Effects of Different Dietary Carbohydrates on Hepatic Enzymes of Copper-Deficient Rats

Abstract

The present study was undertaken to measure the activities of several hepatic enzymes of regulatory importance in the pathways of lipogenesis and gluconeogenesis in rats fed diets marginally deficient in copper (1.2 p g Cu/g of diet) and containing either fructose, glucose, or starch as the carbohydrate sources. Although all copperdeficient rats exhibited the characteristic signs of copper deficiency, they were more pronounced in rats fed the diet containing fructose. Except for the activity of phosphoenolpyruvate carboxykinase which was unaffected either by copper deficiency or by the type of dietary carbohydrate, the hepatic activities of glucose-6-phosphate dehydrogenase, malic enzyme, L-a-glycerophosphate dehydro-362

The Role of Copper as a Modifier of Lipid Metabolism

“…Analysis of hepatic enzymes involved in the lipid and carbohydrate metabolism also indicated that a diet deficient in copper had greatest metabolic effects in combination with fructose, less with glucose and least with starch (71). Glucose-6-phosphate dehydrogenase, malic enzyme, L-alpha-glycerophosphate dehydrogenase and fructose 1-6-diphosphatase were all unaffected by Cu deficiency, but their activities were enhanced most in combination with fructose, suggesting a complementary rather than direct role for fructose in exacerbating copper deficiency (71).…”

Copper deficiency in rats: the effect of type of dietary protein.

“…Since all the rats of the present study consumed fructose, it was not surprising to find that liver size was not affected by the different dietary proteins. It is suggested that metabolism of fructose, which occurs mainly in the liver [18,19] was not altered by the nature of dietary protein.…”

Garlic oil extract ameliorates the severity of copper deficiency.

“…Increased insulin concentration when garlic was fed resulted in a stimulation of lipogenesis by extrahepatic tissues as reflected by the elevated epididymal fat pad weights in Cu-deficient rats fed fructose. Fatty liver is a consequence of fructose but not of glucose (from the digestion of starch) metabolism [9][10][11]. One of the causes of fatty liver in fructose feeding is increased availability of fatty acids in the liver.…”

“…Unlike starch, fructose is very lipogenic and its consump tion results in a fatty liver [9][10][11]. Chronic lipid accumu lation causes the liver cells to become fibrotic, leading to cirrhosis and impaired liver functions.…”