Abstract
Introduction: Populations of black ethnicity have a disproportionately high prevalence of type 2 diabetes (T2D) compared to their white counterparts. Adiposity and dysfunctional lipid metabolism have been shown to trigger and exacerbate tissue-specific insulin resistance. Black communities present with pronounced insulin resistance in the presence of lower visceral and ectopic fat. These findings have been demonstrated in participants without T2D and imply there may be an ethnic distinction in the pathophysiology of T2D.Aim: To use highly sensitive techniques to assess and compare whole-body and tissue-specific insulin sensitivity in black west African (BAM) and white European men (WEM) of normal glucose tolerance (NGT), impaired glucose tolerance (IGT) or type 2 diabetes (T2D), and to assess the association with regional measures of fat and lipolysis.
Methods: Forty-nine BAM (21 NGT, 10 IGT,18 T2D) and 47 WEM (23 NGT, 9 IGT, 15 T2D) underwent a two-step hyperinsulinaemic-euglycaemic clamp with stable glucose and glycerol isotopic tracers to assess insulin sensitivity, and a magnetic resonance imaging scan to assess visceral adipose tissue (VAT) and intrahepatic lipids (IHL).
Results: There were no significant ethnic differences in whole-body or tissue-specific insulin sensitivity between BAM and WEM in any glucose tolerance group (p>0.05). VAT and IHL were significantly lower in BAM than WEM in each glucose tolerance group (p<0.05). There were no ethnic differences in the associations of peripheral or hepatic insulin sensitivity to glucose homeostasis with VAT or IHL (p>0.05). The association between insulin sensitivity to glucose homeostasis with insulin’s antilipolytic actions were weaker in BAM. The antilipolytic action of insulin associated with VAT and IHL in WEM but not BAM.
Conclusions: Black men may have resistance to storing of visceral and ectopic fat and lower levels are found in all glucose tolerance groups. This is observed in the presence of similar whole-body and tissue-specific insulin sensitivity, therefore lower visceral and ectopic fat may be a protective mechanism in black men which prevents pronounced insulin resistance. Visceral fat, hepatic fat and a resistance to insulin’s antilipolytic action all appear to play a role in insulin resistance to glucose homeostasis in both ethnic groups. The latter association is significantly weaker in black men, and the mechanisms behind this relationship may be dependent on fat accumulation in white men but not black men.
| Date of Award | 1 Oct 2020 |
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| Original language | English |
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| Supervisor | Louise Goff (Supervisor) & Stephanie Amiel (Supervisor) |