Maria A G Reid

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We have recently shown that meal-induced insulin sensitization (MIS) occurs after feeding and decreases progressively to insignificance after 24 h of fasting and is caused by action of a hepatic insulin sensitizing substance (HISS). In order to carry out quantitative studies of MIS, some standardized meal intake is required. Our objective was to establish(More)
BACKGROUND In the fed state, the glucose disposal action of insulin can be attributed in approximately equal part to the direct action of insulin and to a hepatic insulin sensitizing substance (HISS) that acts selectively on skeletal muscle. HISS action is absent in the 24-hour fasted state. The objective of this study was to determine whether alcohol(More)
Insulin action is approximately doubled following a meal. The mechanism of postprandial insulin sensitization is dependent on hepatic parasympathetic nerves regulated by the prandial status. The nerves provide a permissive signal to the liver that allows insulin to cause the release of a putative hepatic insulin sensitizing substance (HISS) that selectively(More)
The objective was to compare the ability of the rapid insulin sensitivity test (RIST), the hyperinsulinemic euglycemic clamp (HIEC), and the insulin tolerance test (ITT) to detect hepatic insulin sensitizing substance (HISS) dependent insulin action. HISS action was augmented by feeding and inhibited by fasting, blockade of hepatic nitric oxide synthase, or(More)
Hepatic insulin sensitizing substance (HISS) action accounts for 55% of the glucose disposal effect of a bolus of insulin in the fed state. To determine the effect of continuous versus pulsatile insulin delivery on HISS action in male Sprague-Dawley rats, insulin sensitivity was assessed using the rapid insulin sensitivity test (RIST) before and after a(More)
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