Poster Presentation Australian Diabetes Society and the Australian Diabetes Educators Association Annual Scientific Meeting 2014

Lixisenatide as add-on treatment among patients with different β-cell function levels as assessed by HOMA-β index (#319)

Riccardo Bonadonna 1 , Lawrence Blonde 2 , Mikhail Antsiferov 3 , Rachele Berria 4 , Pierre Goudy 5 , Mensud Hatunic 6 , Viswanathan Mohan 7 , Michael Horowitz 8
  1. Dept of Clinical and Experimental Medicine, University of Parma, Parma, Italy
  2. Ochsner Diabetes Clinical Research Unit, Department of Endocrinology, Ochsner Medical Center, New Orleans, LA, USA
  3. Endocrinology Dispanserium, Moscow Department of Health Care, Moscow, Russia
  4. Sanofi, Bridgewater, NJ, USA
  5. Department of Diabetology, University Hospital Rangueil, Toulouse, France
  6. Mater Misericordiae University Hospital, Dublin, Ireland
  7. Madras Diabetes Research Foundation & Dr. Mohan’s Diabetes Specialities Centre , WHO Collaborating Centre For Non-Communicable Diseases Prevention And Control & IDF Centre of Education, Chennai, India
  8. Discipline of Medicine, Royal Adelaide Hospital, Adelaide, SA, Australia

This study evaluated the effect of lixisenatide, a once-daily prandial glucagon-like peptide-1 receptor agonist, on glycaemic control in patients with type 2 diabetes mellitus (T2DM) inadequately controlled by oral antidiabetics (OADs). Results were stratified by β-cell function, evaluated using the homeostasis model assessment (HOMA-β) index.

The GetGoal-M, -S, and -P trials evaluated the efficacy and safety of lixisenatide treatment in combination with OADs (metformin, sulphonylureas, and pioglitazone, respectively) over 24 weeks in patients with T2DM. This descriptive, post hoc analysis used data from patients (N=980) who received lixisenatide in the intent-to-treat populations of these trials stratified according to baseline HOMA-β levels (high HOMA-β: more than median HOMA-β (28.49%β); low HOMA-β: less than median).

The low HOMA-β cohort included a greater proportion of male and Asian patients, and the cohort tended to be older, with a longer history of known diabetes and duration of OAD treatment compared with patients in the high HOMA-β cohort. Baseline HbA1c, fasting plasma glucose (FPG), and postprandial plasma glucose (PPG) levels were also higher in the low HOMA-β cohort. Lixisenatide treatment was associated with a mean change from baseline in HbA1c of −0.95% and −0.85% for the low and high HOMA-β index patients, respectively (p=0.0865). Declines in mean FPG (low: −1.23 mmol/L vs high: −0.775 mmol/L, p=0.0015) and PPG (low: −6.83 mmol/L vs high: −5.03 mmol/L, p=0.0004) were greater in patients with a lower HOMA-β index at baseline. A higher proportion of patients in the low HOMA-β cohort experienced symptomatic hypoglycaemia (low: 7.76% vs high: 4.49%, p=0.0330).

Lixisenatide was associated with a reduction in HbA1c, and improvements in both FPG and PPG, regardless of β-cell function. These data indicate that lixisenatide treatment is effective in reducing hyperglycaemia, even in the more advanced stages of T2DM.

Funding: Study and editorial assistance (Caudex Medical) were funded by Sanofi.