Ethnicity may be independently linked to beta-cell function
medwireNews: Black West African men have lower levels of insulin secretion in response to a meal than their White Northern European counterparts, irrespective of insulin sensitivity, study findings indicate.
Meera Ladwa (King’s College London, UK) and colleagues also found that “pancreatic fat does not appear to play an independent role in insulin secretory response in either ethnic group.”
The researchers acknowledge that their findings “run counter to much of the literature, where the consensus is that [Black West African] populations hypersecrete insulin and that pancreatic fat is a powerful determinant of their beta-cell function.” They note, however, that emerging evidence “shows that these established findings are not necessarily as consistent as initially thought.”
Their observational study included 23 Black West African and 23 White Northern European men with normal glucose tolerance, who were matched for BMI.
Following an overnight fast and a mixed-meal tolerance test, Ladwa and team found that postprandial beta-cell insulin secretion was significantly lower in Black versus White men after adjustment for insulin sensitivity, with estimated marginal means of 40.5×103 versus 56.4×103 pmol/m2 body surface area per 180 minutes.
The relationship between intrapancreatic lipid levels and insulin secretion varied significantly by ethnicity; there was a significant positive correlation between the two variables in White men, but no such correlation in Black men. However, after adjustment for insulin sensitivity, there was no significant association between intrapancreatic lipid levels and insulin secretion in either group.
In addition, multiple regression analysis revealed that both insulin sensitivity and ethnicity were significant independent predictors of insulin secretion, but pancreatic fat was not.
Writing in BMJ Open Diabetes Research & Care, Ladwa and co-authors say that “pancreatic fat appears to be a proxy of insulin sensitivity and plays a surrogate role rather than directly affecting beta cell function,” but acknowledge that the study only included healthy and non-obese men.
The researchers conclude that their “findings generate the hypothesis that relative impairments in beta cell function may contribute to the greater risk of type 2 diabetes in populations of African ancestry.”
They add: “A better understanding of ethnic-specific differences in metabolism in both health and early disease will be key to refining prevention and treatment options, allowing an evidence-based prediction of responses which can then be tested in interventional studies.”
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