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Stabilizing effect of exenatide in a patient with C‐peptide‐negative diabetes mellitus
Author(s) -
Paisley A. N.,
Savage M. W.,
Wiles P. G.
Publication year - 2009
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.2009.02789.x
Subject(s) - exenatide , medicine , incretin , postprandial , type 2 diabetes , insulin , endocrinology , diabetes mellitus , gastric emptying , sitagliptin , type 2 diabetes mellitus , stomach
Background Exenatide is an incretin mimetic licensed for treatment of Type 2 diabetes poorly controlled despite maximally tolerated doses of oral therapy. Similar in structure to the natural incretin hormone glucagon‐like peptide 1 (GLP‐1), it helps restore underlying pathophysiological abnormalities. Case report We report the successful use of exenatide, combined with insulin, in a 66‐year‐old woman initially diagnosed with Type 2 diabetes in 1989 but now exhibiting a Type 1 phenotype. Diet, lifestyle advice and oral glucose‐lowering agents were commenced but persisting poor control necessitated insulin therapy in 2005. She later presented twice in diabetic ketoacidosis, suggesting conversion to a Type 1 phenotype (postprandial C‐peptide < 94 pmol/l). Despite differing insulin regimens, control remained poor with frequent hyperglycaemic and hypoglycaemic excursions, severely impairing quality of life. Whilst an inpatient in 2007 [glycated haemoglobin (HbA 1c ) 10.2%, body mass index (BMI) 31.5 kg/m 2 ] exenatide was commenced in an attempt to stabilize glycaemic control. Dramatic improvements were seen and continued. Eight months later, HbA 1c had fallen by 2% with an 8‐kg weight loss and 10‐unit reduction in daily insulin dose. Quality of life dramatically improved. C‐peptide remains undetectable. Conclusions This patient with features of both Type 1 and Type 2 diabetes benefited greatly from exenatide with insulin therapy. The improvement seen in glycaemic control could not be attributable to enhanced insulin secretion but could be as a result of a combination of the other incretin effects (postprandial glucagon suppression, delayed gastric emptying and weight loss secondary to increased satiety) all improving insulin sensitivity, reducing insulin dose and smoothing control.