Ketosis-Prone Type 2 Diabetes in Patients of Sub-Saharan African Origin
Open accessAbstract
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 β-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 β-cell dysfunction and insulin resistance reflecting a propensity to glucose toxicity.
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In ketosis-prone diabetes, women are protected unless they are in a hypoestrogenic state.
“In ketosis-prone diabetes, women are protected unless they are in a hypoestrogenic state [43, 45].”
From Sex differences in metabolic homeostasis, diabetes, and obesity (2015) · cites this paper as [43]
The General characteristics of patients at presentation section reports a 3:1 male predominance in the ketosis-prone type 2 diabetes group, consistent with women being less commonly affected. The Discussion also notes strong male predominance. Neither passage establishes that women are protected or that hypoestrogenism removes such protection; searches for estrogen and hypoestrogenic states found no supporting passage. Page numbers were not available in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredA strong male predominance (75%) is observed in ketosis-prone diabetes, a form of type 2 diabetes with a propensity to acute insulin deficiency.
“A strong male predominance (75 %) is also observed in ketosis-prone diabetes (also called idiopathic diabetes), a form of type 2 diabetes with a propensity to acute insulin deficiency [43, 44].”
From Sex differences in metabolic homeostasis, diabetes, and obesity (2015) · cites this paper as [43]
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- Authors
- Mauvais-Jarvis, F., Sobngwi, E., Porcher, R., Riveline, J.-P., Kevorkian, J.-P., Vaisse, C., Charpentier, G., Guillausseau, P.-J., Vexiau, P., & Gautier, J.-F.
- Affiliations
- Department of Endocrinology & Diabetes, Saint-Louis Hospital and University of Paris VII School of Medicine, Paris, France
- Department of Medical Biostatistics, Saint-Louis Hospital and University of Paris VII School of Medicine, Paris, France
- Centre Hospitalier Sud Francilien (FR)
- Department of Internal Medicine B, Lariboisiere Hospital, Paris, France
- University of California, San Francisco (US)
- Hôpital Lariboisière (FR)
- Université Paris Cité (FR)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2004-03-01
- Volume
- 53
- Issue
- 3
- Pages
- 645-653
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2137508233
- Cited by
- 294
- References
- 39
- Citations by year
- 2026: 9 · 2025: 12 · 2024: 12 · 2023: 15 · 2022: 23 · 2021: 16 · 2020: 12 · 2019: 14 · 2018: 19 · 2017: 9 · 2016: 13 · 2015: 22 · 2014: 18 · 2013: 17 · 2012: 13
- FWCI
- 4.94
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Keywords
- ketosis-prone type 2 diabetes, type 1 diabetes, beta-cell dysfunction, insulin resistance, insulin dependence, remission, hyperglycemia, glucotoxicity, insulin secretion, insulin tolerance test, C-peptide
- MeSH terms
- Insulin Secretion, Adult, Blood Glucose, Diabetes Mellitus, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Humans, Insulin, Insulin Antibodies, Insulin Resistance, Islets of Langerhans, Obesity, Cohort Studies, Body Mass Index, Africa South of the Sahara
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