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Free fatty acids level may effect a residual insulin secretion in type 1 diabetes
Agnieszka Zmysłowska1, Krystyna Wyka, Agnieszka Szadkowska
1Department of Pediatrics, Medical University of Lodz, Poland. agnieszka.zmyslowska@umed.lodz.pl
Introduction:
Recent studies on the pathogenesis of type 1 diabetes (T1DM) show that autoimmune activity in human pancreatic 1-cells is accompanied by abnormalities of fatty tissue metabolism, which is the underlying process in type 2 diabetes.The aim of the study was to determine the correlation between C-peptide concentration, indicating residual insulin secretion, and free fatty acids (FFA) level in children with T1DM.
Material And Methods:
We recruited 178 diabetic patients (mean age 10.8 years; M/F 99/79). In all individuals the fasting C-peptide by a radioimmunological method and FFA serum levels using an enzymatic colorimetric method were measured at the onset and after 6 months of the diabetes duration.
Results:
Thirty four (19.1%) of the patients had the C-peptide level above the lower limit of normal range (>0.28 pmol/ml) at both time points. FFA level at onset was significantly higher as compared to the level after 6 months of follow-up (38.4+29.4 vs. 28.9 ± 23.1 mg/dl; p=0.0003). However, both values were positively correlated (r=0.31; p=0.0008). Interestingly, a negative correlation was found between FFA and C-peptide measurements at onset (r=-0.19; p=0.01) and at 6th month of the disease (r=-0.18; p=0.02). Moreover, when the C-peptide level was treated as a binominal variable(above and below 0.28 pmol/ml) higher levels of FFA were observed in children with C-peptide deficiency at onset of diabetes (41.1 vs. 29.9 mg/dl; p=0.03) and a similar trend was noticed at 6th month of the disease (31.0 vs. 23.7 mg/dl; p=0.1). No relation of FFA with age at onset, gender,insulin requirement and HbA1c were revealed.
Conclusions:
The obtained results, which link the FFA level with residual insulin secretion in T1DM,may serve as further evidence supporting the contribution of fatty tissue metabolism in the patho-genesis of T1DM.
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