ESPE Abstracts (2019) 92 FC1.6

A Novel Biochemical Marker, Fatty Acid-Binding Protein 4, in Diabetic Ketoacidosis in Children

Noah Gruber1,2, Idit Ron3, Sharon Sheinvald1, Amir Tirosh3,2, Orit Pinhas-Hamiel1,2


1Pediatric Endocrine and Diabetes Unit, Edmond and Lily Safra Children's Hospital, Sheba Medical Center, Tel Hashomer, Ramat Gan, Israel. 2Sackler School of Medicine, Tel-Aviv University, Tel Aviv, Israel. 3The Dalia and David Arabov Diabetes Research Center, Division of Endocrinology, Diabetes and Metabolism, Sheba Medical Center, Tel-Hashomer, Ramat Gan, Israel


Introduction: Diabetic ketoacidosis (DKA) is the most common cause of hospitalization, cerebral edema, and death among children with type 1 diabetes (T1D). Fatty acid-binding protein 4 (FABP4 or aP2) is one of the most abundant proteins in adipocytes and has been shown to be actively secreted from adipocytes. Circulating FABP4 is regulated by fasting- and lipolysis-related signals and contributes to hyperglycemia by promoting hepatic gluconeogenesis and interfering with peripheral insulin action, implicated in the pathology of many metabolic diseases, including diabetes in humans. Therefore, FABP4 appears as an active adipokine that counter-regulates insulin action and plays crucial hormonal functions in systemic glucose metabolism.

Aims: To determine the correlation between FABP4 and new-onset T1D and to differentiate between DKA and non-DKA situations.

Methods: Clinical and laboratory data were prospectively collected from children who presented with new-onset T1D during the year 2017 from one tertiary medical center. In addition to chemistry and blood gases, FABP4 and free fatty acids (FFA) were collected upon presentation and 48-72 hours after initiation of insulin treatment. The patients were divided to two groups – DKA and non-DKA.

Results: Out of 32 children, with mean age of 9.3±3.5 years, 17 (53%) were male and 13 (40%) presented with DKA. The mean FABP4 level was higher amongst the DKA group, 12.1 ng/ml as opposed to 8.7 ng/ml in the non-DKA group. The delta between the first FABP4 and the second sample after insulin treatment was almost twice in the DKA group compared to the non-DKA group (8.1 vs. 4.5, p-value-0.03). There was a correlation between the FABP4 level and the FFA level in both groups.

Conclusions: We describe a novel biochemical marker, FABP4, which is increased in lipolysis and particularly in DKA. This finding can shed light on the mechanisms involved in DKA.

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