Planta Med
DOI: 10.1055/s-0043-117415
Original Papers
Georg Thieme Verlag KG Stuttgart · New York

Myocardial Glucose Clearance by Aspalathin Treatment in Young, Mature, and Obese Insulin-Resistant Rats

Sybrand Engelbrecht Smit1, Rabia Johnson1, 2, Mignon Alberta Van Vuuren1, Barbara Huisamen1, 2
  • 1Division of Medical Physiology, Stellenbosch University, Cape Town, South Africa
  • 2Biomedical Research and Innovation Platform, South African Medical Research Council, Cape Town, South Africa
Further Information

Publication History

received 10 February 2017
revised 10 July 2017

accepted 17 July 2017

Publication Date:
03 August 2017 (eFirst)

Abstract

Rooibos, an indigenous South African plant ingested as herbal tea, is well known for its antioxidant effects. This in vitro study investigated aspalathin (C21H24O11), a dihydrochalcone unique to rooibos, for hypoglycemic effects in the context of age- and obesity-induced insulin resistance and the mechanisms involved. Male Wistar rats were allocated into three groups: 16 – 30 weeks feeding with either standard rat chow or a high-caloric diet, or 6 – 10 weeks feeding with standard rat chow. Ventricular cardiomyocytes were isolated by collagenase perfusion digestion, and glucose uptake was determined by 2-[3H]-deoxyglucose accumulation. Viability was tested by trypan blue exclusion or propidium iodide staining. The high-caloric diet significantly increased body weight gain (508.5 ± 50.0 vs. 417.3 ± 40.0 g), visceral adiposity (42.30 ± 10.1 vs. 21.75 ± 7.0 g), and fasting blood glucose (5.7 ± 0.4 vs. 4.7 ± 0.1 mM). Aspalathin (10 µM for 90 min) induced 2-[3H]-deoxyglucose uptake in young cardiomyocytes (37.2 ± 13.9 vs. 25.7 ± 2.5 pmol 2-[3H]-deoxyglucose/mg protein) and enhanced insulin-mediated 2-[3H]-deoxyglucose uptake in control cells (32.4 ± 6.4 vs. 23.5 ± 10.0 pmol 2-[3H]-deoxyglucose/mg protein), but failed to induce 2-[3H]-deoxyglucose uptake in high-caloric diet cells. Aspalathin induced glucose uptake in insulin-sensitive cardiomyocytes from young and aged rats, but not in high-caloric diet animals and enhanced the actions of insulin through a PI3K-dependent mechanism, resulting in an additive response.

Supporting Information