Relationship Between Neutrophil-lymphocyte Ratio and Insulin Resistance in Newly Diagnosed Type 2 Diabetes Mellitus Patients

Meiqin Lou; Peng Luo; Ru Tang; Yixian Peng; Siyuan Yu; Wanjing Huang; Lei He

Disclosures

BMC Endocr Disord. 2015;15(9) 

In This Article

Discussion

The present study had shown that the NLR values of the diabetic patients were significantly higher than those of the healthy control (P < 0.001), and the NLR values of the patients with a HOMA-IR value of > 2.0 are notably greater than those of the patients with a HOMA-IR value of ≤ 2.0 (P < 0.001).

Many epidemiological studies have determined that DM is associated with chronic inflammation,[21] which may contribute to the acceleration of diabetic microangiopathy and the development of macroangiopathy;[3,4] IR is a characterized of T2DM, whereas the exact molecular action leading to IR is not yet understood, several studies have associated IR with inflammation[1,6] experimental studies have demonstrated a link between chronic inflammation and insulin resistance through mechanisms involving obesity[22] and atherosclerosis.[23] NLR has been recently defined as a novel potential inflammation marker in cancer and cardiovascular diseases.[14,16] NLR can easily be calculated using the neutrophil-lymphocyte ratio in peripheral blood count. Calculating NLR is simpler and cheaper than measuring other inflammatory cytokines, such as IL-6, IL-1β, and TNF-α.[24]

In addition, NLR was found to be a significant risk factor for IR with DM through logistic regression analysis. The pathological activation of innate immunity leads to inflammation of the islet cells, resulting in a decrease in pancreatic beta-cell mass and impaired insulin secretion.[25] Patients with T2DM are in a state of low-degree chronic inflammation that induces hypersecretion of inflammatory factors, such as CRP, IL-6, TNF-α, and MCP-1, which results in a constantly elevated neutrophilic granulocyte count.[26] One mechanism by which increased levels of neutrophils could mediate IR may be through augmented inflammation. The increase in NLR appears to underlie the elevated levels of pro-inflammation, as evident from the persistent neutrophil activation and enhanced release of neutrophil proteases with T2DM.[27] Moreover, lymphocytes may be also associated with inflammation. Some studies have shown that IR may be related to the signal transduction mediated by T cells and that IR results in a decrease in T-cell count.[28,29] Figure 2 presents the scatter plot of Pearson correlation analysis.

However, some common physical conditions, such as dehydration and Prostate Specific Antigen of the blood specimen can affect the accuracy of the data. Furthermore, physical exercise and release of catecholamine (CA) can cause a drop in neutrophilic granulocyte and lymphocyte. NLR represents a combination of two markers where neutrophils represent the active nonspecific inflammatory mediator initiating the first line of defense, whereas lymphocytes represent the regulatory or protective component of inflammation.[30] NLR is superior to other leukocyte parameters (e.g., neutrophil, lymphocyte, and total leukocyte counts) because of its better stability compared with the other parameters that can be altered by various physiological, pathological, and physical factors.[17,31] Thus, as a simple clinical indicator of IR, NLR is more sensitive compared with the neutrophilic granulocyte count and CRP levels, which are widely used as markers of IR.[32,33]

A logistic regression analysis of the following risk factors was conducted: NLR, TG and HbA1c. In our study, in conjunction with the rising of the level of HbAlc, the degree of IR increased significantly. HbA1c showed an association with early-phase insulin secretion assessed by insulinogenic index.[34] Heianza et al.[35] reported that elevated HbA1c levels of above 41 mmol/mol (>5.9%) were associated with a substantial reduction in insulin secretion and insulin sensitivity as well as an association with β-cell dysfunction in Japanese individuals without a history of treatment of diabetes. Increased accumulation of TG has been observed in human muscle tissue of obese and type 2 diabetic subjects, and associated with IR,[36,37] which is in agreement with the present study. IR reduces the inhibition effect of lipolysis in adipose tissue, resulting in the increase of the free fatty acid (FFA) level in plasma. Plasma FFA levels usually increase in obesity.[38] Infusion of free fatty acids (FFA) has been shown to induce IR in skeletal muscles[39] in several studies. However, in the present study, NLR serves an important function in predicting the risk of IR. IR in diabetic patients is related to chronic inflammation, and NLR may be helpful in assessing the prognoses of these patients.

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