Effect of intragastric triglyceride administration on glucose homeostasis in newborn pigs

Abstract

The fasting hypoglycemia (1.78 +/- 0.29 mmol/l) which develops in 48-h-old pigs is partially reversed (3.85 +/- 0.55 mmol/l) after gastric administration of long-chain triglycerides (LCT). The increase in blood glucose induced by LCT feeding was not secondary to a decreased glucose utilization because glucose disappearance rate increased in LCT-fed piglets but resulted from a twofold increase in glucose appearance. By using the crossover-plot technique, the stimulation of hepatic gluconeogenesis induced by LCT feeding has been localized at 1) the level of pyruvate carboxylase owing to the twofold increase in hepatic acetyl-CoA concentration and 2) the level of glyceraldehyde-3-phosphate dehydrogenase secondary to the increase in reducing equivalents (NADH), which displaces this equilibrium reaction in the direction of gluconeogenesis. As blood lactate, pyruvate, and alanine concentrations increased after LCT feeding, the possible effects of LCT on pyruvate dehydrogenase in peripheral tissues are discussed. These data demonstrate that fatty acids stimulate hepatic gluconeogenesis in 48-h-old fasting piglets and underline the role of fat provision in the regulation of glucose homeostasis during the neonatal period in the pig.

Acetate represents a major product of heptanoate and octanoate β-oxidation in hepatocytes isolated from neonatal piglets

“…The oxidation of fatty acids, which requires free CoA, should theoretically increase the level of acetyl-CoA and lower the content of free CoA in hepatocytes. Consistent with this, neonatal piglet hepatocytes incubated with MCFA displayed a free CoA content much lower than that in blank preparations (Table 2), and liver acetyl-CoA concentration increased with gastric administration of long-chain fatty acids in piglets [36]. Valproate further lowered the free CoA concentration, probably via formation of valproyl-and other acyl-CoA esters.…”

“…in neonatal piglets. It is constructive to emphasize that the concentration of acetyl-CoA was extremely low from neonatal piglets (this study and [35,36]) compared with rats [37]. Explanations for this finding are only speculative, but it is possible that (1) in the presence of MCFA, CoA becomes bound in other acyl-CoA moieties (i.e.…”

Utilization of Medium-Chain Triglycerides by Neonatal Piglets: II. Effects of Even- and Odd-Chain Triglyceride Consumption over the First 2 Days of Life on Blood Metabolites and Urinary Nitrogen Excretion

“…The greater increase in glucose concentration of animals supplemented with even-MCT compared with those supplemented with odd-MCT and LCT may reflect better utilization of even-MCT. Duee et al (1985) have proposed that LCFA oxidation supports hepatic gluconeogenesis by generating ATP and reducing equivalents and also by providing acetyl-CoA, an obligatory cofactor for pyruvate carboxylase (Pegorier et al, 1985). The extent to which this is true for MCFA (Turlan et al, 1983;Pegorier et al, 1983b) is not certain, because short-term infusions of both even-and odd-MCT in dogs have been associated with transient hypoglycemia (Guisard et al, 1973), presumably mediated by an insulin response.…”

Fatty acids and triacylglycerols composition from Tunisian Acacia species seed oil

“…Spady and Dietschy (1985) have suggested that saturated dietary TAG inhibit the activity of hepatic LDL receptors in the Hamster. Other studies have reported the benefic effect of triacylglycerol on glucose homeostasis and on the prevention of obesity and atherosclerosis (Kojima et al, 2010;Pegorier et al, 1985). Acacia seed oil could be used as potential source of TAG with high industrial value; however its safety must be proved.…”