L Ladriere1, T M Zhang, W J Malaisse. 1. Laboratory of Experimental Medicine, Erasmus Medical School, Brussels Free University, Belgium.
Abstract
BACKGROUND: Succinic acid dimethyl ester (SAD) is efficiently metabolized in several cell types as pancreatic islet cells, hepatocytes, and colonocytes. The purpose of this study was to assess the overall nutritional value of SAD in the whole organism. METHODS: SAD was infused at a rate of 80 micromol/g body weight per day in rats starved for either 2 or 4 days. For comparison, similar experiments were conducted in starved rats receiving an equimolar infusion of D-glucose. RESULTS: The ester failed to prevent the starvation-induced fall in body weight, paraovarian fat mass, and liver or muscle protein content. The infusion of SAD minimized, however, the decrease in plasma glucose and insulin concentrations, liver glycogen content, hepatic glucokinase activity, and islet secretory responsiveness to glucose, otherwise caused by starvation. Likewise, the infusion of SAD delayed the rise in free fatty acid and beta-hydroxybutyrate plasma concentration occurring during starvation. Nevertheless, SAD was less efficient than glucose, infused in an equimolar amount, in preventing the starvation-induced fall in liver glycogen content, decrease in the pancreatic B-cell secretory responsiveness to glucose, and stimulation of lipolysis and ketogenesis. CONCLUSIONS: SAD displays a significant nutritional value when infused in starved rats. It could thus be used as a tool to prevent the imbalance between ATP generation and use in selected metabolic situations.
BACKGROUND:Succinic acid dimethyl ester (SAD) is efficiently metabolized in several cell types as pancreatic islet cells, hepatocytes, and colonocytes. The purpose of this study was to assess the overall nutritional value of SAD in the whole organism. METHODS: SAD was infused at a rate of 80 micromol/g body weight per day in rats starved for either 2 or 4 days. For comparison, similar experiments were conducted in starved rats receiving an equimolar infusion of D-glucose. RESULTS: The ester failed to prevent the starvation-induced fall in body weight, paraovarian fat mass, and liver or muscle protein content. The infusion of SAD minimized, however, the decrease in plasma glucose and insulin concentrations, liver glycogen content, hepatic glucokinase activity, and islet secretory responsiveness to glucose, otherwise caused by starvation. Likewise, the infusion of SAD delayed the rise in free fatty acid and beta-hydroxybutyrate plasma concentration occurring during starvation. Nevertheless, SAD was less efficient than glucose, infused in an equimolar amount, in preventing the starvation-induced fall in liver glycogen content, decrease in the pancreatic B-cell secretory responsiveness to glucose, and stimulation of lipolysis and ketogenesis. CONCLUSIONS: SAD displays a significant nutritional value when infused in starved rats. It could thus be used as a tool to prevent the imbalance between ATP generation and use in selected metabolic situations.
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