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33276 
Journal Article 
Abstract 
Nickel chloride-induced changes in glucose metabolism in the rat 
Clary, JJ; Vignati, I 
1973 
Yes 
Toxicology and Applied Pharmacology
ISSN: 0041-008X
EISSN: 1096-0333 
25 
3 
467-468 
English 
WOS:A1973Q218800087 
is part of a larger document 3114922 Abstracts of papers for the Twelfth Annual Meeting of the Society of Toxicology, New York, New York March 18–22, 1973
Exposure to industrial metals may cause subtle long-term health effects. This study was undertaken to explore a heretofore unreported effect of NiC12 on carbohydrate metabolism and elucidate the mechanisms involved. NiC12 was given by various routes: intraperitoneal (8 mg/kg), intratracheal (0.5 mg), and by long-term ingestion (drinking water-225 ppm). In addition, intragastric glucose load (600 mg) was also given to some of the intratracheally injected animals. The following parameters were measured in the serum: glucose, insulin, total lipids, cholesterol and triglycerides. Liver parameters measured were glycogen and glucose-6-phosphatase. Ni63 tissue distribution and excretion were also measured. A single ip injection of Ni to rats caused a rapid, transient fourfold increase in serum glucose and consequent glucosuria. This hyperglycemia was also associated with hyperlipidemia and insulin resistance. Nickel appears to be an antagonist to exogenous insulin. Repeated exposure to ingested Ni (drinking water) also resulted in elevated serum lipids, especially the triglyceride fraction. An increase in pancreatic insulin was also observed. Daily Ni ingestion causes no change in liver glycogen content or in fasting blood glucose values. This study points out the subtle changes in the metabolic pathways which might affect the health of industrial workers exposed to Ni. 
Twelfth Annual Meeting of the Society of Toxicology 
New York 
March 18–22, 1973