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Diabetes 53:645-653, 2004
© 2004 by the American Diabetes Association, Inc.

Ketosis-Prone Type 2 Diabetes in Patients of Sub-Saharan African Origin

Clinical Pathophysiology and Natural History of ß-Cell Dysfunction and Insulin Resistance

Franck Mauvais-Jarvis1, Eugène Sobngwi1, Raphaël Porcher2, Jean-Pierre Riveline3, Jean-Philippe Kevorkian4, Christian Vaisse5, Guillaume Charpentier3, Pierre-Jean Guillausseau4, Patrick Vexiau1, and Jean-François Gautier1

1 Department of Endocrinology & Diabetes, Saint-Louis Hospital and University of Paris VII School of Medicine, Paris, France
2 Department of Medical Biostatistics, Saint-Louis Hospital and University of Paris VII School of Medicine, Paris, France
3 Department of Diabetes and Metabolic Diseases, Sud Francilien Hospital, Corbeil-Essonnes, France
4 Department of Internal Medicine B, Lariboisiere Hospital, Paris, France
5 Diabetes Research Center, Department of Medicine, University of California San Francisco, San Francisco, California

Nonautoimmune ketosis-prone diabetic syndromes are increasingly frequent in nonwhite populations. We have characterized a cohort of patients of sub-Saharan African origin who had ketosis-prone type 2 diabetes (n = 111), type 1 diabetes (n = 21), and type 2 diabetes (n = 88) and were admitted to a hospital for management of uncontrolled diabetes. We compared epidemiological, clinical, and metabolic features at diabetes onset and measured insulin secretion (glucagon-stimulated C-peptide) and insulin action (short intravenous insulin tolerance test) during a 10-year follow-up. Ketosis-prone type 2 diabetes shows a strong male predominance, stronger family history, higher age and BMI, and more severe metabolic decompensation than type 1 diabetes. In ketosis-prone type 2 diabetes, discontinuation of insulin therapy with development of remission of insulin dependence is achieved in 76% of patients (non–insulin dependent), whereas only 24% of patients remain insulin dependent. During evolution, ketosis-prone type 2 diabetes exhibit specific ß-cell dysfunction features that distinguish it from type 1 and type 2 diabetes. The clinical course of non–insulin-dependent ketosis-prone type 2 diabetes is characterized by ketotic relapses followed or not by a new remission. Progressive hyperglycemia precedes and is a strong risk factor for ketotic relapses (hazard ratio 38). The probability for non–insulin-dependent ketosis-prone type 2 diabetes to relapse is 90% within 10 years, of whom ~50% will become definitively insulin dependent. Insulin sensitivity is decreased in equal proportion in both ketosis-prone type 2 diabetes and type 2 diabetes, but improves significantly in non–insulin-dependent ketosis-prone type 2 diabetes, only after correction of hyperglycemia. In conclusion, ketosis-prone type 2 diabetes can be distinguished from type 1 diabetes and classical type 2 diabetes by specific features of clinical pathophysiology and also by the natural history of ß-cell dysfunction and insulin resistance reflecting a propensity to glucose toxicity.

Address correspondence and reprint requests to Franck Mauvais-Jarvis, MD, Department of Medicine, Division of Diabetes, Endocrinology & Metabolism, Baylor College of Medicine, One Baylor Plaza, 520B Houston, TX 77030. E-mail: fmjarvis{at}bcm.tmc.edu


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