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      Visceral Fat Accumulation Is Associated with Asthma in Patients with Type 2 Diabetes

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          Abstract

          Objective

          The number of patients with type 2 diabetes has increased in Japan, and type 2 diabetes has attracted attention as a risk factor for asthma. However, the risk factors for the development of asthma in patients with type 2 diabetes have not been determined. This study was performed to clarify whether visceral fat accumulation (VFA) and insulin resistance are risk factors for the development of asthma in patients with type 2 diabetes.

          Materials and Methods

          A cross-sectional study was conducted. The study group comprised 15 patients with type 2 diabetes with asthma, and the control group comprised 145 patients with type 2 diabetes without asthma. Their fat distribution was evaluated by measuring the VFA by abdominal computed tomography at the umbilical level. Their glucose status was assessed by measuring the fasting plasma glucose (FPG) concentration, fasting immunoreactive insulin concentration, homeostasis model assessment (HOMA) index, and hemoglobin A1c concentration.

          Results

          Among patients with type 2 diabetes, VFA was significantly greater in patients with asthma than those without asthma ( P < 0.0001). The FPG concentration, fasting immunoreactive insulin concentration, and HOMA index were higher in patients with asthma than those without asthma ( P < 0.05, P < 0.0001, and P < 0.0001, respectively). Multiple logistic regression analysis showed that VFA and the HOMA index were significantly associated with asthma in patients with type 2 diabetes (odds ratio, 1.78; 95% confidence interval, 1.31–3.89; P = 0.0115 and odds ratio, 3.65; 95% confidence interval, 1.37–7.85; P = 0.0078, respectively).

          Conclusions

          Our data suggest that VFA and insulin resistance are associated with the development of asthma in patients with type 2 diabetes.

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          Most cited references32

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          Monocyte chemoattractant protein 1 in obesity and insulin resistance.

          Peter Sartipy, David Loskutoff (2003)
          This study identifies monocyte chemoattractant protein 1 (MCP-1) as an insulin-responsive gene. It also shows that insulin induces substantial expression and secretion of MCP-1 both in vitro in insulin-resistant (IR) 3T3-L1 adipocytes and in vivo in IR obese mice (ob/ob). Thus, MCP-1 resembles other previously described genes (e.g., PAI-1 and SREBP-1c) that remain sensitive to insulin in IR states. The hyperinsulinemia that frequently accompanies obesity and insulin resistance may therefore contribute to the altered expression of these and other genes in insulin target tissues. In vivo studies also demonstrate that MCP-1 is overexpressed in obese mice compared with their lean controls, and that white adipose tissue is a major source of MCP-1. The elevated MCP-1 may alter adipocyte function because addition of MCP-1 to differentiated adipocytes in vitro decreases insulin-stimulated glucose uptake and the expression of several adipogenic genes (LpL, adipsin, GLUT-4, aP2, beta3-adrenergic receptor, and peroxisome proliferator-activated receptor gamma). These results suggest that elevated MCP-1 may induce adipocyte dedifferentiation and contribute to pathologies associated with hyperinsulinemia and obesity, including type II diabetes.
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            Omental and subcutaneous adipose tissues of obese subjects release interleukin-6: depot difference and regulation by glucocorticoid.

            S K Fried, D Bunkin, A S Greenberg (1998)
            The purpose of this study was to determine whether human adipocytes from different depots of obese subjects produce interleukin-6 (IL-6) and whether IL-6 release is regulated by glucocorticoids. Fragments of omental and abdominal sc adipose tissue released immunodetectable IL-6 into the medium during acute incubations. Omental adipose tissue released 2-3 times more IL-6 than did sc adipose tissue. Isolated adipocytes prepared from these tissues also released IL-6 (omental > sc), but this accounted for only 10% of the total tissue release. Culture of adipose tissue fragments for 7 days with the glucocorticoid dexamethasone markedly suppressed IL-6 production. These data show for the first time that substantial quantities of IL-6 (up to 75 ng/mL) accumulate in the medium during incubations of both adipocytes and adipose tissue. Although little is known about the effects of IL-6 on adipose tissue, one action is a down-regulation of adipose tissue lipoprotein lipase. The regulated production of this multifunctional cytokine may modulate regional adipose tissue metabolism and may contribute to the recently reported correlation between serum IL-6 and the level of obesity.
            Article 0 comments Cited 185 times – based on 0 reviews     Review now
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              Abdominal fat: standardized technique for measurement at CT.

              T Yoshizumi, T. Nakamura, M Yamane … (1999)
              The authors estimated abdominal fat distribution on the basis of measurements at computed tomography (CT). The attenuation range for fat tissue was defined as the interval within the mean plus or minus 2 SDs considered to be individual variation. Fat areas found with this method were closely correlated with those obtained by means of the computed planimetric method or with a fixed attenuation range from -190 to -30 HU as the standard of reference. Although the average CT numbers obtained with different scanners were distributed widely, the calculated fat areas were almost identical. This method might be a practical and standardized method at CT.
              Article 0 comments Cited 184 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Daisuke Murakami:
                ORCID: http://orcid.org/0000-0002-8794-9141
                Journal
                Journal ID (nlm-ta): J Diabetes Res
                Journal ID (iso-abbrev): J Diabetes Res
                Journal ID (publisher-id): JDR
                Title: Journal of Diabetes Research
                Publisher: Hindawi
                ISSN (Print): 2314-6745
                ISSN (Electronic): 2314-6753
                Publication date Collection: 2019
                Publication date (Electronic): 2 May 2019
                Volume: 2019
                Electronic Location Identifier: 3129286
                Affiliations
                1Department of Otorhinolaryngology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
                2Department of Cardiology, Oita Red Cross Hospital, Oita, Japan
                3Department of Endocrinology, Metabolism, Rheumatology and Nephrology, Faculty of Medicine, Oita University, Oita, Japan
                4Department of Endocrinology, Oita Red Cross Hospital, Oita, Japan
                5Department of Pulmonary, Oita Red Cross Hospital, Oita, Japan
                6Center for Educational Outreach and Admissions, Kyoto University, Kyoto, Japan
                Author notes

                Academic Editor: Gianluca Iacobellis

                Author information
                http://orcid.org/0000-0002-8794-9141
                http://orcid.org/0000-0002-2378-849X
                http://orcid.org/0000-0002-4610-5794
                Article
                DOI: 10.1155/2019/3129286
                PMC ID: 6525865
                PubMed ID: 31192262
                SO-VID: 46fbb1cb-15ae-4922-8992-796e636618c5
                Copyright © Copyright © 2019 Daisuke Murakami et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 30 December 2018
                Date accepted : 7 April 2019
                Categories
                Subject: Research Article

                Data availability:

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