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Ethnic distinctions in the pathophysiology of type 2 diabetes: a focus on black African-Caribbean populations.

Authors
  • Goff, Louise M1
  • Ladwa, Meera1
  • Hakim, Olah1
  • Bello, Oluwatoyosi1
  • 1 Diabetes Research Group, Departments of Diabetes and Nutritional Sciences, King's College London, London, UK.
Type
Published Article
Journal
Proceedings of The Nutrition Society
Publisher
Cambridge University Press
Publication Date
May 01, 2020
Volume
79
Issue
2
Pages
184–193
Identifiers
DOI: 10.1017/S0029665119001034
PMID: 31307560
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Type 2 diabetes (T2D) is a global public health priority, particularly for populations of black African-Caribbean ethnicity, who suffer disproportionately high rates of the disease. While the mechanisms underlying the development of T2D are well documented, there is growing evidence describing distinctions among black African-Caribbean populations. In the present paper, we review the evidence describing the impact of black African-Caribbean ethnicity on T2D pathophysiology. Ethnic differences were first recognised through evidence that metabolic syndrome diagnostic criteria fail to detect T2D risk in black populations due to less central obesity and dyslipidaemia. Subsequently more detailed investigations have recognised other mechanistic differences, particularly lower visceral and hepatic fat accumulation and a distinctly hyperinsulinaemic response to glucose stimulation. While epidemiological studies have reported exaggerated insulin resistance in black populations, more detailed and direct measures of insulin sensitivity have provided evidence that insulin sensitivity is not markedly different to other ethnic groups and does not explain the hyperinsulinaemia that is exhibited. These findings lead us to hypothesise that ectopic fat does not play a pivotal role in driving insulin resistance in black populations. Furthermore, we hypothesise that hyperinsulinaemia is driven by lower rates of hepatic insulin clearance rather than heightened insulin resistance and is a primary defect rather than occurring in compensation for insulin resistance. These hypotheses are being investigated in our ongoing South London Diabetes and Ethnicity Phenotyping study, which will enable a more detailed understanding of ethnic distinctions in the pathophysiology of T2D between men of black African and white European ethnicity.

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