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Veronica Qvisth, Eva Hagström-Toft, Staffan Enoksson, Robert S. Sherwin, Stefan Sjöberg, Jan Bolinder, Combined Hyperinsulinemia and Hyperglycemia, But Not Hyperinsulinemia Alone, Suppress Human Skeletal Muscle Lipolytic Activity in Vivo, The Journal of Clinical Endocrinology & Metabolism, Volume 89, Issue 9, 1 September 2004, Pages 4693–4700, https://doi.org/10.1210/jc.2003-030656
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Effects of circulating insulin and glucose concentrations on skeletal muscle and adipose tissue lipolytic activity were investigated in 10 type 1 diabetes patients with no endogenous insulin secretion. Microdialysis measurements of interstitial glycerol and determination of fractional glycerol release were carried out during standardized combinations of relative hypoinsulinemia/moderate hyperglycemia (11 mmol/liter), hyperinsulinemia/ normoglycemia (5 mmol/liter), and hyperinsulinemia/moderate hyperglycemia, respectively. Local tissue blood flow rates were measured with the 133Xe clearance technique. In response to the change from hypo- to hyperinsulinemia, the fractional release of glycerol decreased from 159.6 ± 17.8 to 85.1 ± 13.7 μmol/liter (P < 0.0001) in adipose tissue, whereas it remained unchanged in skeletal muscle (44.6 ± 6.4 vs. 36.0 ± 7.4 μmol/liter; not significant). When hyperinsulinemia was combined with hyperglycemia, fractional glycerol release was further reduced in adipose tissue (64.5 ± 12.2 μmol/liter; P < 0.05), and in this situation it was also markedly decreased in skeletal muscle (18.1 ± 4.8 μmol/liter; P < 0.0001). Skeletal muscle blood flow was unaltered over the respective study periods. Adipose tissue blood flow decreased by 50% in response to hyperinsulinemia (P < 0.0005), but no further change was seen when hyperinsulinemia was combined with hyperglycemia. It is concluded that in patients with type 1 diabetes, insulin does not exert an antilipolytic effect in skeletal muscle during normoglycemia. However, in response to combined hyperinsulinemia and hyperglycemia, the lipolytic activity in skeletal muscle is restrained in a similar way as in adipose tissue. This may be explained by a glucose-mediated potentiation of the antilipolytic effectiveness of insulin.
