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At least 37 records · Page 2Linked to original sources
PubMed1976

Stoppage of glycogenesis and "over-shoot" of induction of lipogenesis and its related enzyme activities in the liver of fasted-refed rats.

To elucidate the causes of changes of carbohydrate metabolic pathways, the time course of utilization of dietary [U-14C]sucrose and induction of enzyme activities in the livers of rats were investigated. Adult male rats of BHE strain were refed after a fast of 2 days. The nutritionally complete refeeding diet contained 60% sucrose as the only source of carbohydrate. [U-14C]Sucrose was included in the diet on either day 1 or day 2, or both of refeeding. During the first day of refeeding, the radioactivity was incorporated mainly into liver glycogen which rose to over 100 mg/g. During the second day, little 14C appeared in the liver glycogen, which decreased sharply while glucose-6-phosphatase activity increased. The glycogenic pathway thus appeared to be blocked. On the other hand, 14C incorporation in the liver fat was minimal during the first day, but was quite extensive during the second day of refeeding. The enhanced lipogenesis was accompanied by large increases of activities of glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase and NADP-malic dehydrogenase. Results clearly indicate that the carbohydrate load in the liver of intact animals was initially metabolized by the glycogenic pathway. When glycogenesis stopped, carbohydrate was metabolized differently. The enhanced incorporation of [U-14C]sucrose into liver lipids indicates an increased formation of acetyl CoA and an accelerated formation and use of NADPH, probably from increasing dehydrogenase activities. Our data suggest that the blockage of synthesis of glycogen with the continuation of carbohydrate load was a primary cause in over-shooting induction of hepatic dehydrogenase activities and lipogenesis.

Adipose Tissue↗
PubMed1977

Daily rhythms of lipogenesis in fat and lean white-throated sparrows Zonotrichia albicollis.

Lipogenesis was assayed at 6 times a day in the migratory white-throated sparrow Zonotrichia albicollis by measuring the incorporation of label in liver and body lipid 4 h after injection of [3H] acetate. There were daily rhythms of 3H incorporation by liver lipid both in fat birds in the vernal migratory condition and in lean birds in the summer photorefractory condition. Most of the liver lipid incorporation of 3H was restricted to the late afternoon and early evening in both the fat and lean birds. In addition, the total liver incorporation was similar for both groups. On the other hand, nearly twice as much 3H was incorporated in the body lipid of fat birds as in that of lean birds, and a daily rhythm was present only in fat sparrows. Injections of prolactin given simultaneously with [3H] acetate early during the day (at a time when daily injections of the hormone can cause severe losses in body fat stores) drastically reduces liver and body lipid incorporation of 3H. However, injections of prolactin during the afternoon (when daily injections of the hormone produce large increases in body fat stores) have no apparent influence on the incorporation of label. Our results indicate that a principal difference between lean and fat birds resides in a greater capacity in fat birds to transport triglycerides from the liver, in which they are produced, to the body storage depots. The daily rhythm of prolactin in some temporal relations may cause fattening by increasing the transport capacity or cause loss in fat stores in other temporal relations by directly inhibiting hepatic lipogenesis.

Acetates↗
PubMed1977

Effects of maternal dodecanoic or lauric acid (C12:0) feeding on milk fatty acid secretion and lipogenesis in the suckling rat.

Lauric acid feeding induced large alterations in mammary gland fatty acid secretion. It was highly incorported in milk triglycerides, suggesting that mammary gland was not able to efficiently regulate the qualitative aspects of medium-chain fatty acid secretion. These modifications in milk fatty acid secretion did not alter pup growth, lipogenesis balance or the classic parameters of the pup liver during the suckling period. Nevertheless, maternal lauric acid feeding induced important alterations in the qualitative aspects of pup lipogenesis before weaning.

Animal Feed↗
PubMed1978

Lipogenesis in the brain of thiamine-deficient rat pups.

(1) The effect of thiamine deficiency during pregnancy and lactation on lipogenesis in the brain of rat pups was determined. (2) Acetate incorporation to brain lipids in thiamine-deficient rats in vivo was no less than in pair fed control rats, apart from slightly reduced fatty acid synthesis in the cerebrum. (3) Glucose incorporation to brain lipids in vivo was considerably reduced in thiamine-deficient pups. (4) The inducible NADP dependent malic enzyme activity was increased in thiamine-deficient pup brains. (5) The synthesis of acetyl-CoA appears to be the rate limiting step in lipogenesis in thiamine-deficient pup brains.

Acetates↗
PubMed1976

[Fetal and neo-natal development of brown adipose tissue in guinea pigs and rats. Feto-maternal or milk transfer of essential fatty acids : lipogenesis and morphology (author's transl)].

Brown adipose tissue (BAT) lipogenesis (fatty acid, glycerol and CO2 synthesis) and its morphology determined by optical microscopy, were studied in guinea pigs and rats during intra-uterine life and during the suckling period. Following the receptor induction and after the commencement of the hormone sensitive adenylate-cyclase/lipase system (i.e. on the 60th day in guinea pigs, on the 20th day in rats), the fetal BAT releases fatty acids (NEFA) and is capable of allowing the non-shivering thermogenesis. When the maternal diet and, consequently, the fetal or neonatal BAT are supplied with considerable linoleic acid, NEFA contain a large proportion of essential fatty acids. In vitro, the greater the linoleic acid concentration in these NEFA, the less inhibited is the lipogenesis from (2-14C) pyruvate. Thus, in periods just preceding or succeeding birth, fatty acid and glycerol synthesis are higher when the feto-maternal and/or the milk supply are enriched in linoleic acid than when they contain a large proportion of endogenous fatty acids. Morphological studies indicate that the adipose cell evolution could be nonidentical in BAT more or less enriched in essential fatty acids. Linoleic enriched BAT (of animals born to females kept on a sunflower oil diet) seemed to be in a healthy physiological state at birth, perhaps due to rapid lipid renewal and synthesis in their membranes. The control BAT (of animals born to females kept on a lard diet) appeared loaded with fats and in a worse conservation state at the same age.

Adipose Tissue, Brown↗
PubMed1979

Lipogenesis in human adipose tissue in vitro: effect of fat cell size on some enzymatic activities.

The incorporation of [1-C14] palmitate into palmitoyl CoA and triglycerides by homogenates of human adipose tissue have been studied. Adipose tissue samples were taken from three sites varying in adipocytes size (omentum, subcutaneous abdominal wall, buttock). The donors were normal weight women of constant weight. A significant positive correlation was found between initial velocity of palmitoyl CoA synthetase (EC 6.2.1.3) and total [1-C14] palmitate incorporation into triglycerides on one hand and adipocyte cell size on the other hand : these relations with cell size were apparent both within and between individuals. The mechanism of this "size effect" which is unrelated to the higher protein content of larger cells, is still unexplained. Lipogenesis, like most of the metabolic activities of adipose tissue increases with enlarging cell size. Acceleration of a lipogenesis-lipolysis cycle could constitute an energy wasting system able to limit the volume of the adipocytes.

Adipose Tissue↗
PubMed1979

Effects of 2,4-dihydroxybutyrate on lipogenesis in rat hepatocytes.

Hepatocytes were prepared from rats fasted 2 days and refed a high carbohydrate diet for 1 day. These cells contained very high levels of glycogen (about half the defatted dry weight) and carried out high rates of lipogenesis (up to 800 micron at tritium incorporation from 3HOH/g (defatted dry weight)/h), even in the absence of added substrates. Pentose cycle flux was estimated by a method involving the use of [1-14C]galactose (Rognstad, R. (1976) Int. J. Biochem. 7, 221-228). In hepatocytes from normal fasted refed rats, the amount of NADPH produced by the pentose cycle was sufficient for about one-half to three-fourths of that required for fatty acid synthesis. 2,4-Dihydroxybutyrate, a malic enzyme inhibitor (Schimerlik, M.I. & Cleland, W.W. (1977) Biochemistry 16, 565-570) markedly depressed the randomization of 14C in lactate from [6-14C]hexoses, indicating an inhibition of the pyruvate cycle. 2,4-Dihydroxybutyrate (10 mM) had only a slight inhibitory effect on overall lipogenesis, but increased the rate of the pentose cycle by 40 to 90%.

Animals↗
PubMed1979

Lipogenesis in vivo in lean and genetically obese (ob/ob) mice fed on diets with a high fat content.

The effect of variations in the fat content of the diet on fatty acid synthesis in vivo was determined in lean and genetically obese mice, using the 3H2O incorporation technique. In both lean and obese mice the rate of fatty acid synthesis was higher between 21.00 - 22.00 h than between 09.00 - 10.00 h. When lean mice were given a high fat (low-carbohydrate) diet the rate of lipogenesis in adipose tissue and rest of carcass (whole mouse minus liver and adipose tissue) was less than in similar mice given a high-carbohydrate (low-fat) diet. In obese mice, the rate of lipogenesis in adipose tissue and rest of carcass was unaffected, but liver fatty acid synthesis was reduced. In lean mice fed on diets containing a constant percentage of carbohydrate and protein, increasing the fat content of the diet (and decreasing the proportion of cellulose) produced a decrease in fatty acid synthesis in liver, adipose tissue and rest of carcass, when the measurements were made during the night-time feeding period. During the day-time, the effect of increasing the fat content of the diet was less marked. In obese mice, dietary fat did not supress either the day-time or the post-prandial night-time rate of fatty acid synthesis. It is suggested that the hyperinsulinaemia in obese mice may be able to overcome the inhibitory effect of dietary fat on fatty acid syntheses.

Adipose Tissue↗
PubMed1978

[Participation of glutamate and alanine in amino acid biosynthesis, in lipogenesis, and in gluconeogenesis in the brain].

The participation of glutamate and alanine in lipogenesis and gluconeogenesis of brain was investigated. 5(14)C glutamate was injected intracisternally in an amount of 5 mcCu/l g tissue and 3(14)C-alanine was injected subcutaneously 30 mcCu/100 g body weight. Labels from glutamate and alanine were recovered in different lipid franctions -- in phospholipids, glycerides, free fatty acids and cholesterol, as well as in glucose and glycogen. An intensive incorporation of label from 5(14)C glutamate into various amino acids--aspartic acid, glutamine, serine, glycine and alanine--was demonstrated. The data presented indicate the participation of amino acids in lipogenesis and gluconeogenesis of brain.

Alanine↗
PubMed1979

Lipogenesis in Ehrlich ascites tumor cells under anaerobic culture conditions.

Anaerobic culture conditions (95% argon/5% CO2) caused a slightly greater increase in total lipids of Ehrlich ascites tumor cells than a gas phase of 20% O2, 75% N2, 5% CO2. Whereas the rate of [U-14C]acetate incorporation into total lipids and lipid-subclasses rose markedly in the absence of oxygen, a drastic decrease of [U-14C]pyruvate and [1-14C]octanoate incorporation as well as a 30% reduction of 3H incorporation into lipids from tritiated water were observed under these conditions. Since profound changes in the metabolic state of cells cause alterations in the specific activity of the acetyl-CoA pool but do not alter the specific activity of intracellular water, this precursor is considered to be an adequate monitor for lipogenesis under aerobic and anaerobic culture conditions. Therefore, it is concluded that Ehrlich ascites tumor cells are not able to reoxidize NADH/NADPH in the absence of oxygen by a stimulation of biosynthesis of fatty acids as is discussed to be the case in normal cells. The slight increase in total lipids of anaerobically cultured cells seems to be the result of an imbalance between normal uptake and impaired utilization of lipids from serum-supplemented culture medium.

Anaerobiosis↗
PubMed1978

Placental enzymes of glycolysis, gluconeogenesis and lipogenesis in the diabetic rat and in starvation. Comparison with maternal and foetal liver.

The activity of several regulatory enzymes representing the pathways of glycolysis, gluconeogenesis, NADPH generation and lipogenesis was measured in rat placenta maternal and foetal livers on the 20th day of gestation. Streptozotocin diabetes, induced on the 12th day of gestation, or 48 h of fasting did not induce adaptive changes in the activity of placental enzymes while producing a typical insulin deficiency pattern in maternal liver. Foetal liver enzyme activities were unaffected by fasting and in diabetes showed changes suggestive of foetal hyperinsulinaemia. A small increase was observed in the activity of placental pyruvate kinase and a small decrease in that of PEP carboxylase in diabetic and in glucocorticoid-treated rats; these changes were reciprocal to those in the maternal liver and were attributed to hyperglycaemia, as was the increase in placental glycogen. Lack of response to insulin deficiency and to other endocrine alterations indicates that placenta is not sensitive to stimuli which induce adaptive alterations in hepatic enzymes. The only consistent change found in placental enzyme activities was a decrease associated with gestational age.

Animals↗
PubMed1975

Lipogenesis by intact hepatocytes from normal and diabetic rats.

Intact hepatocytes isolated from livers of diabetic rats demonstrate the characteristic decreased lipogenic capacities as compared to normal. Administration of insulin to diabetic rats restores these capacities to near normal levels. The results emphasize the potential that the hepatocyte system has for the study of hormonal regulation of lipogenesis.

Acetates↗
PubMed1979

Lipogenesis in the developing brain: utilization of radioactive leucine, isoleucine, octanoic acid and beta-hydroxybutyric acid.

Incorporation of radioactivity from intracranially injected radioactive leucine, isoleucine (ketogenic amino acids), octanoic acid and beta-hydroxybutyric acid into the brain lipids of 15 to 16 day-old rats was examined. The results showed that radioactivity from all the above precursors was incorporated into brain lipids. Radioactivity from injected isoleucine was incorporated into odd numbered fatty acids indicating an alternate pathway to alpha-oxidation for the biosynthesis of these fatty acids in the brain. For some as yet unclear reasons, a substantial portion of the radioactivity from injected octanoic acid was incorporated into free fatty acids. Utilization of these compounds for providing carbon for lipogenesis during development under unstressed normal conditions is discussed.

Animals↗
PubMed1977

Stimulation of hepatic lipogenesis by eicosa-5,8,11,14-tetraynoic acid in mice fed a high linoleate diet.

Liver slices, from mice fasted for one day and then refed for three days either a 15% corn oil diet or a 15% corn oil diet containing eicosa-5,8,11,14-tetraynoic acid (TYA), were incubated with [1-14C] acetate or [3H] H2O to determine lipogenic capacity. Dietary TYA produced a twofold stimulation in fatty acid and cholesterol synthesis. TYA also caused an increase in the relative proportion of linoleate (C18:2) and a decrease in that of arachidonate (C20:4) in liver. Thus, (a) despite high levels of C18:2, hepatic lipogenesis can be increased, and (b) even short term feeding of TYA can alter the hepatic fatty acid composition presumably by inhibition of arachidonate synthesis from linoleate.

Animals↗
PubMed1975

Rapid modulation of lipogenesis by clofibrate in rat and monkey hepatocytes.

Previous studies have proposed various possible mechanisms for the hypolipidemic actions of clofibrate. In the present study, isolated liver cells freshly prepared from rats and squirrel monkeys were used to investigate the acute effects of sodium clofibrate (sodium chlorophenoxyisobutyrate) on hepatic lipogenesis. Incubation of liver cells with levels of the drug (1 mM) known to lower plasma lipid level in vivo produced a rapid inhibition of [14C]acetate incorporation into cellular lipids. The degree of inhibition caused by the drug was not diminished by preincubation with an excess of unlabeled acetate. Conversion of [14C]acetate to 14CO2 was not significantly altered by sodium clofibrate at 1--3 mM levels, but was decreased at 5--10 mM levels. Incorporation of [14C]acetate into all lipid classes was suppressed by this agent, but inhibition of sterol synthesis was more pronounced than that of fatty acids. Sodium clofibrate (1 mM) reduced the synthesis of sterols from either labeled acetate or labeled mevalonate to a similar degree, but the decline was augmented in each case by a 30-min preincubation of the cells with sodium clofibrate. Addition of fatty acids to cell incubations stimulated sterol generation from [14C] acetate or from [3H] mevalonate, but did not reverse the inhibitory effects of the drug. These results suggest (a) the sodium clofibrate rapidly interferes with hepatic fatty acid and sterol synthesis by direct or indirect actions at diverse loci; (b) that these effects probably occur after acetyl-CoA formation and do not stem from precursor pool dilution; (c) that sodium clofibrate diminishes sterol production at post-mevalonic and perhaps also at pre-mevalonic sites; (d) that a similar pattern of inhibition occurs with sodium clofibrate in the presence of added fatty acids; and (e) that rat and primate livers demonstrate similar metabolic responses to the drug.

Acetates↗
PubMed1979

Regulation of lipogenesis in adipocytes. Independent effects of thyroid hormones, cyclic AMP and insulin on the uptake of deoxy-D-glucose.

Thyroidectomy is known to enhance fat cell phosphodiesterase activity; as a result, the response to lipolytic hormones is markedly reduced. Thyroidectomy also stimulates overall lipogenesis and the uptake of glucose: the present experiments investigated whether there was a correlation between cyclic AMP and glucose uptake. The parameter measured was the transport and phosphorylation (uptake) of deoxy-D-glucose in the presence of two modifiers of the cyclic AMP pool: phosphodiesterase inhibitors and the analogue, dibutyryl cyclic AMP. The inhibition by methylxanthines and dibutyryl cyclic AMP of deoxy-D-glucose uptake observed, was the same in fat cells from normal and thyroidectomized rats: the latter nonetheless still maintained their enhanced glucose uptake. It was therefore concluded that thyroid hormones and cyclic AMP control this step by different, separate pathways. Insulin, well known for its lipogenic effect, enhanced deoxy-D-glucose uptake in fat cells from both normal and thyroidectomized rats to the same extent (about 40%). An additive effect of thyroidectomy and insulin on glucose uptake was thus demonstrated. These results imply that glucose uptake in the adipocyte is controlled by at least three factors: thyroid hormones, cyclic AMP and insulin, each of which can act independently. Maximum glucose uptake is achieved in the presence of a combination of low concentrations of cyclic AMP, of insulin, and in the absence of thyroid hormones.

Adipose Tissue↗
PubMed1978

Early changes in gluconeogenesis and lipogenesis following destruction of the ventromedial hypothalamic nuclei.

Young male rats were injected with tritiated water 6 hr after destruction of the ventromedial hypothalamic nuclei (VMN). One hour later they were sacrificed and the incorporation of tritium into liver and carcass lipids, proteins, and glycogen and into plasma glucose and proteins was measured. It was found that lesioned rats showed increased incorporation into carcass and liver lipid, liver and plasma protein and plasma glucose. Conclusions are that the processes of lipogenesis and gluconeogenesis are accelerated within 6 hr after VMN destruction.

Animals↗
PubMed1978

Control of glucose metabolism in isolated acini of the lactating mamary gland of the rat. Effects of oleate on glucose utilization and lipogenesis.

Oleate (1mM) had only small inhibitory effects on glucose utilization and lipogenesis in acini isolated from rat mammary gland. Esterification of [1-14C]oleate was unaffected by insulin but were decreased by 60% by acetoacetate (2mM). Glycerol (1mM), but not insulin, relieved this inhibition. These experiments provide further support for the role of acetoacetate in regulating substrate utilization by the gland.

Acetoacetates↗