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Ethnic differences in insulin secretory function between black African and white European men with early type 2 diabetes

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Cynthia Mohandas, Riccardo Bonadonna, Fariba Shojee-moradie, Nicola Jackson, Linda Boselli, K. George M. M. Alberti, Janet L. Peacock, A. Margot Umpleby, Stephanie A. Amiel, Louise M. Goff

Original languageEnglish
Pages (from-to)1678-1687
JournalDIABETES OBESITY AND METABOLISM
Volume20
Issue number7
Early online date14 Apr 2018
DOIs
Accepted/In press2 Mar 2018
E-pub ahead of print14 Apr 2018
PublishedJul 2018

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Abstract

Aim
To test the hypothesis that men of black (West) African ethnicity (black African men [BAM]) with early type 2 diabetes (T2D) would have greater insulin secretory deficits compared with white European men (WEM), following prediabetic hypersecretion.

Methods
In 19 BAM and 15 WEM, matched for age, body mass index and duration of diabetes, we assessed and modelled insulin secretory responses to hyperglycaemia stimulated intravenously (hyperglycaemic clamp) and orally (meal tolerance test).

Results
With similar post‐challenge glucose responses, BAM had lower second‐phase C‐peptide responses to intravenous glucose (BAM 70.6 vs WEM 115.1 nmol/L/min [ratio of geometric mean 0.55, 95% confidence interval {CI} 0.37, 0.83]; P = .006) and to oral glucose (BAM 65.4 vs WEM 88.5 nmol/L/min [mean difference −23.2, 95% CI −40.0, −6.3]; P = .009). Peripheral insulin response in BAM to oral glucose was preserved (BAM 47.4 vs WEM 59.4 nmol/L/min [ratio of geometric mean 0.89, 95% CI 0.59, 1.35]; P = .566), with relative reductions in insulin clearance (BAM 506.2 vs WEM 630.1 mL/m2 BSA/min [mean difference −123.9, 95% CI −270.5, 22.6]; P = .095), associated with enhanced incretin responses (gastric inhibitory polypeptide incremental area under the curve: BAM 46.8 vs WEM 33.9 μg/L/min [mean difference 12.9, 95% CI 2.1, 23.7]; P = .021).

Conclusions
In early T2D, BAM had significantly lower insulin secretory responses to intravenous and oral stimulation than WEM. Lower insulin clearance, potentially driven by increased incretin responses, may act to preserve peripheral insulin concentrations. Tailoring early management strategies to reflect distinct ethnic‐specific pathophysiology may improve outcomes in this high‐risk population.

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