Biomedical subjects

C G Lewis

Publications and source records attributed to C G Lewis.

75 records · Page 5Linked to original sources

PubMedDate not supplied

Alcohol consumption mimics the effects of a high-fructose, low-copper diet in rats.

The consumption of a high-fructose diet that is inadequate in copper produces numerous pathologies which eventually lead to the mortality of the animals. In contrast, the consumption of a high-starch diet that is inadequate in copper does not produce abnormalities and the animals survive. Ethanol has been chosen as an agent to mimic the fructose effect in copper deficiency. The administration of 20% ethanol in the drinking water of rats fed a starch-based diet that was inadequate in copper resulted in a depressed growth rate, anemia, pancreatic atrophy, and heart hypertrophy. All these signs were similar to the signs exerted by fructose feeding when it was combined with copper deficiency. Polyol pathway in the liver and kidney was affected by both ethanol and fructose consumption. Ethanol did not aggravate the signs associated with copper deficiency in rats fed fructose, but it exacerbated the signs associated with copper deficiency in rats fed starch. Certain metabolic pathways that are unique for fructose and ethanol may be responsible for the exacerbation of copper deficiency.

Anemia↗

PubMedDate not supplied

Copper-carbohydrate interaction in maternal, fetal and neonate rat.

The present study was undertaken to determine whether the same type of interaction between dietary fructose and copper that affects young growing male rats also affects the fetus and the neonate. Female rats were fed copper-deficient (0.6 microgram Cu/g) or adequate (6.0 micrograms/g) diets containing 62% carbohydrate as fructose or starch either for 8 weeks prior to conception, and during mating, gestation and lactation, or just during gestation. Fetuses were killed at days 14, 18 or 21 of gestation and newborn pups were killed at days 0, 10, or 21 postpartum. Regardless of the duration of dietary copper deprivation, feeding the fructose diet deficient in copper during pregnancy resulted in either fetal resorption or mortality of all newborn pups during the first few hours postpartum. In contrast, copper-deficient rats fed the starch-containing diets delivered live pups. However, 40% of their pups died during the first 2 days postpartum and occurred only when dams had been fed the deficient diet for 12-13 weeks. When fed the deficient diet for a total of 3 weeks only, during pregnancy, all copper-deficient rats fed starch delivered live pups and no mortality occurred during the lactation period. Feeding the copper-adequate fructose diet during lactation resulted in a lower hepatic copper concentration of suckling pups compared with starch feeding. Female pups had higher levels of copper and iron than male pups. The data show that fetal resorption and mortality of the neonate pup was dependent on the type of dietary carbohydrate fed to copper-deficient animals during pregnancy.

Animals↗

PubMedDate not supplied

Responses of insulin to oral glucose and fructose loads in marginally copper-deficient rats fed starch or fructose.

The purpose of this study was to assess the effects of dietary fructose either alone or in combination with marginal copper deficiency in weanling male rats exposed to their respective diets for only 2 wk. This short duration of exposure to inadequate copper intake prevents progressive morbidity brought about by increasing periods of exposure to dietary copper deprivation. Weanling male rats were fed a copper-deficient (0.6 microgram Cu/g) or a copper-adequate (6.0 micrograms Cu/g) diet containing 62% fructose or 62% starch for 2 wk. Either an oral glucose or an oral fructose tolerance test was conducted after an overnight fast. Insulin levels were elevated by either oral glucose or oral fructose at fasting and at 30 min postload in rats fed fructose compared with those fed starch. Despite high levels of plasma, insulin blood glucose was not reduced. Marginal copper deficiency had no effect on either plasma insulin or blood glucose. Data identify fructose as the sole agent responsible for inducing adverse changes in glucose metabolism. Two weeks of fructose consumption was sufficient to produce these changes.

Animals↗