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Impaired postprandial adipose tissue microvascular blood flow responses to a mixed-nutrient meal in first-degree relatives of adults with type 2 diabetes

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journal contribution
posted on 2023-05-21, 09:48 authored by Roberts-Thompson, KM, Hu, D, Russell, RD, Timothy GreenawayTimothy Greenaway, Betik, AC, Parker, L, Kaur, G, Stephen RichardsStephen Richards, Dino PremilovacDino Premilovac, Wadley, GD, Michelle Keske
Adipose tissue microvascular blood flow (MBF) is stimulated postprandially to augment delivery of nutrients and hormones to adipocytes. Adipose tissue MBF is impaired in type 2 diabetes (T2D). Whether healthy individuals at-risk of T2D show similar impairments is unknown. We aimed to determine whether adipose tissue MBF is impaired in apparently healthy individuals with a family history of T2D. Overnight-fasted individuals with no family history of T2D for two generations (FH-, n=13), with at least one parent with T2D (FH+, n=14) and clinically diagnosed T2D (n=11) underwent a mixed meal challenge (MMC). Metabolic responses (blood glucose, plasma insulin, plasma non-esterified fatty acids [NEFA] and fat oxidation) were measured before and during the MMC. MBF in truncal subcutaneous adipose tissue was assessed by contrast ultrasound while fasting and 60 minutes post-MMC. FH+ had normal blood glucoses, increased adiposity, impaired post-MMC adipose tissue MBF (D0.70±0.22 versus 2.45±0.60 AI/sec, p=0.003) and post-MMC adipose tissue insulin resistance (Adipo-IR index; D45.5±13.9 versus 7.8±5.1 mmol/L x pmol/L, p=0.006) compared to FH-. FH+ and T2D had an impaired ability to suppress fat oxidation post-MMC. Fat oxidation incremental area under the curve (35-55 minutes post-MMC, iAUC) was higher in FH+ and T2D, compared to FH- (p=0.002 and 0.004, respectively). Postprandial MBF was negatively associated with postprandial fat oxidation iAUC (p=0.01). We conclude that apparently healthy FH+ individuals display blunted postprandial adipose tissue MBF that occurs in parallel with adipose tissue insulin resistance and impaired suppression of fat oxidation, which may help explain their heightened risk for developing T2D.

Funding

Royal Hobart Hospital Research Foundation

History

Publication title

American Journal of Physiology: Endocrinology and Metabolism

Volume

323

Issue

5

Pagination

E418-E427

ISSN

0193-1849

Department/School

Tasmanian School of Medicine

Publisher

American Physiological Society

Place of publication

United States

Rights statement

Copyright © 2022 the American Physiological Society

Repository Status

  • Restricted

Socio-economic Objectives

Prevention of human diseases and conditions; Expanding knowledge in the biomedical and clinical sciences