Sustained improvement in NEFA suppression during IVGTT 3 years after islet- transplantation. — ASN Events
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Sustained improvement in NEFA suppression during IVGTT 3 years after islet- transplantation. (#318)

Glenn Ward 1 2 3 , Jacqueline Walters 1 4 , Shireene Vethakkan 1 4 , Judith Gooley 1 4 , David Goodman 5 , Alicia Jenkins 4 , Raymond Boston 6 , Jane Holmes-Walker 7 , Philip O'Connell 7 , Thomas WH Kay 8
  1. Endocrinology and Diabetes, St. Vincent's Hospital, Melbourne, Australia
  2. Clinical Biochemistry, St. Vincent's Hospital, Melbourne, Australia
  3. Pathology, University of Melbourne, Melbourne, Australia
  4. University of Melbourne Department of Medicine, St. Vincent's Hospital, Melbourne, Australia
  5. Nephrology, St. Vincent's Hospital, Melbourne, Australia
  6. University of Pennsylvania, Philadelphia, USA
  7. Westmead Hospital, Sydney, Australia
  8. St. Vincent's Institute of Medical Research, Melbourne, Australia

Elevated non-esterified fatty acid (NEFA) levels are associated with beta-cell lipotoxicity. Adequate suppression of NEFA is essential to achieve good metabolic control following islet cell transplantation (ICT).

We evaluated plasma NEFA dynamics over 180 mins following intravenous glucose challenge (IVGTT, 250 mg/kg), at annual intervals, in 3 insulin-independent T1DM ICT recipients, compared to 10 healthy controls. These findings were compared with NEFA kinetics during post-transplant oral glucose tests (OGTT) in the same subjects in which NEFA suppression at 2 hours was similar to controls subjects (97%+1 SEM vs 93+1 respectively).

Similarly to the OGTT, overall NEFA suppression as expressed by the nadir NEFA values during IVGTT was normalised shortly after transplantation and has been sustained in subsequent annual follow up studies (Nadir NEFA at 6mths, 1, 2 and 3years,versus controls: 0.18+0.08, 0.13+0.02, 0.15+0.04, 0.17 +0.08, versus 0.08 +0.02 mmol/l respectively; p=NS, Kruskal-Wallis test).

Unlike the OGTT, the IVGTT is able to evaluate the early NEFA responses, and these were also shown to be similar in the ICT recipients compared to control subjects, (kNEFA at 6mths, 1, 2 and 3years, versus controls: 1.27+0.28, 1.36+0.87, 2.41+0.02, 1.41+1.1 versus 2.14+0.20[% per min] respectively; p=NS, Kruskal-Wallis test).

Our studies show, therefore, that the initial overall normalisation in NEFA dynamics during intravenous glucose tolerance tests is maintained over the prolonged follow up period, and this could be explained by high peri-portal insulin levels (plus proximity of transplanted beta-cells to hepatocytes) in islet cell recipients.