Effect of Copper on Insulin Release by the Intact Rat Pancreas and the Perfused Rat Pancreas

Am, Cohen; Miller, Elizabeth A.

doi:10.1097/00006676-198607000-00003

Cited by 15 publications

(5 citation statements)

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“…Reduced glucose tolerance (Keil and Nelson 1934) Impaired insulin release and binding (Cohen and Miller 1986;Fields et al 1983) Enhancement of defects by fructose relative to those of glucose (Fields et al 1984a) Amelioration of effects by food restriction ; Werman and Bhathena 1993) Inhibition of effects by aminoguanidine (inhibitor of advanced glycation) (Saari 1994) Correlation of defects with glycated Hb…”

Section: Indirect Evidencementioning

confidence: 99%

Copper deficiency and cardiovascular disease: role of peroxidation, glycation, and nitration

Saari

2000

Rev. can. physiol. pharmacol.

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Dietary copper deficiency causes a variety of cardiovascular deficits. Systemic effects include high blood pressure, enhancement of inflammation, anemia, reduced blood clotting, and possibly arteriosclerosis. Effects on specific organs or tissues include weakened structural integrity of the heart and blood vessels, impairment of energy use by the heart, reduced ability of the heart to contract, altered ability of blood vessels to control their diameter and grow, and altered structure and function of circulating blood cells. In some instances, the cause of a defect can be directly attributed to reduced activity of a specific copper-dependent enzyme. However, three nonspecific mechanisms of damage have been implicated in cardiovascular defects of copper deficiency. They are peroxidation, the interaction of oxygen-derived free radicals with lipids and proteins (possibly DNA); glycation, the nonenzymatic glycosylation of proteins; and nitration, the interaction of nitric oxide and its metabolites with peptides and proteins. Though independently these mechanisms present great potential for damage, the possibility that they may interact presents an added reason for concern. Furthermore, the fact that at least two of these mechanisms are associated with diabetes and aging suggests that copper deficiency may exacerbate deficits associated with these two conditions.

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Section: Indirect Evidencementioning

confidence: 99%

Copper deficiency and cardiovascular disease: role of peroxidation, glycation, and nitration

Saari

2000

Rev. can. physiol. pharmacol.

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“…The ability of the endocrine pancreas to release insulin, however, is greatly impaired [7,27]. In the present study, the endocrine pancreas of copperdeficient rats that consumed the adequate iron diet contained very high concentration of insulin.…”

Section: Discussionmentioning

confidence: 44%

Low dietary iron restores functional capabilities of both exocrine and endocrine pancreas in copper-deficient rats

Fields

Lewis

1997

J. Trace Elem. Exp. Med.

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“…Evidence points to an impaired pancreatic release of insulin as the cause [162][163][164]. Evidence points to an impaired pancreatic release of insulin as the cause [162][163][164].…”

Section: Glycationmentioning

confidence: 99%

“…The altered carbohydrate metabolism that is prerequisite to increased glycation is signaled by a reduced glucose tolerance in copper-deficient animals. Evidence points to an impaired pancreatic release of insulin as the cause [162][163][164].…”

Section: Glycationmentioning

confidence: 99%

Cardiovascular effects of dietary copper deficiency

Saari

Schuschke

1999

BioFactors

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Dietary copper deficiency may impair cardiovascular health by contributing to high blood pressure, enhancement of inflammation, anemia, reduced blood clotting and arteriosclerosis. The purpose of this review is to compile information on the numerous changes of the heart, blood and blood vessels that may contribute to these cardiovascular defects. These alterations include weakened structural integrity of the heart and blood vessels, impairment of the use of energy by the heart, reduced ability of the heart to contract, altered ability of blood vessels to control their diameter and to grow, and altered structure and function of circulating blood cells. The fundamental causes of these changes rest largely on reduced effectiveness of enzymes that depend on copper for their activity.

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Effect of Copper on Insulin Release by the Intact Rat Pancreas and the Perfused Rat Pancreas

Cited by 15 publications

References 0 publications

Copper deficiency and cardiovascular disease: role of peroxidation, glycation, and nitration

Copper deficiency and cardiovascular disease: role of peroxidation, glycation, and nitration

Low dietary iron restores functional capabilities of both exocrine and endocrine pancreas in copper-deficient rats

Cardiovascular effects of dietary copper deficiency

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