重點摘要
- 低度的全身性發炎，表現為血中 TNF-α、IL-6、CRP 等濃度升高二到三倍。
- 肥胖增加的脂肪組織會長期活化先天免疫，久了可能導致慢性發炎與第二型糖尿病。
- CRP、TNF-α 偏高與心臟病、糖尿病風險增加有關；脂聯素較高則與胰島素敏感度較好有關，減重通常能改善這些指標。
心臟病、代謝症候群與第二型糖尿病有一個共同點：因為發炎，血液循環中的細胞激素濃度升高，而這是由循環中的多種細胞所調控。
Heart disease, metabolic syndrome, and type 2 diabetes all share increased circulatory cytokine concentration due to inflammation, regulated by cell types in the circulation.
低度的全身性發炎，特徵是血漿中 TNF-α、IL-6 與 CRP 等物質的濃度升高二到三倍。
Low-grade systemic inflammation is characterized by a two to threefold increase in plasma concentrations of cytokines like TNF-α, IL-6, and CRP.
脂肪組織會製造細胞激素，在促進動脈粥狀硬化與心血管疾病上扮演重要角色。脂肪組織主要表現一群稱為「脂肪激素」（adipokines）的多胜肽荷爾蒙，其中脂聯素（adiponectin）是唯一主要由脂肪組織製造的細胞激素。TNF-α、CRP 與脂聯素都在糖尿病中扮演重要角色。
Adipose tissue produces cytokines that play a crucial role in promoting atherosclerosis and cardiovascular disease. Adipose tissue predominantly expresses a group of polypeptide hormones known as adipokines. Adiponectin is the only cytokine that is produced mainly by adipose tissue. TNF-α, CRP and adiponectin all play significant roles in diabetes.
肥胖Obesity
發炎，似乎是動脈粥狀硬化、肥胖與胰島素阻抗之間的共同連結。
Inflammation appears to be a common link between atherosclerosis, obesity and insulin resistance.
肥胖使脂肪組織增加，可能長期活化先天免疫系統，久而久之導致慢性發炎與第二型糖尿病。
Obesity's increased adipose tissue mass can cause chronic activation of the innate immune system, leading to chronic inflammation and type 2 diabetes over time.
C 反應蛋白（CRP）C-reactive protein
促發炎細胞激素長期升高，會在第二型糖尿病中造成一些特定的代謝後果。CRP 濃度升高，與心血管疾病、肥胖、糖尿病、發炎、吸菸及久坐的生活型態都有關聯。
There are several metabolic consequences specific to T2D due to chronic elevation of proinflammatory cytokines. Elevated concentrations of CRP have been associated with CVD, obesity, diabetes, inflammation, smoking and a sedentary lifestyle.
中央型肥胖（腹部肥胖）與 CRP 有關；而在第二型糖尿病患者中，即使體重沒有下降，身體活動本身也與 CRP 降低有關。
Central obesity is linked to CRP, while physical activity, independent of weight loss, has been linked to CRP reduction in patients with type 2 diabetes.
腫瘤壞死因子（TNF-α）Tumor necrosis factor (TNF)
局部突然釋放 TNF-α，可以引發發炎反應來圍堵感染，可能是有益的；但若 TNF-α 在全身急性大量釋放，則會導致敗血症與休克。
The sudden local release of TNF-α can trigger an inflammatory response to contain infections, potentially being beneficial. However, the acute systemic release of TNF-α leads to sepsis and shock.
肥胖者常見 TNF-α 長期偏高，會對葡萄糖代謝造成負面影響，並以多種方式改變胰島素敏感度。
Chronically elevated TNF-α, seen in obesity, negatively impacts glucose metabolism and can alter insulin sensitivity in various ways.
脂聯素（Adiponectin）Adiponectin
脂聯素的作用包括改善葡萄糖與脂質代謝、提升胰島素敏感度、降低氧化壓力與發炎，並促進神經醯胺（ceramide）分解。肥胖者血中的脂聯素濃度會下降。
The effects of adiponectin include improving glucose and lipid metabolism, enhancing insulin sensitivity, reducing oxidative stress and inflammation, and promoting ceramide degradation. Its circulating concentrations are reduced in obesity.
結論Conclusion
對於 CRP、TNF-α 與脂聯素的作用方式，以及它們在調控發炎、進而影響糖尿病發生上的角色，目前已有越來越多的認識。
Increasing knowledge is now available on the modes of action of CRP, TNF-α, and adiponectin, as well as their particular functions in the regulation of inflammation and its consequences for the onset of diabetes.
血漿中 CRP 與 TNF-α 的濃度，與心臟病及糖尿病風險增加相關；相反地，血漿脂聯素濃度較高，則與較好的胰島素敏感度及較低的心臟病風險有關。
Plasma levels of CRP and TNF-α correlate with an increased risk of heart disease and diabetes. However, increased concentrations of plasma adiponectin are related to insulin sensitivity and a lower risk of heart disease.
一般也認為，減重與脂聯素上升、TNF-α 與 CRP 下降有關。
It is generally accepted that losing weight is linked to higher levels of adiponectin and lower levels of TNF-α and CRP.
編者註
CRP 可以在一般抽血中檢測，評估心血管風險時建議檢驗高敏感度 C 反應蛋白（hs-CRP）。TNF-α 與脂聯素多用於研究，不是常規檢查項目。對多數人來說，追蹤糖化血色素、空腹血糖、腰圍與 hs-CRP，就能掌握大方向。
參考文獻References
- Lontchi-Yimagou, E., Sobngwi, E., Matsha, T. E., & Kengne, A. P. (2013). Diabetes mellitus and inflammation. Current Diabetes Reports, 13(3), 435–444. https://doi.org/10.1007/s11892-013-0375-y
- Navarro, J. F., & Mora, C. (2005). Role of inflammation in diabetic complications. Nephrology Dialysis Transplantation, 20(12), 2601–2604. https://doi.org/10.1093/ndt/gfi155
- King, G. L. (2008). The role of inflammatory cytokines in diabetes and its complications. Journal of Periodontology, 79(8S), 1527–1534. https://doi.org/10.1902/jop.2008.080246
- Duran-Salgado MB, Rubio-Guerra AF. Diabetic nephropathy and inflammation. World J Diabetes. 2014 Jun 15;5(3):393-8. doi: 10.4239/wjd.v5.i3.393. PMID: 24936261; PMCID: PMC4058744.
- Alexandraki, K., Piperi, C., Kalofoutis, C., Singh, J., Alaveras, A., & Kalofoutis, A. (2006). Inflammatory process in type 2 diabetes. Annals of the New York Academy of Sciences, 1084(1), 89–117. https://doi.org/10.1196/annals.1372.039
什麼情況該就醫？
- 糖化血色素 ≥ 5.7%，或空腹血糖 ≥ 100 mg/dL
- 腰圍男性 ≥ 90 公分、女性 ≥ 80 公分
- 已經確診糖尿病，但血糖控制不穩定
- 常口渴、頻尿，或體重不明原因下降
本文為衛教資訊，不能取代醫師診斷與治療。若有身體不適，請尋求醫療專業協助。各項檢測與治療需經醫師評估，效果因人而異。
英文原文由本院國際健康諮詢顧問 Menaf 撰寫（Menaf 未具中華民國醫師證書，不在台灣執行診斷與治療）；中文由日安健康編譯，「編者註」為日安健康補充的說明與台灣相關建議。