It was confirmed that the main source of energy for growth and development in the neonatal period was fat. Considerable attention was paid to the development of both white adipose tissue (WAT) and brown adipose tissue (BAT) in the rat and human newborn. Cholesterol metabolism during development was studied in the liver, the small intestine and both WAT and BAT. Brown adipose tissue of rats and adipose tissue from human newborns require carnitine for optimum respiration and fatty acid oxidation. Surprisingly, carnitine enhanced lipolysis in human newborn adipose tissue, Intravenously-fed newborn patients exhibited a rapid decrease of plasma level of carnitine and its esters, indicating a greater requirement for exogenous carnitine than in adult subjects (52 references)
Abnormal cholesterol metabolism, including low intestinal cholesterol absorption and elevated synthesis, is prevalent in diabetes, obesity, hyperlipidemia, and the metabolic syndrome. Diet-induced weight loss improves cholesterol absorption in these populations, but it is not known if endurance exercise training also improves cholesterol homeostasis. To examine this, we measured circulating levels of campesterol, sitosterol, and lathosterol in 65 sedentary subjects (average age 59 years; with at least one metabolic syndrome risk factor) before and after 6 months of endurance exercise training. Campesterol and sitosterol are plant sterols that correlate with intestinal cholesterol absorption, while lathosterol is a marker of whole body cholesterol synthesis. Following the intervention, plant sterol levels were increased by 10 % (p<0.05), but there was no change in plasma lathosterol. In addition, total and LDL-cholesterol were reduced by 0.16 mmol and 0.10 mmol, respectively (p<0.05), while HDL-C levels increased by 0.09 mmol (p<0.05). Furthermore, the change in plant sterols was positively correlated with the change in VO2 max (r = 0.310, p=0.004), independent of other metabolic syndrome risk factors. These data indicate that exercise training reduces plasma cholesterol despite increasing cholesterol absorption in subjects with metabolic syndrome risk factors., K. R. Wilund ... [et al.]., and Obsahuje seznam literatury
The Prague Hereditary Hypercholesterolaemic (PHHC) rat is a strain of the Wistar rat very sensitive to dietary cholesterol.The dynamics of changes in serum and liver lipids and lecithin : cholesterol acyltransferase (LCAT) were studied immediatelly after the switch to a high cholesterol diet. Immediate cumulation of free and esterified cholesterol in the liver after the increase in alimentary cholesterol intake is supposed to be the regulating step leading to a subsequent increase in serum cholesterol concentration. Activity of LCAT was negatively correlated to the concentration of free cholesterol in the liver, very early after the cholesterol diet was introduced, a possibility of a down regulation of enzyme synthesis similarly to the regulation of synthesis of cholesterol in hepatocytes was observed.
Imprinting of an increased sensitivity to a high-fat, high cholesterol (HFHC) diet by dietary manipulation in early life was studied in two strains of rat, i.e. in Prague hereditary hypercholesterolaemic rats (PHHC) and Wistar rats, from which the PHHC strain was obtained by selection and inbreeding. Whereas no effect of early life nutrition on cholesterolaemia induced by HFHC diet was found in control Wistar rats, significant imprinting of increased sensitivity to the same diet was demonstrated in PHHC rats. This imprinting increased the concentration of apoB- containing lipoprotein and liver cholesterol concentration in animals fed HFHC diet for a period of two months after weaning. No effect of this imprinting on endogenous cholesterol synthesis could be demonstrated. It is concluded that imprinting of increased sensitivity to HFHC diet by dietary manipulation in early life is not a general phenomenon but depends on underlying genetic predisposition(s).
Prague hereditary hypercholesterolemic (PHHC) rat – rat strain crossbred from Wistar rats – is a model of hypercholesterolemia induced by dietary cholesterol. Importantly, no bile salts and/or antithyroid drugs need to be added to the diet together with cholesterol to induce hypercholesterolemia. PHHC rats have only modestly increased cholesterolemia when fed a standard chow and develop hypercholesterolem ia exceeding 5 mmol/l on 2 % cholesterol diet. Most of the cholesterol in hypercholesterolemic PHHC rats is found in VLDL that become enriched with cholesterol (VLDL-C/VLDL-TG ratio > 1.0). Concurrently, both IDL and LDL concentrations rise without any increase in HDL. PHHC rats do not markedly differ from Wistar rats in the activities of enzymes involved in intravascular remodelation of lipoproteins (lipoprotein and hepatic lipases and lecithin:cholesterol acyltransferase), LDL catabolism, cholesterol turnover rate and absorption of dietary cholesterol. The feeding rats with cholesterol diet results in development of fatty liver in spite of suppression of cholesterol synthesis. However, even though cholesterolemia in PHHC rats is comparable to human hypercholesterolemia, the PHHC rats do not develop atherosclerosis even after 6 months on 2 % cholesterol diet. Importantly, the crossbreeding experiments documented that hypercholesterolemia of PHHC rats is polygenic. To identify the genes that may be involved in pathogenesis of hypercholesterolemia in this strain, the studies of microarray gene expression in the liver of PHHC rats are currently in progress., J. Kovář ... [et al.]., and Obsahuje seznam literatury