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Effects of subacute low level lead exposure on glucose homeostasis
Insights
This study found that low-level lead exposure in young rats did not affect key gluconeogenic enzymes. However, higher lead doses temporarily altered enzyme activity and increased glucagon levels in six-week-old rats.
Area of Science:
- Biochemistry
- Toxicology
- Endocrinology
Background:
- Lead exposure is a significant public health concern, particularly for developing organisms.
- Understanding the metabolic effects of lead is crucial for assessing its toxicological impact.
Purpose of the Study:
- To investigate the impact of subacute lead exposure on key gluconeogenic enzymes and hormonal regulation in neonate rats.
- To determine the age-dependent sensitivity of rats to lead's metabolic effects.
Main Methods:
- Neonate rats were administered varying doses of lead (0.001–0.1 µg/g/day) from three days to eight weeks of age.
- Hepatic enzyme activities (glucose-6-phosphatase, fructose-1,6-diphosphatase, pyruvate carboxylase, phosphoenolpyruvate carboxykinase), plasma insulin and glucagon, blood glucose, and hepatic glycogen were measured.
- Lead levels in blood, liver, and pancreas were analyzed.
Main Results:
- Low lead doses (up to 0.025 µg/g/day) did not alter gluconeogenic enzyme activities or hormonal levels by eight weeks.
- A higher lead dose (0.1 µg/g/day) transiently enhanced fructose-1,6-diphosphatase and phosphoenolpyruvate carboxykinase activities at six weeks.
- This higher dose also significantly increased glucagon levels and led to lead accumulation in blood and pancreas by six and eight weeks.
Conclusions:
- Subacute lead exposure can transiently affect gluconeogenesis and hormonal balance in young rats, with six-week-old animals showing greater sensitivity.
- Pancreatic tissue demonstrated accumulation of lead, suggesting potential organ-specific toxicity.
- These findings highlight the importance of age in determining the metabolic consequences of lead exposure.
Abstract:
Administration of low levels of lead (0.001, 0.005 and 0.025 micrograms/g/day p.o.) to neonate rats from age three days to eight weeks failed to alter the activities of hepatic glucose-6-phosphatase, fructose-1,6-diphosphatase, pyruvate carboxylase and phosphoenolpyruvate carboxykinase, the four key gluconeogenic enzymes. Administration of lead at a higher dose (0.1 micrograms/g/day p.o.) was also observed to produce no alterations in enzyme activity at eight weeks. However, the higher dose did enhance the activities of fructose-1,6-diphosphatase and phosphoenolpyruvate carboxykinase at age six weeks. Plasma insulin and glucagon were not significantly altered by up to 0.025 micrograms/g exposure to lead until eight weeks of age, although levels of these hormones appear to be slightly dose-responsive tending towards elevated glucagon and decreased insulin levels with increasing lead dosage. At 0.1 micrograms/g/day glucagon was significantly increased at eight weeks. Blood glucose and hepatic glycogen remained unaltered. Blood, hepatic and pancreatic lead levels were unchanged by treatment with lead up to 0.025 micrograms/g/day to eight weeks of age, but there was evidence of lead accumulation in pancreatic tissue whereas levels of the metal in the liver paralleled those in the blood. Significant increases were observed with 0.1 micrograms/g/day lead at six and eight weeks in blood and pancreas. Data are presented which suggest that six week old animals are more influenced by subacute lead exposure than are the eight week old animals, as reflected in some alteration of gluconeogenic enzyme activity in younger rats.