Insulin-mediated skeletal muscle vasodilation is nitric oxide dependent. A novel action of insulin to increase nitric oxide release.

Steinberg, Helmut O.; Brechtel, Ginger; Johnson, Ann; Fineberg, Naomi S.; Baron, Alain

doi:10.1172/jci117433

Cited by 1,137 publications

(703 citation statements)

References 38 publications

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“…Similarly, other studies have shown that endothelium-dependent vasodilation was impaired in thoracic aorta rings from rats infused with glucosamine and that this was a result of the inhibition of NOS by glucosamine [19]. Since both the insulin-mediated increases in total flow [15,36] and capillary recruitment [16] have been suggested to be NOSdependent, this could be the mechanism for the glucosamine-mediated inhibition of capillary recruitment and total flow. The effects of glucosamine on gene expression in endothelial cells [37] should also be considered, if longer-term exposure occurs.…”

Section: Discussionmentioning

confidence: 77%

“…Evidence from a number of laboratories indicates that limb blood flow is controlled by insulin acting via a NO-dependent mechanism presumed to be initiated via vascular endothelial cells [15,36,39]. However, the role of limb blood flow in insulin-mediated glucose uptake is at best controversial [40].…”

Section: Discussionmentioning

confidence: 99%

“…When infused locally [15], inhibitors of nitric oxide synthase (NOS) block insulin-mediated increases in blood flow, and also block insulin-mediated capillary recruitment when infused systemically [16]. For capillary recruitment, the higher sensitivity to insulin [17] and the fact that time course studies show capillary recruitment to be the earliest change caused by insulin in vivo [18] suggest that endothelial cells, in particular endothelial nitric oxide synthase (eNOS), are the source of nitric oxide (NO).…”

Section: Introductionmentioning

confidence: 99%

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Acute glucosamine-induced insulin resistance in muscle in vivo is associated with impaired capillary recruitment

et al. 2005

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Aims/hypothesis: Glucose toxicity and glucosamine-induced insulin resistance have been attributed to products of glucosamine metabolism. In addition, endothelial cell nitric oxide synthase is inhibited by glucosamine. Since insulin has endothelial nitric-oxide-dependent vasodilatory effects in muscle, we hypothesise that glucosamine-induced insulin resistance in muscle in vivo is associated with impaired vascular responses including capillary recruitment. Materials and methods: Glucosamine (6.48 mg kg −1 min −1 for 3 h) was infused with or without insulin (10 mU kg −1 min −1 ) into anaesthetised rats under euglycaemic conditions. Results: Glucosamine infusion alone increased blood glucosamine (1.9±0.1 mmol/l) and glucose (5.4±0.2 to 7.7± 0.3 mmol/l) (p<0.05) but not insulin. Glucosamine induced both hepatic and muscle insulin resistance as evident from measures of glucose appearance and disposal as well as hindleg glucose uptake, which was inhibited by approx. 50% (p<0.05). Insulin-mediated increases in femoral arterial blood flow and capillary recruitment were completely blocked by glucosamine. Conclusion/interpretation: Glucosamine mediates a major impairment of insulin action in muscle vasculature associated with the insulin resistance of muscle. Further studies will be required to assess whether the impaired capillary recruitment contributes to insulin resistance.

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Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Acute glucosamine-induced insulin resistance in muscle in vivo is associated with impaired capillary recruitment

et al. 2005

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“…It is, therefore, tempting to speculate that the increased stiffness found in subjects with type 2 diabetes may be due in part to insulin resistance. 41 …”

Section: Type 2 Diabetes Mellitus and Endothelial Dysfunctionmentioning

confidence: 99%

Arterial stiffness, hypertension and diabetes mellitus

2000

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“…The acute vascular effect of insulin in healthy men is vasodilation by stimulation of nitric oxide production and secondarily by stimulation of vasodilating prostaglandins. 3,4 Early in the course of insulin-dependent diabetes mellitus (IDDM), before the occurrence of overt retinopathy, a decrease in retinal blood flow is present that correlates with plasma glucose levels. 5 In contrast, in IDDM with poor metabolic control, elevated cardiac output and forearm blood flow Correspondence: Dr PC Chang, Department of Nephrology, C3-P, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands Received 9 July 1998; revised and accepted 19 October 1998 vascular resistance were related to the plasma glucose concentrations both glucose infusions were equipotent.…”

Section: Introductionmentioning

confidence: 99%

Acute hyperglycaemia in the forearm induces vasodilation that is not modified by hyperinsulinaemia

Veen¹,

Frölich

1999

J Hum Hypertens

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Objective: To evaluate whether acute elevations of local plasma glucose concentrations could influence forearm blood flow (FBF) and how this interacts with local hyperinsulinaemia in healthy volunteers. Methods: Using the perfused forearm technique, in random order, glucose 20% or saline 0.9% as a control was infused in three dose steps (0.3, 1.0, and 3.0 ml/min) for 5 min each in eight healthy men. The infusion experiments were repeated, in random order, during local hyperinsulinaemia by intra-arterial infusion of insulin 0.05 mU/kg/min. The ratio of FBF of the infused over the FBF in the control arm (FR) was measured at 15-sec intervals during the infusions. Results: Glucose infusion increased the FR dosedependently by 172% ± 39% (M ± SE) at the highest dose (P Ͻ 0.01). During hyperinsulinaemia the glucoseinduced increase in FR was significantly (P Ͻ 0.01) less, 96% ± 26%, however, when changes in FR or forearm

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Insulin-mediated skeletal muscle vasodilation is nitric oxide dependent. A novel action of insulin to increase nitric oxide release.

Abstract: The purpose of this study was to examine whether insulin's effect to vasodilate skeletal muscle vasculature is mediated by endothelium-derived nitric oxide (EDNO)

Cited by 1,137 publications

References 38 publications

Acute glucosamine-induced insulin resistance in muscle in vivo is associated with impaired capillary recruitment

Acute glucosamine-induced insulin resistance in muscle in vivo is associated with impaired capillary recruitment

Arterial stiffness, hypertension and diabetes mellitus

Acute hyperglycaemia in the forearm induces vasodilation that is not modified by hyperinsulinaemia

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