Publicaciones científicas
Circulating glucagon is associated with inflammatory mediators in metabolically compromised subjects
Ortega FJ, Moreno-Navarrete JM, Sabater M, Ricart W, Fruhbeck G, Fernandez-Real JM.
Background
Acute phase mediators promote metabolic changes by modifying circulating hormones. However, there is virtually no data about the link between glucagon and inflammatory parameters in obesity-related chronic low-grade inflammation.
Study design
We performed both cross-sectional and longitudinal (diet-induced weight loss) studies.
Methods
Circulating glucagon concentrations (ELISA), parameters of glucose and lipid metabolism, interleukin-6 (IL-6), and complement factor B (CFB), were analyzed in 316 subjects (250 men and 66 women). The effects of weight loss were investigated in an independent cohort of 20 subjects.
Results
Circulating glucagon significantly correlated with glucose (r=0.407, p<0.0001), glycated hemoglobin (r=0.426, p<0.0001), fasting triglycerides (r=0.356, p=0.001), and parameters of innate immune response system such as IL-6 (r=0.342, p=0.050) and CFB (r=0.404, p=0.002) in obese subjects with altered glucose tolerance (AGT), but not in individuals with normal glucose tolerance (NGT). In obese and NGT subjects, glucagon was associated with fasting triglycerides (r=0.475, p=0.003) and CFB (r=0.624, p=0.001). In obese subjects, glucagon (p=0.019) and CFB (p=0.002) contributed independently to 26% of fasting triglycerides variance (p<0.0001) after controlling for the effects of age and fasting serum glucose concentration in multiple lineal regression models. Moreover, concomitantly with fat mass, fasting triglycerides, and CFB, weight loss led to significantly decreased circulating glucagon (-23.1%, p=0.004).
Conclusions
According to current results, acute phase reactants such as IL-6 and CFB are associated with fasting glucagon in metabolically compromised subjects. This suggests that glucagon may be behind the association between inflammatory and metabolic parameters in obesity-associated chronic low-grade inflammation.
CITA DEL ARTÍCULO Eur J Endocrinol. 2011 Jul 28. [Epub ahead of print]
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