|Year : 2019 | Volume
| Issue : 1 | Page : 212
Association between BMI and inflammation among diabetic polyneuropathy patients
Tayebeh Mottaghi1, Fariborz Khorvash2, Farzin Khorvash3, Mohammadreza Maracy4, Majid Kheirrollahi5, Gholamreza Askari6
1 Food Security Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
2 Department of Neurology, Isfahan University of Medical Sciences, Isfahan, Iran
3 Department of Infectious Diseases, Isfahan University of Medical Sciences, Isfahan, Iran
4 Department of Epidemiology and Biostatistics, School of Health, Isfahan University of Medical Sciences, Isfahan, Iran
5 Pediatric Inherited Diseases Research Center, Research Institute for Primordial Prevention of Non-communicable Disease and Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
6 Department of Community Nutrition, School of Nutrition and Food Science, Isfahan University of Medical Sciences, Isfahan, Iran
|Date of Submission||28-Jan-2018|
|Date of Acceptance||02-Nov-2018|
|Date of Web Publication||10-Dec-2019|
Department of Community Nutrition, School of Nutrition and Food Science, Isfahan University of Medical Sciences, Isfahan
Source of Support: None, Conflict of Interest: None
Background: Inflammation is defined as body tissues response to harmful stimuli. Obesity-related inflammation leads to increased risk chronic diseases including diabetic polyneuropathy (DPN). The present study was performed to determine association between body mass index (BMI) and inflammatory markers including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) in DPN patients. Methods: In this cross-sectional study, 200 DPN patients with a mean (SD) of age 58.76 (9.53) years were selected. All patients completed the questionnaire including demographic data and chronic disease history. In addition, anthropometric measures and clinical laboratory tests were taken. Multivariate linear regression was used to detect the association between BMI, CRP, and ESR levels. Results: BMI was associated with increase in ESR and CRP levels (β-ESR = 4.67, P < 0.001 and β-CRP = 0.71, P < 0.001). Also, this association remained after adjustment for other different variables. Conclusions: These findings indicate that higher BMI is related to increase inflammatory markers including CRP and ESR in DPN patients. Therapies for DPN and reducing inflammation should target the weight loss among obese patients.
Keywords: Body mass index, C-reactive protein, diabetes, erythrocyte sedimentation rate, polyneuropathy
|How to cite this article:|
Mottaghi T, Khorvash F, Khorvash F, Maracy M, Kheirrollahi M, Askari G. Association between BMI and inflammation among diabetic polyneuropathy patients. Int J Prev Med 2019;10:212
|How to cite this URL:|
Mottaghi T, Khorvash F, Khorvash F, Maracy M, Kheirrollahi M, Askari G. Association between BMI and inflammation among diabetic polyneuropathy patients. Int J Prev Med [serial online] 2019 [cited 2020 Jul 11];10:212. Available from: http://www.ijpvmjournal.net/text.asp?2019/10/1/212/272631
| Introduction|| |
Inflammation is defined as a physiological response to physical, chemical, and biological stimuli. Inflammation is linked to obesity, characterized by increased levels of C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR)., Obesity is related to different risk factors such as increased consumption of energy and reduced physical exercise., The source of inflammation in obesity is known, however, obesity-related inflammation is followed by the immune system activation. Obesity is associated with chronic diseases such as diabetic polyneuropathy (DPN). The pathogenesis of DPN is not completely known. Inflammation, oxidative stress, and mitochondrial dysfunction have been involved in the pathogenesis of DPN. About 50% of diabetic patients are expected to observe symptoms of diabetic neuropathy.Diabetic neuropathy can be attributed to disability related to foot ulceration, amputation, and walking disturbance. The DPN prevalence estimated 53% in Iran. The high concentrations of inflammatory markers among obese patients seem to be effective in the progression of DPN.
Recently, researchers have found an increased interest in the relationship between obesity and inflammation., No studies have been conducted to investigate the relationship between body mass index (BMI) and inflammation among DPN patients. The objective of the present article is to investigate association between BMI and inflammation in patients with DPN.
| Methods|| |
The present study was approved by the ethical committee of the Isfahan University of Medical Sciences. Baseline started in 4th March 2017 and ended in 23rd October 2017. A total of 50 patients were excluded due to missing values for BMI (n = 10), CRP (n = 20), ESR (n = 20), and other variables (n = 5). Finally, 200 patients were entered in the final analysis.
Assessment process and data collection
Participants selected from the Khorshid and Imam Mousa Sadr clinics. Random sampling method was used. Currently smoking and education were reported by self-report. Hypertension was expressed as systolic/diastolic blood pressure ≥140/90 mm Hg or using antihypertensive medication. Diabetes was expressed as fasting blood sugar ≥7.0 mmol/L or using antidiabetic treatment. Height and weight were measured to the nearest 0.1 cm and 0.01 kg using a Seca scale and height gauge, respectively. Patients with no shoes and light clothing.
BMI was defined as body weight in kilograms divided by height squared in meters. Venous blood samples were collected on admission after a 12-h overnight fast and were immediately sent to laboratory for analysis based on the clinical routine. Two hundred patients undergoing electromyography and nerve conduction velocity (EMG–NCV) for diagnosis of DPN were selected in the present study. CRP was measured with the enzyme-linked immunosorbent assay (ELISA) method. ESR was determined using the Westergren method.
Statistical analyses were performed using the STATA, version 13 software (StataCorp). P values <0.05 were considered significant. Quantitative variables were expressed as mean [standard deviation (SD)] and qualitative variables were expressed as frequency (percentage). Multivariate linear regression analysis was used to evaluate the relationship between BMI and inflammatory markers including ESR and CRP.
| Results|| |
A total of 200 patients (101 men) with a mean (SD) of age 58.76 (9.53) years were included in this cross-sectional study. About 9% of the participants reported a history of smoking. The mean years of education for patients were 5.61 years. The prevalence of hypertension, coronary heart disease, hyperlipidemia, and non-proliferative diabetic retinopathy among all diabetic patients were 40%, 31.5%, 75%, and 37%, respectively. The demographic characteristics and clinical examination of the patients are demonstrated in [Table 1]. Type I and II of diabetes patients with DPN assessment were selected. From these participants, 75 patients with DPN treated with insulin, 85 patients in combinations of insulin and oral antidiabetic drugs, and 40 with oral antidiabetic drugs. CRP and ESR concentration among patients with diabetic neuropathy were 9.81 mg/dl and 49.02 mg/dl, respectively. Patients with higher BMIs had high level of CRP and ESR. This result is obtained from crude model.
|Table 1: Demographic and clinical characteristics diabetic polyneuropathy patients|
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The multivariate linear regression model indicated that CRP and ESR were positively related to BMI. After adjusting for age, education, sex, and smoking (Model 1), 1 unit increase in BMI was related to increase of 0.73 unit CRP and 4.99 unit ESR (P< 0.001) [Table 2]. The relationship remained significant after adjustment for other variables in Model 2 [Table 2].
| Discussion|| |
The present study demonstrates a positive association between BMI and serum levels of CRP and ESR among patients with DPN. Obese patients demonstrated significantly higher inflammation.
The finding is consistent with findings of other studies.,,, The relationship might be confounded using covariate variable such as chronic diseases. Therefore chronic diseases such as coronary heart disease, hypertension, hyperlipidemia, non-proliferative diabetic retinopathy, and other related factors were controlled in Model 2. Also, the existence of medical features related to inflammation was excluded.
Increased serum levels of inflammatory markers play an important role among diabetic patients with higher BMI. However, the mechanism of relationship between CRP and blood sugar remains unclear. In fact, adipose tissue as a producer tissue of inflammatory markers indicates the positive association between higher BMI and inflammation. Adipose tissue as inflammatory markers can increase lipogenesis, and response of the systemic inflammatory phase.
The sources of inflammation activated by hyperglycemia and metabolic disease are immune cells such as increased macrophage, mast cells, and natural killer T cells that contribute for expression of tissue cytokine., Obesity increases metabolic stress related to the immune system activation and inflammation, as a risk factor for cardiovascular disease, colon cancer, breast cancer, dementia, and depression. Also, inflammation is related to increased intake of calorie and other nutrients such as intake of high fat and carbohydrate. Increased of proinflammatory macrophages are inversely related to sensitivity insulin.
Studies have demonstrated that weight loss is related to decrease inflammatory markers., Also, weight loss among people with gastric bypass indicate decreased levels of inflammatory markers.
These findings about association between BMI and increased CRP and ESR levels highlight susceptible to various outcomes of inflammation such as chronic diseases.
The present study has several strengths. Our study is the first cross-sectional study about the association between BMI and inflammation among DPN patients in Iran, Isfahan. Second, the results of present study have been controlled for covariate variables. Besides, this study has several limitations. First, design of present study is cross-sectional and could not determine causal relationship for these factors. Second, two inflammatory markers were considered in this study for assessment of inflammation.
In conclusion, increased BMI was related to increased levels of CRP and ESR among DPN.
| Conclusions|| |
These findings indicate that higher BMI is related to increase inflammatory markers including CRP and ESR in DPN patients. Therapies for DPN and reducing inflammation should target the weight loss among obese patients.
This study was extracted from PhD dissertation which was approved by School of Nutrition and Food Science, Isfahan University of Medical Sciences (code : IR.MUI.REC.1395.2.286).
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Monteiro R, Azevedo I. Chronic inflammation in obesity and the metabolic syndrome. Mediators Inflamm 2010;2010. doi: 10.1155/2010/289645.
Rodriguez-Hernandez H, Simental-Mendia LE, Rodriguez-Ramirez G, Reyes-Romero MA. Obesity and inflammation: Epidemiology, risk factors, and markers of inflammation. Int J Endocrinol 2013;2013:678159.
Dalmas E, Rouault C, Abdennour M, Rovere C, Rizkalla S, Bar-Hen A, et al
. Variations in circulating inflammatory factors are related to changes in calorie and carbohydrate intakes early in the course of surgery-induced weight reduction. Am J Clin Nutr 2011;94:450-8.
Stavropoulos-Kalinoglou A, Metsios GS, Panoulas VF, Nevill AM, Jamurtas AZ, Koutedakis Y, et al
. Underweight and obese states both associate with worse disease activity and physical function in patients with established rheumatoid arthritis. Clin Rheumatol 2009;28:439-44.
Hotamisligil GS. Inflammation and metabolic disorders. Nature 2006;444:860-7.
Luís Griera J, María Manzanares J, Barbany M, Contreras J, Amigó P, Salas-Salvadó J. Physical activity, energy balance and obesity. Public Health Nutr 2007;10:1194-9.
Nijhuis J, Rensen SS, Slaats Y, van Dielen FM, Buurman WA, Greve JW. Neutrophil activation in morbid obesity, chronic activation of acute inflammation. Obesity (Silver Spring) 2009;17:2014-8.
Roman-Pintos LM, Villegas-Rivera G, Rodriguez-Carrizalez AD, Miranda-Diaz AG, Cardona-Munoz EG. Diabetic polyneuropathy in type 2 diabetes mellitus: Inflammation, oxidative stress, and mitochondrial function. J Diabetes Res 2016;2016:3425617.
Deli G, Bosnyak E, Pusch G, Komoly S, Feher G. Diabetic neuropathies: Diagnosis and management. Neuroendocrinology 2013;98:267-80.
Lopez-Garcia E, van Dam RM, Qi L, Hu FB. Coffee consumption and markers of inflammation and endothelial dysfunction in healthy and diabetic women. Am J Clin Nutr 2006;84:888-93.
Sobhani S, Asayesh H, Sharifi F, Djalalinia S, Baradaran HR, Arzaghi SM et al
. Prevalence of diabetic peripheral neuropathy in Iran: A systematic review and meta-analysis. J Diabetes Metab Disord 2014;13:97.
Bochud M, Marquant F, Marques-Vidal PM, Vollenweider P, Beckmann JS, Mooser V, et al
. Association between C-reactive protein and adiposity in women. J Clin Endocrinol Metab 2009;94:3969-77.
Shemesh T, Rowley KG, Jenkins A, Brimblecombe J, Best JD, O'Dea K. Differential association of C-reactive protein with adiposity in men and women in an aboriginal community in northeast arnhem land of Australia. Int J Obes (Lond) 2007;31:103-8.
Choi J, Joseph L, Pilote L. Obesity and C-reactive protein in various populations: A systematic review and meta-analysis. Obes Rev 2013;14:232-44.
Kao TW, Lu IS, Liao KC, Lai HY, Loh CH, Kuo HK. Associations between body mass index and serum levels of C-reactive protein. S Afr Med J 2009;99:326-30.
Koca TT. Does obesity cause chronic inflammation? The association between complete blood parameters with body mass index and fasting glucose. Pak J Med Sci 2017;33:65-9.
Fronczyk A, Moleda P, Safranow K, Piechota W, Majkowska L. Increased concentration of C-reactive protein in obese patients with type 2 diabetes is associated with obesity and presence of diabetes but not with macrovascular and microvascular complications or glycemic control. Inflammation 2014;37:349-57.
Makki K, Froguel P, Wolowczuk I. Adipose tissue in obesity-related inflammation and insulin resistance: Cells, cytokines, and chemokines. ISRN Inflamm 2013;2013:139239.
Hajianfar H, Hosseinzadeh MJ, Bahonar A, Mohammad K, Askari GR, Entezari MH, et al
. The effect of omega-3 on the serum visfatin concentration in patients with type II diabetes. J Res Med Sci 2011;16:490-5.
Hajianfar H, Bahonar A, Entezari MH, Askari G, Yazdani M. Lipid profiles and serum Visfatin concentrations in patients with type II diabetes in comparison with healthy controls. Int J Prev Med 2012;3:326-31.
Gregor MF, Hotamisligil GS. Inflammatory mechanisms in obesity. Annu Rev Immunol 2011;29:415-45.
Ringseis R, Eder K, Mooren FC, Kruger K. Metabolic signals and innate immune activation in obesity and exercise. Exerc Immunol Rev 2015;21:58-68.
Kruger K, Klocke R, Kloster J, Nikol S, Waltenberger J, Mooren FC. Activity of daily living is associated with circulating CD34+/KDR+ cells and granulocyte colony-stimulating factor levels in patients after myocardial infarction. J Appl Physiol 2014;116:532-7.
El-Salem K, Ammari F, Khader Y, Dhaimat O. Elevated glycosylated hemoglobin is associated with subclinical neuropathy in neurologically asymptomatic diabetic patients: A prospective study. J Clin Neurophysiol 2009;26:50-3.
Nicoletti G, Giugliano G, Pontillo A, Cioffi M, D'Andrea F, Giugliano D, et al
. Effect of a multidisciplinary program of weight reduction on endothelial functions in obese women. J Endocrinol Invest 2003;26:RC5-8.
[Table 1], [Table 2]