Lipogenesis in iron-deficient adult rats

Iron-deficient (5 ppm Fe) or control (307 ppm Fe) diets were fed ad libitum to female rats for 7 weeks, and then meal-fed for 4 weeks. Body weights, hemoglobin levels, and hematocrits were lower (p<0.01) in deficient group (184±7, 7.1±0.4, 32.7±0.6) than in the control group (220±10, 16.9±0.3, 51.8±0.8) at the end of the 11-week experiment. Animals were killed 1 hr after meal feeding, and liver slices, mesenteric adipose tissue, and segments of mid-jejunum were incubated in vitro with [U-¹⁴C] glucose or³H₂O. Adipose tissue from deficient rats had incorporation of [U-¹⁴C] glucose into triglycerides two to three times greater than control rats (p<0.01). Release of¹⁴CO₂ from glucose was greater in adipose tissue of deficient rats than controls (p<0.05). Incorporation of³H₂O into triglycerides was also two to three times greater in deficient adipose tissue than in controls (p<0.02). In liver slices, incorporation of glucose in polar lipids was slightly higher in deficient rats than in control rats (p<0.05). No significant differences were found in incorporation of³H₂O or [U-¹⁴C] glucose into lipids or CO₂ in jejunum. Thus, iron- deficient adult rats have greater lipid synthesis from³H₂O and glucose in adipose tissue than rats fed adequate levels of iron.     

Serum lipids in suckling and post-weanling iron-deficient rats

Serum lipids were studied in iron-deficient and control rats during suckling and after weaning at 21, 30, and 60 days of age. Diets providing 5 or 307 ppm iron were fed to dams and their offspring during gestation, lactation, and after weaning. Rats on the deficient diet throughout the experimental period developed a hyperlipidemia characterized by elevated triglycerides, cholesterol, and phospholipids which was present at 21, 30, and 60 days. Control pups weaned to the deficient diet developed anemia at 30 days of age and hypertriglyceridemia at 60 days of age. Repletion of deficient rats with iron after weaning caused a rapid decline in serum lipid levels after only 9 days on the control diet. The hyperlipidemia of iron deficiency thus appears to be reversible with iron supplementation. The time required to develop hypertriglyceridemia in iron deficiency is longer postweaning than during suckling.     

Fatty acid oxidation in relation to cholesterol biosynthesis in rats

Groups of male and female rats were fed diets containing (calorie basis) 2% corn oil (low-fat, LF), 42% corn oil (CO) or 2% corn oil plus 40% beef tallow (BT) for 2 weeks. Then rats of each sex and diet group were given an intraperitoneal injection of¹⁴C-acetate,- stearate- oleate or linoleate. Acetate incorporation into cholesterol and rate of oxidation of each fatty acid were determined. Specific activity of cholesterol was higher in females than males, higher with 40% lipid in the diet than with 2% corn oil and higher for CO than BT. Linoleate was oxidized more rapidly than oleate which exceeded stearate. An index of dietary lipid oxidation was computed based on fatty acid oxidation rate, per cent of each fatty acid in the diet and per cent of lipid calories in the diet. Serum cholesterol-¹⁴C was found to be proportional to dietary lipid oxidation index.     

Fatty acid composition of liver lipids in rats fed brominated fatty acids

Feeding rats diets containing brominated corn oil or di- or tetrabromostearate as the monoglyceride produced changes in fatty acid composition of liver lipids. Those changes associated with the feeding of brominated corn oil or tetrabromosterates could be explained by the accumulation of triglyceride, and the changes associated with the feeding of dibromostearate could result from the proliferation of a membrane system. A unique response to the feeding of diets containing brominated corn oil is an increase in the level of γ-linolenic acid.     

Reduction of hepatic stearoyl-CoA desaturase activity in rats fed iron-deficient diets

The effect of feeding iron-deficient diets to rats on the hepatic stearoyl-CoA desaturase activity was examined since iron is present in the Δ9 desaturation system. Separate groups of rats were fed low iron diets without fat (FF-Fe) or containing either 14% hydrogenated coconut oil (HCNO-Fe) or 14% corn oil (CO-Fe) for 10 weeks. Diets supplemented with iron (FF+Fe, HCNO+Fe and CO+Fe) were fed to the corresponding control groups. Stearoyl-CoA desaturase activity in the liver microsomes of rats in the CO+Fe group (2.55±0.17 nmol oleate produced/min/mg protein) was about half of that in the HCNO+Fe (4.76±0.15) and FF+Fe (5.38±0.18) diet groups. In rats which were fed iron-deficient diets, hepatic desaturase levels were reduced significantly as compared to those of controls (1.0±0.06, CO-Fe; 2.11±0.13, HCNO-Fe; 3.65±0.1, FF-Fe). The hemoglobin (Hb) and hematocrit (Hct) levels in blood showed moderate iron depletion only in the CO-Fe group. Hence, dietary polyunsaturated fat promotes the onset of iron deficiency. Furthermore, even before the blood Hb and Hct values express iron depletion, the effect of feeding low iron diets was observed by the reduction of hepatic Δ9 desaturase activity in rats fed HCNO-Fe and FF-Fe diets.