Phosphorus Balance in Rats with Hypophosphatemia Induced by Lanthanum Carbonate
Munehiro Yoshida, Ryôta Hosomi, M. Kunimatsu, Mikiko Nakamura, Kenji Fukunaga, Seiji Kanda, Toshimasa Nishiyama
Abstract
Open-access reader
Munehiro Yoshida, Ryôta Hosomi, M. Kunimatsu, Mikiko Nakamura, Kenji Fukunaga, Seiji Kanda, Toshimasa Nishiyama
Abstract
Open-access reader
To examine whether lanthanum carbonate can induce a low phosphorus status in experimental animals, we examined phosphorus balance in rats administered lanthanum carbonate. Male 8-week-old Wistar rats were fed a basal case-in-based semi-purified diet or the basal diet supplemented with 0.45% or 0.90% lanthanum as lanthanum carbonate for 4 weeks. Lanthanum administration did not influence body or several organ weights and liver function. In rats administered lanthanum, a very small quantity of lanthanum was detected in several organs although the apparent absorption was almost zero. The highest lanthanum concentration was observed in the liver followed by the femur and kidney. Lanthanum was not clearly detected in the brain. Differences in organ lanthanum between 0.45% and 0.90% administration groups were not significant; lanthanum accumulation in the body is very low and may reach a plateau in a certain range of intake. Serum phosphorus was decreased and fecal phosphorus was increased by lanthanum administration dose-dependently. Urinary phosphorus excretion was significantly decreased by lanthanum. Since urinary phosphorus of rats fed 0.45% lanthanum diet decreased to near zero, the highest phosphorus balance was observed in rats fed 0.45% lanthanum diet. This high balance is considered to be adaptation to the low phosphorus status induced by lanthanum carbonate. These results indicate that lanthanum carbonate can induce hypophosphatemia without any direct side effects and be used to examine the effect of removing phosphorus from the diet in animal nutritional studies.
OpenAlex reports 1 citations for this work. Citation counts describe recorded attention and do not establish research quality.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
To examine whether lanthanum carbonate can induce a low phosphorus status in experimental animals, we examined phosphorus balance in rats administered lanthanum carbonate. Male 8-week-old Wistar rats were fed a basal case-in-based semi-purified diet or the basal diet supplemented with 0.45% or 0.90% lanthanum as lanthanum carbonate for 4 weeks. Lanthanum administration did not influence body or several organ weights and liver function. In rats administered lanthanum, a very small quantity of lanthanum was detected in several organs although the apparent absorption was almost zero. The highest lanthanum concentration was observed in the liver followed by the femur and kidney. Lanthanum was not clearly detected in the brain. Differences in organ lanthanum between 0.45% and 0.90% administration groups were not significant; lanthanum accumulation in the body is very low and may reach a plateau in a certain range of intake. Serum phosphorus was decreased and fecal phosphorus was increased by lanthanum administration dose-dependently. Urinary phosphorus excretion was significantly decreased by lanthanum. Since urinary phosphorus of rats fed 0.45% lanthanum diet decreased to near zero, the highest phosphorus balance was observed in rats fed 0.45% lanthanum diet. This high balance is considered to be adaptation to the low phosphorus status induced by lanthanum carbonate. These results indicate that lanthanum carbonate can induce hypophosphatemia without any direct side effects and be used to examine the effect of removing phosphorus from the diet in animal nutritional studies.
Key concepts: Lanthanum carbonate, Lanthanum, Hypophosphatemia, Chemistry, Phosphorus, Phosphate binder, Phosphate, Internal medicine