Masafumi Koga1, Takumi Hirata2, Soji Kasayama3, Yuko Ishizaka4, Minoru Yamakado4. 1. Department of Internal Medicine, Kawanishi City Hospital, Hyogo, Japan. Electronic address: m-koga@kawanishi-city-hospital.com. 2. Foundation for Biomedical Research and Innovation, Hyogo, Japan. 3. Department of Medicine, Nissay Hospital, Osaka, Japan. 4. Center for Multiphasic Health Testing and Services, Mitsui Memorial Hospital, Tokyo, Japan.
Abstract
BACKGROUND: Glycated albumin (GA) is known to be negatively regulated by body mass index (BMI) in non-diabetic subjects and patients with type 2 diabetes mellitus (T2DM). In non-diabetic subjects, a mechanism has been proposed in which chronic inflammation associated with obesity increases albumin metabolism and negatively regulates GA levels. However, whether this same mechanism exists in T2DM is unclear. We investigated the factor(s) which influence GA levels in T2DM patients. METHODS: This study included 179 T2DM patients from among people undergoing complete medical examinations. Correlations between GA and the following variables were examined among fasting samples for T2DM patients: BMI, C-reactive protein (CRP), homeostasis model assessment for β-cell function (HOMA-β) and homeostasis model assessment for insulin resistance (HOMA-R). RESULTS: BMI was significantly positively correlated with CRP, but CRP was not significantly correlated with GA. HOMA-β was significantly positively correlated with BMI and significantly negatively correlated with GA. Multivariate analysis showed that HOMA-β was a significant explanatory variable for GA, but not CRP and HOMA-R. CONCLUSIONS: Our findings suggest that insulin secretion plays a greater role than chronic inflammation in the mechanism by which BMI negatively regulates GA in T2DM patients.
BACKGROUND: Glycated albumin (GA) is known to be negatively regulated by body mass index (BMI) in non-diabetic subjects and patients with type 2 diabetes mellitus (T2DM). In non-diabetic subjects, a mechanism has been proposed in which chronic inflammation associated with obesity increases albumin metabolism and negatively regulates GA levels. However, whether this same mechanism exists in T2DM is unclear. We investigated the factor(s) which influence GA levels in T2DM patients. METHODS: This study included 179 T2DM patients from among people undergoing complete medical examinations. Correlations between GA and the following variables were examined among fasting samples for T2DM patients: BMI, C-reactive protein (CRP), homeostasis model assessment for β-cell function (HOMA-β) and homeostasis model assessment for insulin resistance (HOMA-R). RESULTS: BMI was significantly positively correlated with CRP, but CRP was not significantly correlated with GA. HOMA-β was significantly positively correlated with BMI and significantly negatively correlated with GA. Multivariate analysis showed that HOMA-β was a significant explanatory variable for GA, but not CRP and HOMA-R. CONCLUSIONS: Our findings suggest that insulin secretion plays a greater role than chronic inflammation in the mechanism by which BMI negatively regulates GA in T2DM patients.
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