Alteration of Glucose and Insulin Metabolism in Congenital Heart Disease

Abstract

Children with left-to-right shunt, with and without congestive heart failure, were found to have impaired glucose tolerance tests (GTT). In cyanotic children normal levels of glucose were found in association with abnormally high levels of insulin following oral GTT. Several possible mechanisms are proposed to explain the different glucose tolerance alterations: (1) Suppression of insulin release appeared to partially explain the low levels of insulin in congestive heart failure. This suppression may be related to the high levels of circulating norepinephrine found in these patients. (2) Excessive clearance of insulin by the lung may also be responsible for the reduced arterial insulin levels in patients with left-to-right shunt, and underclearance of insulin for the abnormally higher arterial insulin levels in patients with right-to-left shunts in whom a significant amount of venous blood has bypassed the lung. (3) Hypoxia of the pancreas and the liver in cyanotic patients and those with congestive heart failure may explain the reduction of insulin levels in the hepatic vein following i.v. glucose tolerance tests. An excess production of a glucagonlike gastrointestinal factor in cyanotic children may partially explain the abnormally high levels of insulin following oral GTT.

Congenital Heart Disease in the Older Adult

“…51 There is evidence for abnormal glucose metabolism in ACHD patients. 69 Abnormal glucose metabolism is recognized as a powerful predictor of cardiac morbidity and mortality. The pathogenesis is probably multifactorial and lesion specific.…”

Decreased serum insulin-like growth factor-I associated with growth failure in newborn lambs with experimental cyanotic heart disease.

“…Growth hormone levels are also elevated in high altitude dwellers with chronic hypobaric hypoxemia (34). Although IGF levels have not been previously measured in patients with cyanotic congenital heart disease, abnormalities of insulin release have been demonstrated (17,18), and insulin plays a significant role in the control of IGF-I production (10). Our finding of decreased IGF-I in association with normal levels of growth hormone is partially consistent with the findings ofprevious studies during other chronic stresses.…”

“…Although there have been several previous investigations to determine the etiology of growth failure during chronic hypoxemia, the exact mechanisms are still not well defined (5)(6)(7)(8)(9)(10). Hypermetabolism (5,6), reduced visceral blood flow (1 1), tissue hypoxemia (12), reduced caloric intake (1,12), abnormalities in digestive enzymology (13)(14)(15)(16), and alterations in growth hormone and insulin metabolism (17,18) have been proposed as etiologies. However, previous studies in infants and children with cyanotic congenital heart disease have been complicated by difficulties in controlling for the multiple variables present in the clinical setting (6,8,(19)(20)(21)(22)(23).…”

Chronic Hypoxemia in the Newborn Lamb: Cardiovascular, Hematopoietic, and Growth Adaptations

“…Increased oxygen and substrate demand (41), abnormal hormonal status (42), inadequate caloric intake (43) or malabsorption (44), and local tissue alterations in blood flow and metabolism (35) have all been suggested as causes of failure to thrive in infants with congenital heart disease. Increased total body oxygen consumption and decreased insulin response to oral glucose (45,46) have been described in normoxemic infants in congestive heart failure, but not in hypoxemic infants with cyanotic heart disease (41,47).…”