy Clin Immunol. 2006;1182:389-395. [CrossRef] [PubMed]
 

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References

Sood A, Qualls C, Seagrave J, et al. Effect of specific allergen inhalation on serum adiponectin in human asthma. Chest. 2009;1352:287-294. [CrossRef] [PubMed]
 
Ludwig M, Klein HH, Diedrich K, Ortmann O. Serum leptin concentrations throughout the menstrual cycle. Arch Gynecol Obstet. 2000;2633:99-101. [CrossRef] [PubMed]
 
Hara K, Horikoshi M, Yamauchi T, et al. Measurement of the high-molecular weight form of adiponectin in plasma is useful for the prediction of insulin resistance and metabolic syndrome. Diabetes Care. 2006;296:1357-1362. [CrossRef] [PubMed]
 
Seino Y, Hirose H, Saito I, Itoh H. High molecular weight multimer form of adiponectin as a useful marker to evaluate insulin resistance and metabolic syndrome in Japanese men. Metabolism. 2007;5611:1493-1499. [CrossRef] [PubMed]
 
Seino Y, Hirose H, Saito I, Itoh H. High-molecular-weight adiponectin is a predictor of progression to metabolic syndrome: a population-based 6-year follow-up study in Japanese men. Metabolism. 2009;583:355-360. [CrossRef] [PubMed]
 
Nakashima R, Kamei N, Yamane K, Nakanishi S, Nakashima A, Kohno N. Decreased total and high molecular weight adiponectin are independent risk factors for the development of type 2 diabetes in Japanese-Americans. J Clin Endocrinol Metab. 2006;9110:3873-3877. [CrossRef] [PubMed]
 
Shore SA, Schwartzman IN, Mellema MS, Flynt L, Imrich A, Johnston RA. Effect of leptin on allergic airway responses in mice. J Allergy Clin Immunol. 2005;1151:103-109. [CrossRef] [PubMed]
 
Shore SA, Terry RD, Flynt L, Xu A, Hug C. Adiponectin attenuates allergen-induced airway inflammation and hyperresponsiveness in mice. J Allergy Clin Immunol. 2006;1182:389-395. [CrossRef] [PubMed]
 
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