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. 2018 Mar 29;17(1):37-43.
doi: 10.1007/s40200-018-0336-8. eCollection 2018 Jun.

Acute phase ketosis-prone atypical diabetes is associated with a pro-inflammatory profile: a case-control study in a sub-Saharan African population

Eric Lontchi-Yimagou  1 , Philippe Boudou  2 , Jean Louis Nguewa  3 , Jean Jacques Noubiap  4 , Vicky Kamwa  5 , Eric Noel Djahmeni  6 , Babara Atogho-Tiedeu  1 , Marcel Azabji-Kenfack  7 , Martine Etoa  6 , Gaelle Lemdjo  6 , Mesmin Yefou Dehayem  6 , Jean Claude Mbanya  1   6   8 , Jean-Francois Gautier  2   3 , Eugène Sobngwi  1   6   8
Affiliations

Acute phase ketosis-prone atypical diabetes is associated with a pro-inflammatory profile: a case-control study in a sub-Saharan African population

Eric Lontchi-Yimagou et al. J Diabetes Metab Disord. .

Abstract

Background: It is unknown whether inflammation plays a role in metabolic dysfunction on ketosis-prone diabetes (KPD). We aimed to assess the inflammatory profile in sub-Saharan African patients with KPD during the acute ketotic phase as well as during non-ketotic hyperglycemic crises.

Methods: We studied 72 patients with non-autoimmune diabetes: 23 with type 2 diabetes mellitus (T2D), and 49 with KPD, all admitted in hyperglycemic crisis (plasma glucose ≥250 mg/dl). The T2D and KPD groups were matched by sex, age, and Body Mass Index. KPD was sub-classified into new-onset ketotic phase (n = 34) or non-ketotic phase (n = 15). We measured TNF-α, MCP-1, MIP1-α, IL-8, MIP1-β, and VEGF in the serum of all participants.

Results: TNF-α and IL-8 were higher in participants with KPD compared to those with T2D (p = 0.02 TNF-α; p = 0.03 IL-8). TNF-α and IL-8 were also higher in the ketotic phase KPD group compared to the T2D group (p = 0.03 TNF-α; p < 0.001 IL-8) while MIP1-α was lower in people with ketotic phase KPD compared to their T2D counterparts (p = 0.03). MIP1-α was lower in the ketotic phase KPD group compared to the non-ketotic phase KPD group (p = 0.04). MCP-1 was lower in non-ketotic phase KPD compared to T2D (p = 0.04), and IL-8 was higher in non-ketotic phase KPD compared to T2D (p = 0.02).

Conclusions: Participants with KPD had elevated pro-inflammatory cytokines compared to their T2D counterparts. Ketotic phase KPD is associated with a different pro-inflammatory profile compared to non-ketotic phase KPD, and the inflammatory profile appears to be comparable between non-ketotic phase KPD and T2D patients.

Keywords: Inflammation; Ketosis-prone diabetes; Sub-Saharan Africa; Type 2 diabetes.

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Conflict of interest statement

This study was performed in accordance with the guidelines of the Helsinki Declaration and was approved by the National Ethics Committee of Cameroon. All participants provided written informed consent.Not applicable.The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Concentrations of TNF-α (a), MCP-1 (b), MIP1-α (c), IL-8 (d), MIP1-β (e), and VEGF (f) according to the diabetes phenotype (Ketotic phase KPD, non-ketotic phase KPD, and type 2 diabetes). TNF-α: Tumor necrosis factor alpha, MCP-1: Monocyte Chemoattractant Protein-1, MIP1-α: Macrophage inflammatory protein one alpha, IL-8: Interleukin-8, MIP1-β: Macrophage inflammatory protein one beta, VEGF: Vascular endothelial growth factor. KPD: Ketosis prone diabetes. The results are presented as median and interquartile range (25th and 75th). * = p < 0.05
See this image and copyright information in PMC

References

    1. Leahy JL, Hirsch IB, Peterson KA, Schneider D. Targeting beta-cell function early in the course of therapy for type 2 diabetes mellitus. J Clin Endocrinol Metab. 2010;95(9):4206–4216. doi: 10.1210/jc.2010-0668. - DOI - PubMed
    1. Dobrian AD, Galkina EV, Ma Q, Hatcher M, Aye SM, Butcher MJ, Ma K, Haynes BA, Kaplan MH, Nadler JL. STAT4 deficiency reduces obesity-induced insulin resistance and adipose tissue inflammation. Diabetes. 2013;62(12):4109–4121. doi: 10.2337/db12-1275. - DOI - PMC - PubMed
    1. Kiely A, McClenaghan NH, Flatt PR, Newsholme P. Pro-inflammatory cytokines increase glucose, alanine and triacylglycerol utilization but inhibit insulin secretion in a clonal pancreatic beta-cell line. J Endocrinol. 2007;195(1):113–123. doi: 10.1677/JOE-07-0306. - DOI - PubMed
    1. Souza KL, Gurgul-Convey E, Elsner M, Lenzen S. Interaction between pro-inflammatory and anti-inflammatory cytokines in insulin-producing cells. J Endocrinol. 2008;197(1):139–150. doi: 10.1677/JOE-07-0638. - DOI - PubMed
    1. Lontchi-Yimagou E, Sobngwi E, Matsha TE, Kengne AP. Diabetes mellitus and inflammation. Curr Diab Rep. 2013;13(3):435–444. doi: 10.1007/s11892-013-0375-y. - DOI - PubMed

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