Pola Penanda Glikemik dan Inflamasi dalam Perkembangan Penyakit Diabetes Melitus Tipe 2 pada Pria Obesitas Sentral

Miftakh N. Rahman, Indriyanti R. Sukmawati, Irma M. Puspitasari

Abstract


Obesitas sentral merupakan masalah kesehatan yang prevalensinya terus bertambah. Obesitas sentral telah diketahui menjadi faktor risiko yang berasosiasi kuat dengan diabetes melitus (DM). Obesitas sentral memicu inflamasi yang menyebabkan resistensi insulin dan peningkatan fungsi sel beta pankreas sebagai kompensasi hingga akhirnya mengalami kerusakan. Oleh karena itu, perlu diketahui pola penanda glikemik dan inflamasi dalam perkembangan penyakit DM. Penelitian ini bertujuan untuk mengetahui pola penanda glikemik dan inflamasi dalam perkembangan penyakit DM pada pria dengan obesitas sentral. Penelitian dilakukan dengan pendekatan potong lintang terhadap 70 orang pria berusia 30–50 tahun di Jakarta, Bandung, Semarang, dan Bogor dengan lingkar perut lebih dari 90 cm yang memenuhi kriteria inklusi dan eksklusi dan diperiksakan HbA1c, insulin puasa, glukosa puasa, serta hsCRP. HOMA-IR dan HOMA-B diperoleh dari permodelan matematika untuk insulin puasa dan glukosa puasa. Rekrutmen dilakukan pada bulan November–Desember 2017. Diperoleh hasil bahwa terdapat korelasi positif antara lingkar perut dengan HbA1c (r=0,484; p<0,05), insulin puasa (r=0,629; p<0,05), HOMA-IR (r=0,602; p<0,05), HOMA-B (r=0,540; p<0,05), dan hsCRP (r=0,522; p<0,05), juga terdapat pola peningkatan HbA1c, glukosa puasa, insulin puasa, dan HOMA-IR pada setiap tahap perkembangan DM. HOMA-B meningkat hingga pre-DM kemudian turun pada DM. Insulin puasa, HOMA-IR, HOMA-B, dan hsCRP lebih tinggi pada obesitas sentral non-DM dibandingkan kontrol. Terdapat korelasi positif antara hsCRP dengan HbA1c (r=0,484; p<0,05), insulin puasa (r=0,629; p<0,05), HOMA-IR (r=0,602; p<0,05), dan HOMA-B (r=0,540; p<0,05). Terdapat peningkatan insulin puasa dan HOMA-IR pada obesitas sentral dengan pre-DM dibandingkan dengan obesitas sentral non-DM. Penelitian ini memberikan informasi pola penanda glikemik dan inflamasi pria dengan obesitas sentral pada perkembangan penyakit DM. Pengetahuan mengenai pola perkembangan DM dapat memberikan informasi bahwa DM pada obesitas sentral dapat dicegah sedini mungkin sehingga prevalensinya dapat dikendalikan.

Kata kunci: Diabetes melitus, inflamasi, obesitas sentral, resistensi insulin

 

Glycemic and Inflammation Markers Pattern of Type 2 Diabetes Mellitus Disease Progression in Centrally Obese Men

Abstract
Central obesity is a health problem whose prevalence continues to increase. Central obesity has been known to be a risk factor that is strongly associated with diabetes mellitus (DM). Central obesity triggers inflammation which causes insulin resistance and increases the function of pancreatic beta cells as compensatory mechanism before its exhausted. Therefore, we need to know the patter of glycemic and inflammatory markers in the disease development of DM. This study aimed to determine the pattern of glycemic and inflammatory markers in the development of DM in men with central obesity. This study was conducted with a cross-sectional approach to 70 men aged 30–50 years in Jakarta, Bandung, Semarang, and Bogor with waist circumference of more than 90 cm who met the inclusion and exclusion criteria and examined HbA1c, fasting insulin, fasting glucose, and hsCRP. HOMA-IR and HOMA-B were obtained from mathematical modeling for fasting insulin and fasting glucose. Recruitment is carried out in November–December 2017. The result shows that there was significantly positive correlation between waist circumference with HbA1c (r=0.484; p<0.05), fasting insulin (r=0.629; p<0.05), HOMA-IR (r=0.602; p<0.05), HOMA-B (r=0.540; p<0.05), and hsCRP (r=0.522; p<0.05). There was an increasing pattern of HbA1c, fasting glucose, fasting insulin, HOMA-IR, and hsCRP, in every step of DM progression. Meanwhile, HOMA-B increased until central obesity with pre DM condition and decreased in central obesity with DM condition. There was an increase of fasting insulin, HOMA-IR, HOMA-B, and hsCRP in central obese without DM-men compared to control. There was a positive correlation between hsCRP and HbA1c (r=0.484; p<0.05), fasting insulin (r=0.629; p<0.05), HOMA-IR (r=0.602; p<0.05), and HOMA-B (r=0.540; p<0.05). There was an increase of fasting insulin and HOMA-IR in central obese without DM-men compared to central obese with pre DM-men. This study provides information on patterns of glycemic and inflammatory markers of men with central obesity in the disease development of DM. Knowledge about the pattern of DM development can provide information that DM in central obesity can be prevented as early as possible so that its prevalence can be controlled.

Keywords: Central obesity, diabetes mellitus, insulin resistance, inflammation


Keywords


Diabetes melitus, inflamasi, obesitas sentral, resistensi insulin

References


McArdle MA, Finucane OM, Connaughton RM, McMorrow AM, Roche HM. Mechanisms of obesity-induced inflammation and insulin resistance: Insights into the emerging role of nutritional strategies. Front Endocrinol. 2013;44:52. doi: 10.3389/fendo.2013.00 052

Castro AVB, Kolka CM, Kim SP, Bergman RN. Obesity, insulin resistance and comorbidities–Mechanisms of association. Arq Bras Endocrinol Metabol. 2014;58(6):600–9. doi: 10.1590/0004-2730000003223

Rachmi CN, Li M, Alison Baur L. Overweight and obesity in Indonesia: Prevalence and risk factors—a literature review. Public Health. 2017;147:20–9. doi: 10.1016/j.puhe.2017.02.002.

Meiliana A, Wijaya A. Metaflammation, NLRP3 inflammasome obesity and metabolic disease. Indones Biomed J. 2011;3(3):168–84. doi: 10.18585/inabj.v3i3.148

World Health Organization. The Asia Pacific perspective: Redifining obesity and its treatment. Sydney : Health Communications Australia. 2000.

Badan Penelitian dan Pengembangan Kesehatan Kementerian Kesehatan Republik Indonesia. Riset kesehatan dasar 2013. Jakarta: Kementerian Kesehatan Republik Indonesia; 2013.

Badan Penelitian dan Pengembangan Kesehatan Kementerian Kesehatan Republik Indonesia. Riset kesehatan dasar 2007. Jakarta: Kementerian Kesehatan Republik Indonesia; 2007.

World Health Organization. Global report on diabetes. World Health Organization; 2016.

Song Y, Manson JE, Tinker L, Howard BV, Kuller LH, Nathan L, et al. Insulin sensitivity and insulin secretion determined by homeostasis model assessment and risk of diabetes in a multiethnic cohort of women: the Women’s Health Initiative Observational Study. Diabetes Care. 2007;30(7):1747–52.

Tjokroprawiro A. Formula klinik praktis bidang diabetologi-endokrinologi-metabolisme. Edisi ke-5. Surabaya: Pusat Diabetes dan Nutrisi Surabaya-Fakultas Kedokteran Universitas Airlangga-RSUD Dr. Soetomo; 2017.

American Diabetes Association. Standards of medical care in diabetes—2009. Diab Care. 2009;32:(1):S13–61. doi: 10.2337/dc09-S013

Ye J. Mechanisms of insulin resistance in obesity. Front Med. 2013;7(1):14–24. doi: 10.1007/s11684-013-0262-6.

Mayans L. Metabolic syndrome: Insulin resistance and prediabetes. FP Essent. 2015;435:11–6.

Alejandro EU, Gregg B, Blandino-Rosano M, Cras-Méneur C, Bernal-Mizrachi E. Natural history of β-cell adaptation and failure in type 2 diabetes. Mol Aspects Med. 2015;42:19–41. doi: 10.1016/j.mam.2014.12.002.

Soewondo P, Pramono LA. Prevalence, characteristics, and predictors of pre-diabetes in Indonesia. Med J Indones. 2011;20(4):283–94. doi: 10.13181/mji.v20i4.465

Ashcroft FM, Rorsman P. Diabetes mellitus and the β cell: The last ten years. Cell. 2012;148(6):1160–71. doi: 10.1016/j.cell.2012.02.010.

Butler AE, Dhawan S. β-Cell identity in type 2 diabetes: Lost or found? Diabetes. 2015;64(8):2698–700. doi: 10.2337/db15-0550

Russo GT, Giorda CB, Cercone S, Nicolucci A, Cucinotta D, BetaDecline Study Group. Factors associated with beta-cell dysfunction in type 2 diabetes: the BETADECLINE study. PLoS One. 2014;9(10):e109702. doi: 10.1371/journal.pone.0109702

Baranyi A, Amouzadeh-Ghadikolai O, von Lewinski D, Rothenhäusler H-B, Theokas S, Robier C, et al. Branched-chain amino acids as new biomarkers of major depression—A novel neurobiology of mood disorder. PLoS One. 2016;11(8):e0160542.doi: 10.1371/journal.pone.0160542.

Stokes A, Collins JM, Grant BF, Scamuffa RF, Hsiao C-W, Johnston SS, et al.Obesity progression between young adulthood and midlife and incident diabetes: A retrospective cohort study of u.s. Adults. Diabetes Care. 2018;41(5):1025–31. doi: 10.2337/dc17-2336.

Kim ES, Jeong JS, Han K, Kim MK, Lee SH, Park YM, et al. Impact of weight changes on the incidence of diabetes mellitus: A Korean nationwide cohort study. Sci Rep. 2018;8(1):3735. doi: 10.1038/s41598-018-21550-3




DOI: https://doi.org/10.15416/ijcp.2019.8.4.281

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