Lipocalin-2, glucose metabolism and chronic low-grade systemic inflammation in Chinese people

Abstract

BackgroundLipocalin-2 is a novel adipokine with connection to insulin resistance. In this study, we aimed to investigate the association of serum lipocalin-2 with glucose metabolism and other metabolic phenotype in a large-scale Chinese population.MethodsWe evaluated serum lipocalin-2 in a cross-sectional sample of 2519 Chinese aged from 50 to 82 year in a Shanghai downtown district by ELISA. Glucose, insulin, lipid profile, inflammatory markers, and adipokines were also measured.ResultsSerum lipocalin-2 was significantly higher in subjects with isolated impaired fasting glucose, isolated impaired glucose tolerance, combined impaired fasting glucose/impaired glucose tolerance and newly-diagnosed type 2 diabetes than in those with normal glucose regulation. Lipocalin-2 elevation was clearly associated with a higher risk for impaired glucose regulation (OR 1.30 for each 10 ng/ml increase in serum lipocalin-2, 95% CI 1.23-1.62, p = 0.009) after adjustment of age, gender, smoking, alcohol drinking, family history of diabetes, serum CRP, serum adiponectin, serum CXCL5, HOMA-IR, BMI, and waist/hip ratio. The OR for participants with impaired glucose regulation and type 2 diabetes was 1.31 (95% CI 1.21-1.69, p < 0.001).ConclusionsOur findings suggest that elevated serum lipocalin-2 is closely and independently associated with impaired glucose regulation and type 2 diabetes.

The relationship between circulating neutrophil gelatinase-associated lipocalin and early alteration of metabolic parameters is associated with dietary saturated fat intake in non-diabetic Korean women

“…Wang et al reported that serum NGAL levels in obese individuals, particularly those with diabetes, were higher than those in lean non-diabetic individuals, even when adjusted for age and sex, although the significance disappeared when further adjusted for BMI [13]. A cross-sectional study conducted by Huang et al in 2,519 Chinese subjects showed that serum NGAL levels in subjects with impaired glucose tolerance, impaired fasting glucose, and newly diagnosed type 2 diabetes were significantly higher than those in subjects with normal glucose regulation [14]. Moreover, NGAL levels showed a positive correlation with insulin resistance (IR), measured with the homeostasis model assessment-estimated IR (HOMA-IR) [14].…”

“…A cross-sectional study conducted by Huang et al in 2,519 Chinese subjects showed that serum NGAL levels in subjects with impaired glucose tolerance, impaired fasting glucose, and newly diagnosed type 2 diabetes were significantly higher than those in subjects with normal glucose regulation [14]. Moreover, NGAL levels showed a positive correlation with insulin resistance (IR), measured with the homeostasis model assessment-estimated IR (HOMA-IR) [14]. Ni et al reported that serum NGAL levels in patients with coronary artery disease (CAD) were higher than those in non-CAD subjects.…”

“…It also accumulates in the renal cortical tubules and blood vessels [32]. As mentioned above, recent studies have shown positive correlations between serum NGAL levels and the risk of obesity, MetS, diabetes, and CVD [13][14][15][16]. According to Wang et al, NGAL levels are positively correlated with adiposity indexes such as BMI, waist circumference, and body fat percentage [13].…”

“…Body weight and height were measured in the morning, with participants lightly clothed and without Recent studies have suggested that serum levels of neutrophil gelatinase-associated lipocalin (NGAL) are associated with obesity, MetS, diabetes, and CVD [13][14][15][16]. NGAL, also known as lipocalin-2 or growth factor-stimulated superinducible protein 24, is a 25 kDa secretory glycoprotein [17] that was first identified as a protein secreted from human neutrophils [18].…”

Neutrophil gelatinase-associated lipocalin as a potential therapeutic integrator of glycolipid metabolic and inflammatory signaling

“…Elevated serum NGAL is closely and independently associated with impaired glucose regulation and type 2 diabetes. 23,24 However, on the other hand its disruption in mice resulted in significantly potentiated diet-induced obesity, dyslipidemia, fatty liver disease, and insulin resistance. 25,26 NGAL-/-mice have increased hepatic gluconeogenesis, decreased mitochondrial oxidative capacity, impaired lipid metabolism, and increased inflammatory state under the high fiber diet condition.…”