In vitro influence of lactate on function of peritoneal fibroblasts.

A. Breborowicz, L. Martis, D. G. Oreopoulos

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

The authors studied the effect of sodium lactate (NaLact) on the function of human peritoneal fibroblasts (F) in vitro. NaLact inhibits the proliferation of fibroblasts in a dose-dependent way: at a concentration of 40 mM, it decreases the growth of these cells by 34%. A similar effect was observed with other solutes (glucose, mannitol, sodium chloride) at identical concentrations, suggesting that the factor responsible for slower growth of the cells was hyperosmolality. When applied to fibroblast monolayers, NaLact (40 mM) increased the synthesis of total proteins by 10%. Exposure of the fibroblasts to NaLact did not increase noncollagen protein production, and the observed increase in total protein synthesis was due to the increased synthesis of collagen. We could not reproduce this effect of lactate on fibroblast collagen synthesis with other osmotic solutes. Our results suggest that dialysis fluid hyperosmolality may be one of the factors responsible for the decrease of the cellular components within the peritoneal interstitium; whereas NaLact is specifically responsible for the increased production of collagen by peritoneal fibroblasts, leading to the deposition of masses of collagen in the extracellular space.

Original languageEnglish (US)
Pages (from-to)225-229
Number of pages5
JournalAdvances in peritoneal dialysis. Conference on Peritoneal Dialysis
Volume10
StatePublished - 1994
Externally publishedYes

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Lactic Acid
Fibroblasts
Collagen
Sodium Lactate
Proteins
Extracellular Space
Mannitol
Growth
Sodium Chloride
In Vitro Techniques
Dialysis
Glucose

ASJC Scopus subject areas

  • Medicine(all)

Cite this

In vitro influence of lactate on function of peritoneal fibroblasts. / Breborowicz, A.; Martis, L.; Oreopoulos, D. G.

In: Advances in peritoneal dialysis. Conference on Peritoneal Dialysis, Vol. 10, 1994, p. 225-229.

Research output: Contribution to journalArticle

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